Herpes human papilloma. Genital herpetic and papillomavirus infections. HSV and HPV what is it in women

Most people have heard about a disease such as herpes. There is a lot of information, but only a few can say exactly what it is. Doctors always say that any infection is always easier to prevent than to treat. To know how to deal with infections such as papilloma virus (HPV) and herpes, you must first understand what kind of virus it is and where it comes from in the human body.

Basic information

The name of the disease papillomavirus (HPV) and herpes, or as they are called in other words, human papillomavirus, comes from the Latin meaning Human Papillomavirus HPV. This is a special group of viruses belonging to the papillomavirus family. In total, this group includes 5 genera.

In simpler words, the papilloma virus is called a herpes infection and belongs to a group of diseases that originate from the herpes simplex virus. The disease is characterized by damage not only to the mucous membrane, but also to the entire central nervous system, skin, and other human systems and organs.

The word “herpes” translated from Greek means creeping. This disease was first discussed in Greece. The healer of this country described in detail the symptoms of this disease back in the 1st century BC. He observed the rash on the lips.

The papilloma virus is a herpes infection and is localized externally on the genitals; it is designated genital herpes or GG. Today, this disease is a significant problem in clinical virology and gynecology. Doctors in Russia, the CIS and doctors from other countries are looking for ways to combat this disease.

We must remember! The danger of the papilloma virus is associated with reproductive functions. A woman infected with herpes often either suffers from infertility or the inability to bear a child. Subsequently, the virus can develop into dysplasia and lead to cervical cancer.

Classification of herpes

Any disease begins with a virus entering the body. If everything is left to chance and the disease is not dealt with, the disease will begin to develop and gradually move into subsequent stages that are more dangerous for people. The same thing happens with herpes.

The virus manifests itself in the following forms of the virus:

• herpes simplex type 1;
• herpes simplex type 2;
• Varicella zoster or in other words called shingles virus;
• Epstein-Barr;
• cytomegalovirus;
• human herpes;
• human herpes type eight;
• papillomas.

Each form is dangerous in its own way and causes complications on certain organs and systems.

Features of papilloma virus (HPV)

This virus is one of the most common infections. Infection occurs through sexual contact. The virus is highly specific and has the property of not only infecting, but also easily transforming into epithelial cells.

In total, more than a hundred types of HPV have been found, with 35 species capable of infecting the human urogenital tract. The virus instantly affects the integumentary epithelium and mucous membrane of the genital organs.

HPV infection is one of the most common; it infects most of the world's people, and this is precisely the group of viruses that provoke the occurrence of tumors and the development of cancer. It has been proven that 95 percent of squamous cells of cervical cancer contain HPV DNA. Over the past ten years, infections have increased by 12 percent.

Etiology

Papillomaviruses belong to the papovirus family. They are capable of infecting almost all vertebrates. Virions (or virus cells) do not have an envelope; their diameter ranges from 50 to 55 nm. The virus is well preserved at temperatures up to 50 degrees Celsius for half an hour and is resistant to alcohol ethers. During the replication cycle, from 8 to 10 products of protein origin are expressed.

HPV types are classified, depending on oncological activity, as follows:

Mechanism of infection

Infection occurs as follows:

• the HPV virus enters the basal cells of the body;
• the cell structure gradually begins to change;
• cells divide, grow;
• a papilloma appears or, translated from Latin, a certain “nipple” is formed, and translated from Greek – “tumor”, that is, a new phenomenon, the so-called genital wart, is formed.

Infection

There are several ways to become infected with the virus:

1. Sexual intercourse, which also includes anal sex and oral-genital contact.
2. Infection during childbirth. Newborns become infected from their mother.
3. Sometimes infection occurs through household means; one touch is enough. That is, pools, baths, toilets, and gyms can become places of infection. Viruses can enter through scratches or abrasions on the skin.
4. Cases of self-infection or autoinoculation have been reported. Possibly during shaving and hair removal.

Therefore, you can protect yourself by observing hygiene and sanitary rules.

Risk factors

There are many factors that provoke the spread of infection. These include:

• unfavorable socio-economic situation;
• sexual behavior;
• disruption and weakening of the immune system;
• infection with sexually transmitted diseases (gonorrhea, syphilis, chlamydia, etc.);
• young age;
• pregnancy;
• bad habits (alcohol, smoking);
• hypo- and vitamin deficiency.

Homosexuals are most likely to contract HPV infection.

Forms of the disease

The incubation period for anogenital warts ranges from 1 to 90 days. Usually, HPV infection does not appear immediately; symptoms do not appear at first. HPV infection of an oncological nature takes from 5 to 30 years.

The forms of the disease are as follows:

1. Clinical (it can be seen with the naked eye);
2. Subclinical (there are no symptoms, cannot be seen with the naked eye, can only be identified as a result of special studies);
3. Latent (usually in this form there are no changes in HPV DNA);
4. Cervical or also called intraepithelial neoplasia.

Clinically, HPV type infections manifest themselves as follows:

• as single genital warts;
• as fibroepithelial neoplasms on the skin and mucous membranes;
• as single nodules on a broad base resembling a “cauliflower” shape.

Endophytic condylomas are flat and inverted, most often located on the cervix, and in appearance they resemble raised plaques. It can only be determined with extended colposcopy.

In the subclinical form, small flat warts form; the disease can only be diagnosed by colposcopy.

Treatment

If viruses are in hibernation, then it is impossible to get rid of them. No cure has yet been invented for this disease. You can only expel viruses when they are active. There have been cases where HPV disappeared on its own. But this only applies to herpes viruses that constantly live in the body.

Treatment is based on achieving remission, or in other words, keeping the infection latent for as long as possible, and in no way allowing the disease to develop.

Viruses reach their active phase when the body is vulnerable and the immune system is weakened. That is, stress, illness, pregnancy and menstrual days.

The best treatment for herpes and papillomavirus is constant immune support. A healthy, correct lifestyle helps protect the body. If, nevertheless, the virus makes itself felt and “woke up” in the body, then you should immediately start taking immunostimulants.

There is good news that a vaccine against herpes viruses has already been created, but it can only be given to those people who are not infected.

Human papillomavirus (HPV)

Human papillomavirus is an epitheliotropic virus. The places where it is most often affected include the skin, genital mucosa, and oral cavity. Currently, more than 100 types of HPV are known. According to clinical manifestations, they are divided into cutaneous and anogenital types.

Papillomaviruses are the only group of viruses that induce tumor formation in natural conditions. In particular, they contribute to the degeneration of papilloma into carcinoma.

According to the degree of malignancy, papillomaviruses are divided into 3 groups: HPV of high, medium and low oncogenic risk. The most common types of HPV with high oncogenic risk are: 16, 18, 31, 33, 35, 39, 45, 52, 58, 59, 67.

Routes of transmission of HPV:

• Household route of infection (virus penetration through microtraumas in the skin);
• Sexual (it has been proven that the risk of infection is higher in sexually active women);
• The virus can be transmitted from mother to child during childbirth.

Clinical manifestations

Some types of HPV viruses cause the familiar “warts” (benign growths of integumentary tissue), while others cause genital warts. The latter also belong to benign tissue growths, but in some cases they can become malignant, in other words, lead to cancer.

The incubation period for genital HPV infection ranges from 3 to 8 months. In most cases, HPV infection is short-term and resolves on its own within 12-24 months (if there is no re-infection), which is determined by the activity of antiviral immunity.

As a rule, a woman can become infected with the papilloma virus in her youth at the beginning of sexual activity, but the virus does not immediately and relatively rarely manifest its pathogenicity, remaining for many years in a hidden (latent) state. Activation of the virus and the occurrence of a malignant neoplasm of the cervix can occur many years later - at 50-70 years of age under the influence of a wide variety of provoking factors.

Diagnostics

HPV infection is very insidious, and the changes associated with it that precede cancer not only do not cause any concern or discomfort, but are often not detected during a routine examination by a gynecologist. The human papillomavirus test (HPV test) is a reliable assistant to the doctor: identifying the virus draws the doctor’s special attention to the problem of the possible development of cancer and forces additional examinations. It should be added that at the moment, many European countries use cervical screening, which includes regular examination of women for the virus (HPV test) and/or Pap test (determines changes in cells associated with the virus). Every woman undergoes such an examination once every 3-5 years. Experience in a number of countries has shown that this practice can reduce the likelihood of developing cervical cancer by more than 1,000 times.

HSV and HPV what is it in women

I am 19 years old. I was tested for hidden infections and found dysbacteriosis, ureaplasma, HPV-16 and HSV-1,2. Treatment was prescribed for the first two diseases + ointment for herpes (it popped up on the labia, two gynecologists persistently called it irritation after shaving, as if it became clear only after tests). The worst thing for me is to find out that I have HPV, since I heard from Malysheva’s programs that it leads to cervical cancer, and there is also erosion. And in general, please tell me, are herpes and HPV curable?

So much infection. Is HPV also sexually transmitted?

There is no cure for either one. You can treat the manifestations of viruses, increase immunity, suppress the activity of viruses. But the viruses themselves will remain in your body and you will infect your partners.
All oncogenic HPVs can cause cancer. Or they may not call.

3. Sagittarius is the zodiac scribe

“The same bullshit with HPV(“

I have the same thing: HPV 16, the herpes virus is recurrent, although no matter how many times I took tests (smear), herpes was never found. and the bubbles of herpetic origin pop up, the gynecologists themselves examined them. This is such crap. You need to increase your immunity. For HPV I was injected with allakin-alpha, 6 ampoules every other day, very painful. My friend also injected herself with this drug for HPV and fainted from the pain; I tolerated the injections more or less normally. For herpes rashes: Genferon suppositories 1,000,000 rectally, Herpferon ointment or acyclovir, acyclovir tablets, Immunal drops! I am undergoing complex treatment.

It has not been proven that HPV leads to cancer. It’s just that half of those with cancer were diagnosed with this virus.

Tina) It has been proven that a certain type of HPV leads to cervical cancer, etc.

Guest) there is so much infection) Check yourself first!) transmission of HPV and HSV can occur not only through sexual contact but also through household contact!

And I found this article that there is no clear evidence that HPV causes cancer
http://magov.net/blog/zagovor/1625.html

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Herpes and papillomatosis: similarities and differences, causes, relationships

Papilloma and herpes are viral diseases that have a similar clinical picture and develop for identical reasons. According to statistics, up to 90% of adults are infected with one or both pathologies, while not everyone develops an active form of the disease. How to distinguish herpes simplex (HSV) from human papillomavirus (HPV)?

Ways of infection with herpes and HPV

The main feature by which diseases differ is the method of infection. The first spreads through airborne droplets, the second through skin contact. In this case, the disease must be in an active form. What does it mean?

Most of the time, the causative agent of herpes or papilloma hides in remote places of the human body: HSV-1 (simple) is found in the brain, genital - in the sacrum, and HPV - in the mucous membrane of the genital organs. If a person has a strong immune system, the virus may never manifest itself, but when the protective functions weaken, the first manifestations of pathology on the skin begin to appear.

Thus, the significant difference between the diseases is that even young children can catch herpes. Papillomavirus is more often spread through sexual contact, since the rashes are localized mainly in the genital area.

Moreover, the presence of one of the pathologies does not in any way affect the infection of the other - HPV does not cause herpes and vice versa. These are two different viruses that manifest themselves for similar reasons - due to weakened immunity, stress, overwork, smoking, etc.

Symptoms of HPV and HSV

Another way to distinguish viruses is the appearance of rashes in the active phase of the disease.

Herpes simplex looks like transparent blisters in the area of ​​the mouth and wings of the nose; the skin around the rash becomes inflamed. Over time, the contents of the blisters darken and they burst, opening ulcers. Without treatment, the active course of the disease can last up to 12 weeks.

Papillomavirus can appear on any part of the body, but most often provokes the appearance of growths near the genitals. If the active phase of the disease occurs inside the vagina of a woman giving birth, the child can pick up the pathogen during childbirth. The rashes are papillomas - processes on epithelial tissue. They are usually painless and have the color of the skin or mucous membrane, without standing out against its background.

Thus, herpes and papilloma viruses are similar, but they can be distinguished from each other. Despite the fact that they are easy to become infected with, they do not pose a danger to a healthy person with a strong immune system. Only a specialist can carry out differential diagnosis. If any rash appears on the body, you should contact a medical facility for examination.

Papilloma and herpes: what are the differences?

Two very common types of viral infections are transmitted through unprotected sex: HPV and HSV. Some experts are inclined to consider papillomavirus and herpes virus to be synonymous, but in fact they have more differences than similarities.

What are the types of infections?

Herpes and HPV are divided into several types. There are more than 100 strains of HPV, but there are only two subtypes of herpesvirus: herpes simplex virus (HSV, or type 1) and simplex (type 2). HSV affects the mouth area, and the second subtype provokes the development of ulcers on the genitals. Papilloma and herpes in the anogenital zone are visually very similar to each other, although the tumors are caused by completely different viruses. The statistical indicators of the prevalence of HSV and HPV also differ. Approximately 10% of adults are infected with the siplex virus. HSV is more common and affects almost 40% of the world's population. But about 70% of patients in gynecological and venereological clinics suffer from HPV.

MINISTRY OF HEALTH OF THE RF: Papillomavirus is one of the most oncogenic viruses. Papilloma can become melanoma - skin cancer!

As for symptoms, papillomavirus is asymptomatic in most cases. Genital warts appear in only 10% of cases. Less commonly, tumors can develop into cervical or penile cancer. But HSV is almost always accompanied by rashes: in the oral cavity with the first type, and in the genital area with the simplex type.

Prevention and treatment of two different viral infections

Both herpes and papillomavirus require mandatory treatment. In the first case, doctors prescribe antiviral drugs in the form of tablets to treat rashes in the genital area, and creams to treat all other areas. In severe cases, patients may take medications throughout the year, rather than just during outbreaks, to reduce the frequency of relapses. Treatment of HPV includes a course of antiviral and immunomodulatory drugs, as well as physical removal of abnormal changes in the skin.

The good news is that people can easily prevent contracting the above infections. It is enough to refrain from close relationships with unverified people (avoid kissing, treating wounds without gloves), and also use a condom during sexual intercourse. Additionally, women can get a special vaccination to prevent papillomavirus. Also at the stage of clinical trials is the Vitagerpavak vaccine, designed to protect the body from herpes infection. The first official results prove the high effectiveness of the domestic drug.

THE MINISTRY OF HEALTH WARNS: “Papillomas and warts can become melanoma at any time. "

Herpetic infection is a group of diseases caused by the herpes simplex virus, characterized by damage to the mucous membranes, skin, central nervous system, and other human organs and systems.

Herpes - translated from Greek as "creeping" - was known back in the first century BC. and was described by Roman doctors who observed characteristic rashes on the lips.

Clinical symptoms of herpetic infection are quite diverse - from short-term skin manifestations to multiple organ systemic lesions that are life-threatening.

A herpetic infection localized on the external genitalia - genital herpes (GG) - is one of the significant medical and social problems in gynecology and clinical virology, although according to statistics, the number of visits to doctors of various specialties for GG in Russia and the CIS countries is no more than 15 % of the actual incidence of the disease.

Modern observations show that genital herpes is caused by both related forms of the Herpes simplex virus. Thus, in the USA, type I herpes virus causes from 10 to 20% of genital herpes, in Japan - 35%. According to WHO, at least 22 million people suffer from chronic genital herpes infection in Russia and the CIS countries. According to data from the Department of Gynecological Endocrinology of the Scientific Center for Acceptance of the Russian Academy of Medical Sciences, during a survey of a closed population in Moscow, the frequency of HH infection in women of reproductive age in 1997 was 19.6% (Marchenko L.A., 1997).

Herpesvirus infections play one of the dominant roles in the etiology and pathogenesis of spontaneous abortions and premature births, disorders of embryo- and organogenesis. Viral infections in general and genital herpes in particular are acquiring leading importance in the formation of pathology of human reproductive function, the development of anatomical and physiological disorders in the mother and developmental anomalies in the fetus and newborn.

Herpes viruses are associated with a number of cancer diseases and can act as a cofactor in carcinogenesis, inducing the development of dysplasia and cervical cancer.

Etiology, classification, pathogenesis of herpetic infection

HSV I - mainly affects the mucous membranes and skin of exposed parts of the body (face, skin of extremities, oral mucosa, conjunctiva, etc.

HSV type II most often affects the epidermis and mucous membrane of the urogenital tract.

Infection of the sensory ganglia of the autonomic nervous system and lifelong persistence of HSV in them is the leading point in the pathogenesis of HSV. Primary infection is accompanied by replication of the virus at the site of invasion, as the pathogen penetrates the ganglia by hematogenous and oxoplasmic routes. The tropism of the virus for epithelial and nerve cells explains the polymorphism of the clinical manifestations of herpes infection.

Genital Herpes Clinic

Clinical manifestations of herpetic infection are directly dependent on the following factors:

• Localization of lesions
• Gender (women suffer more often from genital herpes)
• Age (peak incidence occurs in people over forty)
• Intensity of the inflammatory process
• Strain virulence
• The body's ability to perform protective immunological reactions

Depending on the indicated components in case of damage to the urogenital area, three stages of herpetic infection of the urogenital tract are distinguished (Kozlova V.I., Puchner A.F., M., 1995):

Stage 1 - herpes infection of the external genitalia.
Stage 2 - herpetic colpitis, cervicitis, urethritis
Stage 3 - herpetic lesions of the endometrium, uterine appendages, bladder

According to clinical and morphological manifestations, genital herpes is divided into four types:

• The first clinical episode of primary genital herpes (there are no antibodies to HSV in the blood)
• First clinical episode of existing genital herpes (presence of antibodies to HSV of one type, superinfection with HSV of another type and no history of episodes of HSV)
• Recurrent genital herpes (presence of antibodies to HSV and history of HH episodes)
• Atypical, asymptomatic

Atypical HS is found in 30-60% of cases and is characterized by a mild abortive course. The most common atypical variant of the course of HH occurs in a chronic, recurrent version of the infection, is difficult to treat, is accompanied by chronicity of the process, and impaired sexual and reproductive function in the patient.

In the typical form of genital herpes, the affected area swells, turns red, and a vesicular rash appears against this background. The blisters open after 1-2 days, weeping erosions form, which subsequently epithelialize without scarring. Patients are concerned about itching and pain in the affected area, inguinal adenopathy, systemic affects (fever, general weakness, headache, nausea). The virus is shed for one to three months after infection, mostly between the first and third week. Then comes a latent period, interpreted as recovery. Episodes of reactivation of latent virus lead to recurrent herpes infection, which is usually less severe and limited to the same location as the primary one.

It is difficult to distinguish between the primary form and the first attack of non-primary herpes. Employees at the University of Washington recommend identifying primary genital herpes by the presence of three or more signs:

• Two extragenital symptoms, including fever, myalgia, headache and nausea;
• Multiple bilateral genital lesions with severe local pain and hyperemia for 10 days or more
• Persistence of genital lesions for more than 16 days;
• Distal HSV lesions of the fingers, buttocks, oropharynx (Brow A. Et al., 1987);

Diagnosis of herpetic infection

Diagnostic examination algorithms are based on clinical and laboratory tests.

• Strokes - prints from scrapings of cells in the area of ​​damage. A diagnostic sign of herpes infection is the presence of giant multinucleated cells and changes in nuclear chromotin in smears.
• Fluorescent antibody method (MFA) to assess the number of antigen-containing cells, to detect viral antigens in infected cell cultures - PIF, RNIF - are used to detect antibodies to HSV and evaluate their dynamics in the blood serum of pregnant women.
• Enzyme-linked immunosorbent assay (ELISA) for the determination of HSV antigens in biological samples: saliva, urine, blood, cervical mucus, separated from vesicles on the skin and mucous membranes.
• Virological method the most reliable in diagnosing HSV. The material for research is obtained by isolating fluid from skin vesicles and inoculating it into a cell culture. Material from the cervical canal, urethra, cerebrospinal fluid, mucus from the throat, and breast milk are also examined. HSV multiplies in tissue culture of various origins (dicloid fibroblasts, chicken embryos, Vero cells). In infected cultures, the virus causes the formation of giant multinucleated cells; the cytopathogenic effect manifests itself on days 3–5.
• Polymerase chain reaction (PCR), hybridization reaction (HyC) is highly specific. Their main drawback is the likelihood of false-positive reactions due to contamination of the test material with foreign DNA.
• Serological diagnosis HSV in adults is of no clinical value, since 80% - 90% of the population has antibodies to HSV. The absence of antibodies to both types of HSV excludes the diagnosis of HH. If antibodies to HSV are not detected in the blood material taken during the acute period, but appear after 2-3 weeks, then we can talk about a primary herpetic infection.

When forming a diagnosis of genital herpes based on clinical and laboratory data, the following points must be taken into account:

• If an HSV infection is suspected, a virological examination of the discharge of the urogenital tract is carried out 2-3 times a month, because a single negative result does not exclude the diagnosis of GG.
• For asymptomatic forms of herpes and especially herpetic infection of the internal genital organs, it is necessary to examine the maximum number of samples of biological materials: blood, cervical mucus, epithelium, endometrium, peritoneal fluid.
• Identification of specific IgM Without IgG or a 4-fold increase in titers of specific Ig G in paired sera obtained from a patient with an interval of 10-12 days indicates primary GI.
• Identification of specific IgM on the background IgG, in the absence of an increase in Ig G titers in paired sera, indicates an exacerbation of HH.

Differential diagnosis of herpetic infection

In a typical course, the clinical picture of herpes in most cases allows a correct diagnosis to be made without the use of additional laboratory and instrumental methods. Difficulties in differential diagnosis may arise with atypical forms of HSV or other diseases localized in the anogenital area.

Soft chancre may resemble herpetic rashes in the phase of formation of erosions and ulcers, accompanied by pain. Differential diagnostic signs are the absence of grouped vesicles, rounded outlines of lesions, a more pronounced reaction of regional lymph nodes, detection of the causative agent of chancroid.

In primary syphilis, multiple hard chancre may resemble HS. Distinctive features are: infiltration at the base, painful primary affect, pronounced regional inguinal lymphadenitis, detection of treponema pallidum.

Differential diagnosis of GG sometimes has to be made with scabies, traumatic lesions of the genitals, contact dermatitis, streptococcal impetigo, Hailey-Hailey pemphigus, Darier, Behcet's, and Crohn's diseases.

Particular difficulties in differential diagnosis may arise when a combination of HSV infection and the above diseases occurs. In such cases, anamnesis of the disease and screening clinical diagnostic tests contribute to the correct diagnosis. In some complex cases, it is advisable to use histomorphological studies.

Treatment of human herpes viral infections

Despite obvious successes in the treatment of acute phases of the most common herpes viral infections, the problem of individual and population prevention of these diseases remains unresolved throughout the world. Immunotherapy and vaccine therapy do not have the necessary effectiveness, and chemotherapy drugs do not guarantee the maximum therapeutic effect of herpes viral infection.

The main components of complex therapy for herpes viral diseases at the present stage are:

• Suppressing viral replication to limit the spread of infection.
• Normalization of the immune response in order to form a complete defense of the macroorganism.

In this regard, domestic herpetologists continue to create comprehensive programs for the treatment of severe recurrent herpes viral diseases. Such programs are based on a combination or sequential use of chemotherapy and immunotherapy for herpes infection. Several similar programs have been developed in Russia, differing from each other in the set of immunomodulators, vaccines and acyclic nucleazides, as well as the sequence of application of immunotherapy, chemotherapy, and efferent treatment methods.

Stage 1. Treatment in the acute (or recurrent) period is chemotherapy: local and systemic forms of acyclic nucleazides for 5-10 days in a full dose to suppress the replication of herpes viruses.

a) nucleazid analogues ( enteral administration):

• Acyclovir 200 mg x 5 times peros 7-10 days
• Valtrex 500 mg 1 time peros 7-10 days
• Famvir 150 mg x 3 times peros 5-7 days
• Herpesin 250 mg x 4 times peros 7-10 days local ointment applications:
• Acyclovir 5% ointment x 4-6 times externally for 5-10 days
• Virolex 3% ointment x 5 times externally 7-15 days
• Gossepol 10% ointment x 3-5 times externally for 7-15 days
• Interferon- beta and gamma (cream) 3 times 5-6 days
• Cyclovir 5% ointment x 5-6 times externally for 5-10 days
• Epigenes- aerosol x 6 times externally for 5 days
• Panavir-gel 5% topically 3-4 times 5-10 days

b) pyrophosphate analogues(act directly on the DNA polymerase of the virus, have high virus-neutralizing activity, reducing viremia):

• Foscarnet 2.4%
• Helepin 1% ointment 2 times externally for 15-20 days

Stage 2. Treatment in the repair or remission phase with immunomodulators, courses of interferons or inducers of their products, or (if indicated) a course of general-purpose immunomodulators. The duration of this stage of treatment is from 14 to 60 days, depending on clinical and laboratory indicators of disease activity.

c) interferons and inducers of interferonogenesis:

• Interferon alpha-2a(intramuscular, subcutaneous or into the lesion) up to 12 ml IU doses and treatment regimen are selected individually, the duration of treatment is 7-10 days
• Interlock IM 5000 IU per day for 14 days
• Cycloferon 12.5% solution 2 ml IM per day 10-15 days
• Panavir 0.004% solution 5 ml IV slowly with an interval of 48 hours 3-5 days
• Arbidol 200 mg peros 3 weeks
• Viferon 500,000 IU rectal suppositories 10 days
• Immunoglobulin human normal 3.0 IM 5-7 days
• Recombinant - alpha 2-interferon in combination with KIP suppositories vaginally or rectally 30 days
• Dekaris 150 mg 1 time per 4 weeks
• Diuciphone 100 mg 3 times peros 2-3 weeks
• Lisavir 200-400 mg 2-4 times peros 7-10 days
• Lycapid 10 mg 1-2 times under the tongue for 10 days
• Methyluracil 500 mg x 4 times peros for 2 weeks
• Myelopid 1.0 ml 1 time IM 14 days
• Nucleinad 300 mg 3 times peros for 30 days

Stage 3. Specific vaccine therapy: begin vaccine therapy no earlier than 2 months after the end of the active phase of the disease.

- Polyvalent antiherpetic vaccine 0.2 ml intravenously 1 time every 3 days, course duration 5 injections. After 2 weeks, repeat 0.3 ml intravenously once every 10 days 5.

Efferent (extracorporeal) treatment methods

Hemosorption, hemooxygenation, plasmapheresis, plasmasorption

The mechanism of action of efferent treatment methods on specific body systems:

1) detoxification

• elimination of toxic substances
• unblocking natural detoxification systems
• extracorporeal biotransformation of toxic substances

2) rheocorrection

3) immunocorrection

• elimination of antigens, antibodies, CEC, immunocompetent cells
• unblocking the immune system
• changes in the direction of the immune response

4) increased sensitivity to endogenous and medicinal substances

The course of treatment includes up to 3 sessions of plasmapheresis with the removal of 30% -50% of the VCP in 1 session, which refers to the average volume of plasma exfusion. The break between sessions is 1-2 days. After a course of plasmapheresis against the background of herpetic infection

• the titer of immunoglobulins M, G decreases by 1.5 - 2 times
• remission increases by an average of 5 months
• the titer of total T and B lymphocytes increases
• the content of T-helper link T lymphocytes increases
• Coagulation potential decreases with normal levels of fibrinolysis
• the concentration of CEC decreases almost 2 times

Herpetic infection and pregnancy

The clinical symptoms of HSV during pregnancy have the same features and the same spectrum of severity as in non-pregnant women.

Primary infection of the mother with HSV during pregnancy is associated with intrauterine infection of the fetus, which occurs in approximately 5% of cases in the population.

There are three main routes of HSV expansion to the embryo and fetus:

• Transcervical, when HSV from the vagina and cervix penetrates through the membranes into the amniotic fluid.
• Transplacental, when HSV in the mother’s blood penetrates the placenta.
• Transovarial - penetration of HSV from the abdominal cavity.

The manifestation of HSV infection in the fetus is determined by the gestational age at which infection occurs and the route of penetration of the pathogen. Infection of the fetus with HSV in the first trimester can lead to micro- and hydrocephalus, intracranial calcification, cataracts and other malformations of organs and systems.

The rate of spontaneous abortions increases after primary HSV infection during the first trimester by 13 - 34% (Whitley R. et al., 1988).

Infection of the fetus with HSV in the 2nd and 3rd trimesters causes hepatosplenomegaly, anemia, jaundice, chorioretinitis, fetal growth restriction syndrome, pneumonia, and meningoencephalitis.

The highest risk of HSV infection for a newborn occurs during childbirth. Up to 85% of infections occur in the second stage of labor in the presence of lesions in the vulva, vagina or cervix, or with asymptomatic HSV release.

Clinical manifestations of HSV infection in the fetus are determined mainly by the following factors:

• gestational age at which infection occurred;
• mechanism of pathogen invasion into the body.

An unfavorable pregnancy outcome for the fetus during herpesvirus infections is observed during hematogenous transmission of the infectious agent.

In 50% of cases, postnatal manifestations of HSV occur in a disseminated or localized form.

Disseminated form: The disease develops 9-11 days after birth. The brain, liver, and skin are affected. If left untreated, 80% of those affected die. But even with antiviral therapy, the mortality rate is 15 - 20%.

Localized - neurological form: The primary neurological form appears in infants 15 - 17 days after birth, in 33% of them no skin manifestations of HSV are detected.

The mortality rate for this form if untreated is 17%. Approximately 60% of surviving children experience long-term neurological complications.

Damage to the skin and mucous membranes is 20%. This form develops 10 to 12 days after birth. Up to 25% of infants may develop neurological complications later in life.

Diagnosis of intrauterine viral infection due to the nonspecificity of its clinical manifestations is extremely difficult. Clinical, instrumental and immunological examination methods help to establish a presumptive diagnosis:

• assessment of the mother’s health status, determination of the presence of virus carriage and the frequency of seroconversion of herpes infection;
• specific immune response to virus expression;
• metabolic changes in the mother's body;
• ultrasound and other research methods.

But a reliable diagnosis can only be made using invasive research methods: chorionic villus biopsy, amniocentesis, cordocentesis.

Management of pregnancy and childbirth

Strategic approaches to antenatal HSV screening vary across Europe and the Americas. Reliable diagnosis is not available through routine examination methods, so the issue of termination of pregnancy must be approached very carefully.

The American Academy of Pediatrics in 1980 recommended culture-based diagnosis of HSV in the third trimester in pregnant women with a history of herpes infection. For women with herpetic lesions or positive culture and serology for HSV during the week preceding delivery, cesarean section is recommended.

In the UK, women with a history of HSV or a sexual partner with a history of HSV are screened from 32 weeks of pregnancy. If herpetic lesions are detected within 21 days preceding the date of delivery, a cesarean section is recommended.

In a antenatal clinic, an obstetrician-gynecologist monitors the course of pregnancy, the state of the feto-placental complex, and the pregnant woman’s immune system.

The risk of developing HSV in a newborn depends on:

• maternal susceptibility to the virus
• gestational age
• the presence of clinical manifestations of genital herpes in the mother.

The degree of transmission of the virus from mother to fetus varies depending on the stage of the disease in the mother, because The primary variant of HSV infection poses a high (up to 50%) risk of intrauterine infection for the fetus.

The likelihood of neonatal herpes infection is very high when clinical symptoms of primary HSV infection appear after 34 weeks of pregnancy or the first episode of recurrent herpes, which, in the presence of maternal antibodies to HSV, is less dangerous and the risk of neonatal infection is not higher than 5%. Delivery in these cases is carried out by cesarean operation. section and, if possible, before rupture of the membranes to avoid ascending infection.

If a cesarean section is performed against the background of a long (more than 6 hours) anhydrous period, the administration of Acyclovir according to the generally accepted regimen is indicated.

The administration of nucleazides and their analogues in the third trimester of pregnancy is important only in the treatment of primary herpetic infection or in the prevention of herpes in children born to mothers with cervical or other local genital manifestations of herpetic infection during childbirth.

Indications for the treatment of severe disseminated forms of herpetic infection in pregnant women and newborns with Acyclovir are absolute and are again carried out according to the generally accepted scheme.

Depending on the indications, symptomatic, restorative therapy is carried out, in combination with immunoglobulins and efferent methods of treatment. The tactics for managing pregnancy and childbirth are determined based on the results of clinical, laboratory and virological studies, and data from the feto-placental complex.

It is necessary to carry out careful clinical and laboratory monitoring of all newborns exposed during pregnancy and childbirth to HSV infection.

To exclude late clinical manifestations of herpetic infection, newborns are observed inpatiently for 12 - 18 days.

If infection during childbirth cannot be ruled out, a cultural and serological examination of urine, feces, discharge from the eyes, and pharynx is performed. If symptoms of HSV infection or verification according to HSV examination data in newborns appear, treatment with antiviral drugs is prescribed.

Immunization

Immunization prior to pregnancy does not play a decisive role in preventing HSV infection in the antenatal period due to the lack of an appropriate vaccine.

Human papillomavirus

ICD X revision, section A 63

Genital papillomavirus infection is a common sexually transmitted disease.

Human papillomavirus (HPV) is a highly human-specific infection from the Papovaviridea family, which has the ability to infect and transform epithelial cells. More than a hundred types of HPV have been identified, of which 35 infect the human urogenital tract, causing damage to the integumentary epithelium of the skin and mucous membranes of the genital organs. Today, HPV infection is one of the most common and important STIs, which infects most of the sexually active population of the planet; papillomaviruses are the only group of viruses for which the induction of tumors in humans has been proven. Epidemiological and virological studies confirm that at least 95% of all squamous cell carcinomas of the cervix contain HPV DNA. The number of infected people in the world has increased 12 times over the last decade (V.A. Molochkov, 2004).

The peak incidence of HPV infection occurs at the age of 18-25 years and decreases after 30 years, when the incidence of dysplasia and cervical cancer increases significantly, the peak of which occurs at 45 years.

Etiology

Papillomaviruses infect a wide range of vertebrates and belong to genus A of the papovaviridae family. Virions do not have an envelope, their diameter is 50-55 nm. The virus is stored at a temperature of 50 C for 30 minutes, resistant to ethers and alcohols. During the replication cycle, the viral genome expresses 8 to 10 protein products. Early proteins control viral replication, transcription and cellular transformation; oncoproteins E6 and E7 are responsible for the oncogenic properties of the virus. The E6 and E7 genes are always detected in tumor cells infected with HPV, while other fragments of the viral genome may be lost during its long-term persistence.

Pathogenesis

HPV is highly tropic towards proliferating cell populations and infects epithelial cells of the basal layer of the epithelium and epidermis. Virus invasion occurs through microdamage to tissues (mechanical, bacterial, etc.), when their depth reaches the basal layer of the epidermis.

Penetrating through microtraumas, HPV infects stem cells of the basal layer, which then become a constant source of infection of epithelial cells, which subsequently undergo successive stages of differentiation with a persistent replicatively inactive virus.

Viruses infect dividing immature cells of the basal cell layer and transitional types of epithelium, where proliferating cells are close to the surface, this fact may explain the frequency of infection of the cervix and the lower third of the vagina and vulva. When viral DNA becomes incorporated into the nuclear material of the host cell, viral integration is said to occur. The integrated form of HPV is capable of malignant transformation as the viral DNA begins to control the cellular genetic material for the reproduction of HPV-encoded proteins. When HPV DNA is integrated, no viral particles are produced, this is called nonproductive HPV infection. Integration of high-risk HPV into the host cellular genome potentiates the production of two oncoproteins: E6 and E7, which interact with endogenous cellular regulatory proteins leading to deregulation of the cell progression cycle, which is a critical point in the formation of cervical squamous cell neoplasia, the formation of non-productive flat condylomas, invisible to the naked eye. . A non-integrated infection is productive because it produces intact viral particles. A distinctive feature of a productive infection is the formation of genital warts, which have a low probability of developing neoplastic processes in the epithelium and epidermis. Dissemination of the virus often occurs against the background of changes in the immune system, and local manifestations of infection are recorded as quickly as possible from the moment of infection and invasion of tissue by the virus.

Epidemiology.

HPV infection of the genital organs (both the skin and mucous membranes in general) occurs in the presence of microtraumas, and it should be taken into account that the reservoir of HPV infection can be the urethra, Bartholin’s glands, and seminal fluid. The most well-known manifestations of HPV infection to practitioners are anogenital warts and genital warts, the number of cases of which, according to the Ministry of Health of the Russian Federation in 1999, amounted to 23.5% per 10,000 population (Rogovskaya S.I., 2003). Across European countries, these data vary from 36% in women under 25 years of age, to 2.8% in women 45 years of age and older (Burk R.D. et al, 1996).

At least 50% of sexually active adults are infected with one or more types of HPV, and in most cases, genital HPV infection in them is unrecognized, subclinical or asymptomatic. Genital HPV infection is highly contagious and is acquired during the first few sexual contacts; Infection with a single sexual contact occurs in approximately 60% of cases.

Risk factors. Recent studies have established that HPV is a necessary but not sufficient factor in cervical neoplasia. Risk cofactors for the development of the disease may be:

• disorders of cellular and humoral immunity
• unfavorable socio-economic status;
• sexual behavior;
• concomitant sexually transmitted diseases (herpes, chlamydia, trichomoniasis, gonorrhea, syphilis, etc.);
• hypo- and vitamin deficiencies;
• young age;
• smoking;
• pregnancy;
• dysbiosis of the vaginal biotope.

The development and course of genital HPV infection also depends on sexual orientation. We are talking about the frequent occurrence of anogenital HPV infection of high and low oncogenic risk among homosexuals of both sexes, as well as the high incidence of anal cancer, registered in the United States in 35 cases per 100 thousand homosexual men

Given the high prevalence of genital HPV infection, cases of its perinatal transmission to infants born from infected mothers during vaginal delivery due to aspiration of amniotic fluid, cervical or vaginal secretions have become more frequent. In this case, the infection can persist for many years in the cells of the child’s oral mucosa and be the cause of the characteristic juvenile laryngeal papillomatosis associated with HPV-16 and type 18, which has become more frequent in recent years. Juvenile laryngeal papillomatosis can develop if the mother has a history of genital warts, as well as if she has a subclinical genital HPV infection. Cases of papillomatosis of the larynx, trachea, and bronchi in children born by cesarean section have been described, which, according to some authors, indicates the possibility of transplacental transmission of infection and the inappropriateness of using cesarean section for the sole purpose of preventing HPV infection of the newborn (20, 21).

Clinic

Clinical manifestations of HPV infection can be different: genital warts, fibroepithelial formations on the surface of the skin and mucous membranes on a thin stalk, less often on a broad base in the form of single nodules, or in the form of multiple outgrowths like “cauliflower”.

The surface is covered with stratified squamous epithelium of the dyskeratosis type. In the underlying stroma there are atypical vessels and inflammation. Localization of OC varies, mainly in places of possible maceration: clitoris, labia minora, urethral orifice, vagina, cervix, anus. In 85% of OK patients, additional foci of HPV are detected during examination; in almost every fourth of them, cervical diseases and cervical intraepithelial neoplasia of varying severity are associated with HPV (Shabalova I.P. et al., 2001).

• Clinical forms (visible to the naked eye):
• exophytic condylomas (typical pointed, papillary, papular);
• vestibular papillomatosis (small papillomatous formations of the vestibule of the vagina)
• Subclinical forms (not visible to the naked eye and asymptomatic, detected only by colposcopy and/or cytological or histological examination):
• flat condylomas (typical structure with many koilocytes);
• small forms (various lesions of MPE and metaplastic epithelium with single koilocytes);
• condylomatous cervicitis/vaginitis
• Latent forms (absence of clinical, morphological or histological changes upon detection of HPV DNA)
• Cervical intraepithelial neoplasia (squamous intraepithelial lesions):
• CIN - CIN 1 - mild dysplasia +/- koilocytosis, dyskeratosis;
• CIN II - severe dysplasia +/- koilocytosis, dyskeratosis;
• CIN III or CIS - severe dysplasia or carcinoma in situ +/- koilocytosis, dyskeratosis;
• Microinvasive squamous cell carcinoma.

The incubation period for genital warts usually varies from 1 to 3 months, but is often longer. In most cases, HPV infection does not manifest itself, remaining asymptomatic. Progression of high-risk HPV infection to cervical intraepithelial neolasia and carcinoma in situ usually occurs within 5 to 30 years and rarely within less than 1 year.

Exophytic forms - genital warts - are the most typical manifestation of infection caused by benign types of the HPV6 and HPV11 viruses.

Endophytic condylomas can be flat and inverted, located on the cervix and have the appearance of flat or slightly raised plaques, determined by extended colposcopy. These types of condylomas may be the result of infection with oncogenic types of the virus.

The manifestation of genital HPV infection is accompanied by the appearance of genital warts; the subclinical form is detected only during extended colposcopy in the form of small flat warts or is established on the basis of a characteristic histological picture - koilocytosis. The absence of clinical and histological signs of infection when HPV DNA is detected indicates a latent or asymptomatic infection

In women, the following areas are affected: labia frenulum, labia, clitoris, urethra, pubis, perineum, perianal area, vestibule of the vagina, entrance to the vagina, hymen, vagina, cervix. The external opening of the urethra in women is affected in 4-8% of cases , deeper damage to the urethra causing the phenomenon of sluggish urethritis.

Anal warts are more common in people who have anal sex and are rarely located above the dentate line of the rectum.

In persons who practice oral-genital intercourse, genital warts can affect lips, tongue, palate.

Genital warts are usually associated with low-risk HPV: most often (80%) with HPV-6, which is detected in immunocompetent people; less often - with HPV-11 - the causative agent of genital warts during immunosuppression. The development of anal warts in passive homosexuals is associated with it.

Genital warts are usually asymptomatic and are often discovered incidentally during examination or on the basis of a Pap smear. In this regard, at first, patients do not complain about the discomfort associated with them. However, large or injured warts, ulcerated or subjected to secondary infection, are accompanied by itching, pain, discharge, and an unpleasant odor, and urethral warts in men can cause a bifurcation of the urine stream and even obstruction of the urethral opening.

Genital warts pose a big problem when pregnancy. Perinatal HPV infection can lead to laryngeal and genital papillomatosis in infants and children.

Laryngeal papillomatosis is a rare but severe clinical manifestation of HPV infection, potentially life-threatening. It affects both newborns and adults.

In 28% of cases it occurs in the first 6 months of life, leading in some cases to airway obstruction.

In patients, especially with impaired cellular immunity (HIV infection, immunosuppressive therapy, Hodgkin's disease) or pregnancy, very large genital warts develop - giant Buschke-Levenshtein condyloma, invasive and destructive tumor associated with HPV types 6 and 11.

HPV infection caused by high oncogenic risk virus types (HPV-16 and 18) is the etiological agent of a rather heterogeneous group of diseases: bowenoid papulosis, cervical intraepithelial neoplasia, cervical cancer, and less commonly, cancer of the vagina, vulva, and anus.

Bowenoid papulosis is associated with HPV-16, as well as other types of HPV -1,6,11,18,31-35,39,42,48,51-54 and manifests itself as dome-shaped and flat papules and spots with a smooth, velvety surface. Bowenoid papulosis usually develops in men who have multiple sexual partners. In the partners of such patients, cervical HPV infection and cervical intraepithelial neoplasia are detected; the course of bowenoid papulosis is usually benign. In some patients, bowenoid papulosis can persist for years, transforming (especially in older people and/or people with immunosuppression) into Bowen's disease and squamous cell carcinoma

In 25% of women, genital warts appear not only on the external genitalia, but also on the cervix and vagina. In the vast majority of cases, these are flat warts, which are a manifestation cervical or vaginal intraepithelial neoplasia transforming into cervical cancer.

Numerous epidemiological and laboratory data have established that in 100% of cases, the primary event in the pathogenesis of cervical cancer is infection with HPV during sexual contact (while HPV-16 is mainly present in squamous cell cancer of the cervix, adenocarcinomas and poorly differentiated tumors of the vulva, vagina and cervix - HPV-18).

In general, up to 90% of cases of HPV infection end in spontaneous recovery; only in 10% of cases does a persistent infection develop, which triggers the mechanisms of malignant transformation of epithelial cells.

Infection of epithelial cells with HPV is a necessary but not sufficient event for cancer development. According to Molochkov V.A. et al. (2004), the formation of irreversible neoplasia requires: active expression of the E6 and E7 genes, with highly oncogenic types HPV-16 and 18, induction of metabolic mechanisms for the conversion of estradiol to 16a-OH, as well as induction of multiple chromosomal damage DNA in an infected cell that completes the process of degeneration. At the first stage of CIN I neoplasia, active replication of the virus and its asymptomatic shedding are observed. The transformation of CIN I into invasive cancer occurs with a very high frequency and, as a rule, is accompanied by the integration of viral DNA into the genome of the host cell, and tumor transformation is more likely to occur when HPV interacts with other carcinogenic or infectious agents (herpes simplex virus type 2, C. trachomatis, cytomegaloviruses, myco- and ureaplasma).

Diagnosis of papillomavirus infection

Laboratory diagnosis of HPV infection is carried out on the basis of cytological, histological examination of biopsy specimens, determination of antibodies to HPV, detection of HPV DNA and E7 oncoprotein

It is also very important to examine the patient for the presence of concomitant STDs. According to Molochkov V.A. (2004.) in 25,783 adult patients of the PCR laboratory in Moscow, papillomavirus infection of high oncogenic risk was detected in 29.6%, low risk - in 13.3%, C. trachomatis - in 6.1%, Micoplasma hominis - in 14, %, Micoplasma genitalium - in 2.6%, N. gonorrhoeae - in 2.6%, G. vaginalis - in 39.5%, human herpes simplex virus types 1 and 2 - in 11.7%, C. albicans - in 18.3%

Clinical examination examination of the external genitalia, vulva, and vagina should be performed in good lighting, preferably using vulvoscopy. To detect subclinical genital HPV infection, an extended colposcopy is performed. False-positive results with this method are usually a consequence of inflammatory and dyskeratic processes of the vulva and vagina.

Colposcopy and biopsy are indicated for all women with class II (CIN II) or class III (CIN III) cerical intraepithelial neoplasia, regardless of confirmation of HPV infection.

The simplest methods for identifying HPV are immunological method s: RSK, IFA, PiF.

Diagnosis of HPV infection of the cervix includes testing by Paponikolaou(PAR - test).

Molecular biological methods - in situ hybridization reaction, PCR, DNA probe.

Histological examination biopsy samples of epithelial and epidermal tissues.

PAP testing is convenient to use at the initial stages of diagnosing cervical pathology, with the aim of selecting patients for colposcopy and histological analysis.

These techniques are also used for low-symptomatic or asymptomatic forms of viral diseases of the genitals.

The use of molecular biological research methods is advisable to prove the presence of HPV with its typing, since both DNA hybridization and polymerase chain reaction make it possible to identify oncogenic types of the virus 16 and 18.

The effectiveness of these methods does not exceed the effectiveness of pathohistological examination, but allows one to identify patients at high risk of this infection (Kozlova V.I., Puhner A.F., 1997). The importance of detecting HPV DNA and typing the virus is due to the fact that 15-28% of women with the presence of HPV DNA (with normal cytology) develop squamous intraepithelial neoplasia within 2 years, and in women with the absence of HPV DNA, only 1-3% develop the disease. cases.

The main method for diagnosing HPV is cytological - detection of koilocyte cells in a biopsy specimen of the cervical epithelium (MPE cells of the intermediate and superficial type with a multinuclear structure), pathognomonic for HPV.

If flat condyloma (PC) is detected in combination with koilocytoatypia, a repeat knife biopsy of the cervix with curettage of the cervical canal of the cervix is ​​necessary to exclude dysplasia and preinvasive cancer in young women. Clarification of all diagnostic and clinical criteria for HPV infection allows the pathologist to give a competent histological conclusion and helps the attending physician develop rational tactics for patient management and determine a reliable prognosis of the disease.

The disadvantages of cytological examination include the fact that it allows diagnosing only clinical and subclinical forms of infection. Taking into account the human factor, there is the possibility of false negative results in the presence of high-grade squamous intraepithelial lesions (invasive cancer from 15 to 55%, pre-invasive cancer from 20 to 70%), and the sensitivity of this method varies from 50-80%.

At histological examination genital warts show moderate thickening of the stratum corneum with papillomatosis, parakeratosis and acanthosis; Mitotic figures may be present. Diagnostically important is the presence in the deep areas of the Malpighian layer of koilocytes - large epithelial cells with round hyperchromic nuclei and pronounced perinuclear vacuolization.

Serological tests are not informative enough for the clinical diagnosis of HPV infection, but may be useful for epidemiological research.

The significance of this method increases with follow-up to determine the risk of relapse or progression of the disease. Sensitivity and specificity increase significantly when the cytological method and HPV testing are used in combination, especially in patients with questionable cytological data.

TREATMENT

When choosing a treatment method for HPV infection, the age, medical history, somatic status of the patient, previous antiviral therapy, as well as the location, number, size of warts, genital and flat condylomas are taken into account. Treatment tactics should be individualized, taking into account the tolerability of certain treatment methods. Treatment of other concomitant infectious diseases and correction of dysbiotic disorders of the vaginal biotope are mandatory (Rogovskaya S.I., 1997).

Local treatment of PVI is aimed at removing condylomas and atypically changed epithelium, using various types of chemical coagulants, cytostatics and physiosurgical treatment methods, however, the recurrence rate of PVI remains high from 30 to 70%. Therefore, after removal of papilomatous growths, local and general therapy with antiviral drugs, interferon inducers, and nonspecific immunomodulators is necessary to prevent relapse of PVI. Patients with HPV should be warned that this infection is a sexually transmitted disease, therefore examination and treatment should be carried out on both partners, and barrier methods of contraception should be recommended for the period of therapy and the next 6 to 9 months.

Local treatment of HPV

1. Cytotoxic treatments:

- Podophyllin- 10-25% solution. Podophyllinotoxin 0.5% solution or gel Resin with cytotoxic effect. The solution is applied to the pathologically changed area, washed off after 4-6 hours with an interval of 3-6 days. The course of treatment is 5 weeks.
- Condilin- 0.5% solution of podophyllotoxin analogue is applied with an applicator to the affected areas, avoiding contact with healthy skin. 2 times a day, course of treatment - 3 days.
- Feresol- a mixture of 60% phenol and 40% tricreazole. Condyloma treatment is carried out once every 10 days until the clinical effect is achieved.
- 5-fluorouracil - 5% cream. Cytotoxic drug for the treatment of condylomas. Apply once a day at night for 10 days.

Drugs with a cytotoxic, antimitotic mechanism of action are not used for the treatment of perianal, rectal, urethral, ​​vaginal and cervical warts. Possible adverse reactions - vomiting, nausea, weeping dermatitis. It is not recommended to apply the drug to an area larger than 10 cm2. The drugs are contraindicated for pregnant women and children.

2. Chemical destructive methods of therapy:

- Solcoderm- a mixture of organic and inorganic acids. Apply to the affected area with an applicator after treating with alcohol. An area of ​​up to 4-5 cm is treated at the same time. The break between sessions is 1-4 weeks. The drug can be used to treat PVI of the vulva and perineum in pregnant women.
- Epigen spray- the main active ingredient is glycyrrhizic acid - it has antiviral, antipruritic, immunomodulatory, interferonogenic effects. Treatment is carried out by irrigating the surface of the elements 6 times a day for 7 days. If warts are localized in the vagina, the drug can be used using a vaginal attachment 3 times a day for 5 days. The remaining elements are removed by methods of physical or chemical destruction, after which a second course of treatment of epithelial areas with epigene is carried out.

Trichloroacetic acid - 80-90% solution. The drug causes local coagulative necrosis. Recommended for mildly expressed genital warts and genital warts. Prescription for pregnant women is possible. Treatment course is 6 weeks: one application per week. The drug should be applied only to the altered surface, avoid contact with healthy tissue. The effectiveness of treatment is 70%. if after the recommended course of treatment there is no positive dynamics, physical destructive methods of treatment with systemic administration of immunocorrective and protoviral drugs are indicated.

3. Physical destructive methods of treatment:

- Diathermocoagulation. The technique is contraindicated if the patient has a pacemaker or a heart rhythm disorder of organic origin. Leaves rough scars on the skin and mucous membranes.
- Laser therapy- removal of formations using a high-energy laser. It is carried out both in a hospital and on an outpatient basis. Laser vaporization of the cervix is ​​performed without prior anesthesia on days 5-7 of the menstrual cycle. Laser coagulation is OK; warts can also be performed in the first phase of the menstrual cycle under infiltration anesthesia. Treatment of large elements of OC and warts is carried out in parts with multiple sessions. A relative contraindication to the use of CO2 laser on an outpatient basis is hemorrhagic syndromes - Willibrandt's disease and Werlthoff's disease.
- Radiosurgery- removal of tumors using high-frequency electrosurgery. The cutting effect is achieved without physical manual pressure. In electrodissection mode, it is recommended for the removal of genital warts of the vulva, vagina, and anorectal area. In electrocoagulation mode - for the removal of genital warts, flat condylomas of the cervix, dysplasia. The processing area should not exceed 5 sq.cm.

The method is relatively contraindicated for use on an outpatient basis in patients with thrombohemorrhagic syndromes.

- Cryodestruction- removal of tumors using liquid nitrogen.

The cryodestruction method ensures the death of tumor cells through the formation of extra- and intracellular ice crystals, followed by tissue necrosis, as well as activation of the humoral and cellular immune response of the macroorganism to cryoexposure. The effect is achieved by a single application of a cryoprobe (cryospray) with an exposure of 10-12 seconds. If necessary, the procedure is repeated after 1-2 weeks.

Cryodestruction is recommended for a limited number of small elements (4-5); the treatment area should not exceed 5 cm2. Local anesthesia is recommended, especially if the patient has more than two warts. Contraindicated for the treatment of vaginal genital warts, as there is a high risk of mucosal perforation.

- Surgical excision

Contraindications for physical surgical treatment methods are: acute inflammatory diseases of the genital organs, malignant neoplasms, when the extent of the process is above the lower third of the cervical canal, since it is impossible to control the boundaries of the effect on the tissue.

Currently, physical methods are considered the most effective in the pathogenetic treatment of HPV infection; they have a minimal number of complications and contraindications.

- Panavir- solution in ampoules of 5.0 ml, colorless, transparent, odorless. The drug is prescribed intravenously at a dose of 5.0 ml with an interval of 48 hours. The course of treatment is 5 injections (25.0 ml), 0.002% protective gel Panavir (biologically active polysaccharide from the class of hexose glycosides). It is used topically as monotherapy for limited manifestations of PVI, and in adjuvant therapy after destructive or surgical treatment to prevent relapses and complications, as well as rapid regeneration of the skin and mucous membranes. 2-3 times a day for 2-3 weeks.
- ridoxol 0.5% and bonauton 2% ointment- applied to affected areas 5-6 times a day for 2-3 weeks.
- Indinol- a drug, a derivative of indinol - 3 - carbinol, selectively inhibits estrogen-dependent expression of the E7 gene, causing apoptosis of cells infected with HPV. The drug is available in capsules in a dose of 200 mg. The course of treatment is 400 mg per day for 10-12 weeks.

The use of interferons in the complex treatment of PVI is effective not only for treating the disease, but also for preventing clinical relapses, as well as for removing patients from a state of immunodeficiency. Interferon derivatives are recommended for use both before and after destructive and surgical treatments for PVI.

- Human leukocyte interferon(CHLI) in the form of applications for 14 days, injections intracondyloma or under the papilloma (CHLI 100-500 thousand IU; up to 1 million IU daily dose). 3 times a week for 3 weeks.
- Reaferon candles 10 thousand IU or Viferon 100 and 500 thousand IU 3 times a week for 3 weeks.
- Interferon ointment 40 IU - externally 3 times a day for 10 days.

6. Adaptogens: Chinese Schisandra extract, Eleutherococcus;

7. Group vitamins: B, D, ascorbic acid, tocopherol acetate (according to the generally accepted scheme)

8. Sedatives: Valerian extract 1 tablet x 3 times a day for 2-3 weeks, Persen 1 tablet x 2 times a day for 3-4 weeks, Novopassit 1 tablet x 2 times a day for 14 days, Relanium 1 tablet at night x 10 days.

Requirements for treatment results - achieving clinical cure, reducing the number of relapses.

Follow-up. In order to identify precancerous dysplastic conditions in women infected with HPV 16 b type 18, it is necessary to conduct cervical cytological and molecular biological studies in combination with colposcopy twice a year.

Human papillomavirus infection in pregnant women

Due to gestational immunodeficiency during pregnancy, the risk of occurrence and exacerbation of PVI increases. Condylomas can increase in size, sometimes causing obstruction of the birth canal. Antenatal or intranatal infection of the fetus with the development of papillomatosis of the larynx and bronchi is possible.

CO2 laser therapy is considered one of the effective methods for treating condylomas in pediatric gynecology and pregnant women. Laser treatment is performed no later than 35 weeks of pregnancy. Laser therapy allows you to destroy any formations locally and under the control of a colposcope. Electrosurgical and radiosurgical excision of skin and mucous condylomas, flat condylomas of the cervix. Relapses of PVI after destructive and surgical treatment methods are 2-15%.

• Due to the risk of adverse effects on the fetus, topical use of podophyllin and fluorouracil is contraindicated.
• condylomas are treated with 3-chloroacetic acid 1-2 times a day for 3 days
• CO 2 laser therapy, radiosurgical treatment methods in combination with adjuvant therapy with interferons.

HPV infection itself is not an indication for cesarean section.

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20. Sukhikh G.T., Vanko L.V., Kulakov V.I. Immunity and genital herpes. Ed. NGMA, Nizhny Novgorod - Moscow, 1997.
21. Khakhalin L.N. VZV and CMV infections in pregnant women and newborns. In the book. - Unknown epidemic: herpes. Smolensk, 1997, p. 93-100.
22. Koutsky L.A., Kiviar N.B. Genital human papillomavirus. In: Sexual Transmittral Diseases /Ed. K. K. Holmes et al. -3rd ed.-Mc.Grow-Hill., 1999.-New York,-P.347-160.
23. Syrjanen K.J. Long-term consequences of genital HPV infections in women //Ann.Med.-1992.-Vol.24.-P.233-245.

Regina 2015-12-24 13:48:28

Genital herpes is probably the most unpleasant disease of all that I have had to experience. Being pregnant, I don’t know why, my herpes came out, so I suffered with it.... It’s unbearable itching, pain, fever, in general hell. Infagel ointment saved me, it was prescribed by a gynecologist, it cost 60 rubles at that time. I smeared the herpes for 4 days, and everything went away without a trace.

HPV vs herpes

Even with safe sex, there is still a chance of contracting sexually transmitted diseases and infections. Only a small percentage of “safe sex” is still not that safe. Using condoms and other birth control is still very helpful to keep your genitals free of viruses, diseases, and other infections.

The most common sexually transmitted infection is human papillomavirus or HPV among youth who are sexually active (in a global setting). On the other hand, herpes is one of the most common sexually transmitted diseases in the United States. About a million people become ill each year in the United States.

It's important to know the differences between them so you can avoid them, or you can determine if you have them and treat them right away.

HPV comes in 70 different forms. These forms come in the form of genital warts, anal warts, cervical cancer, penile cancer, miscarriages and many more. This virus feeds on the moist parts of the skin of the human body: the mouth, anus and especially the genital area. HPV is spread through direct skin contact such as sex, oral sex and kissing. For example, if you have open sores and have direct contact with a person who has genital warts, the virus can be directly transferred to your body. Once the HPV virion has invaded your cells, it will take at least several months to a year before it can be clinically detected. A normal infection may last a year or two. However, after 15-20 years, about 5-10% of affected women develop precancerous cervical lesions, which ultimately lead to cervical cancer. The good news is that HPV is preventable. There are two vaccines available to prevent infection with the virus. These vaccines are Gardasil and Cervarix.

Herpes, on the other hand, comes in two forms: genital herpes and oral herpes. Oral herpes is the most common form of herpes that a person can get from infection with the herpes simplex virus. Symptoms include cold sores or fever blisters. Genital herpes is also an infection of the herpes simplex virus and includes symptoms of keratitis, encephalitis, Mollaret's meningitis and Bell's palsy. Herpes is transmitted through direct contact of broken skin with the skin of an infected person. It is like a blister pack that lasts from 2 to 21 days. Genital herpes is often asymptomatic, meaning you can have it without symptoms. Once infected, the virus resides within the body as it travels within sensory nerves and is carried through an axon to the nerve endings in the skin. A person who is infected with herpes suffers constant episodes and can still infect others. There is no known cure for this disease. But this can be prevented by barriers such as condoms. Vaccines for herpes are still undergoing clinical testing.

To avoid these diseases and all the troubles and problems they bring, abstinence is the best thing to do.

HPV is the most common sexually transmitted infection among youth who are sexually active (in a global setting), while herpes is the most common sexually transmitted disease in the United States. 2.

HPV has warts for symptoms and herpes has sores or blisters for symptoms. 3.

HPV simply disappears over time if you have a strong immune system, while Herpes will remain until you pass it on to your next sexual partner. 4.

HPV has 70 forms, whereas herpes has 2 forms. 5.

Vaccines for HPV are already available, while herpes is still in clinical trials.

Human papillomavirus (HPV), a virus from the Papovaviridea family, has the ability to infect and transform epithelial cells. More than 100 types of HPV have been identified, of which 35 infect the human urogenital tract, causing damage to the integumentary epithelium of the skin and mucous membranes of the genital organs. Today, HPV infection is one of the most common and important sexually transmitted infections, which infects most of the sexually active population of the planet. Papillomaviruses are one of the groups of viruses that have been proven to induce tumors in humans. Epidemiological and virological studies confirm that at least 95% of all squamous cell carcinomas of the cervix contain HPV DNA. But not only papillomaviruses have transforming ability against epithelial cells.

Herpes viruses are associated with a number of oncological diseases and are considered as a cofactor of carcinogenesis, inducing the development of dysplasia and cervical cancer. Of the large family Herpesviridae, which unites more than 100 viruses identical or similar in morphology, only 8 infect humans: HSV-1 and HSV-2 types, Zoster virus (herpes virus type 3), Epstein-Barr virus (herpes virus type 4), cytomegalovirus (herpes virus type 5), herpes virus type 6 is the causative agent of sudden exanthema, herpes virus type 7 is detected in patients with chronic fatigue syndrome, HSV-8 is implicated in the occurrence of Kaposi's sarcoma. Herpes viruses have pantropism, i.e. affect almost all organs and tissues. HSV-2, EBV and CMV can be found more often than other herpes in the human urogenital tract. That is why these viruses are most interesting as synergists for the course of HPV infection. Herpes can reach a latent state, and thus ensure lifelong carriage. This occurs due to the incorporation of the nucleic acid of the virus into the DNA of the host cell (the so-called integration) or through the formation of an episome - an extrachromosomal DNA molecule of the virus, lying separately in the kareoplasm or cytoplasm of the infected cell. In this state, herpes viruses are able to persist for a long time in the human body, but with a decrease in immune defense, reactivation and active replication of the virus occurs. By integrating into the structure of human DNA, herpes viruses can act as mutagens, incl. carcinogens. Changing the activity of some human genes that control cell growth and proliferation is an extremely important property for herpes viruses, because uncontrolled intensive proliferation of infected cells ensures more pronounced and efficient reproduction of viral particles. At the same time, it is known that HPV is highly tropic towards proliferating cell populations and most actively infects epithelial cells in this phase.

Thus, the activation of herpes viruses on the mucous membrane of the urogenital tract leads to the creation of ideal conditions for the penetration of HPV into epithelial cells. From the above, we can conclude that patients with severe immunodeficiency conditions constitute a risk group for HPV infection, and therefore, the risk of developing dysplasia and cervical cancer in such patients is significantly higher. First of all, women diagnosed with HIV infection fall into this group. This disease is accompanied by severe damage to the immune system and therefore reactivation of herpetic infections is not uncommon for these patients.

The purpose of our study was to study the prevalence of herpes viruses - HSV type 2, EBV and CMV in the urogenital tract of HIV-infected patients at the Lipetsk AIDS Center, and the incidence of combined herpes infection with HPV.

Materials and methods. The studies were carried out in the clinical and immunological laboratory of the State Healthcare Institution “LOCPBS and IZ”. For analysis, urogenital scrapings were taken and examined by polymerase chain reaction (PCR) for the presence of HPV DNA, its genotype and quantity, EBV DNA, CMV and HSV type 2.

For the study, we used test systems from NPF “DNA-technology”, Moscow - “CMV-gene”, “VEB-gene”, “HSV-gene”, NPF “Litekh”, Moscow - “Gerpol-2”, “Vipapol” complex”, LLC “InterlabService” Central Research Institute of Electronics of Rospotrebnazor, Moscow - “AmliSens-VKR-screen-FL” and “AmpliSens-VKR-genotype-FL”.

Results. An analysis of the prevalence of herpes viruses and HPV in the urogenital tract of HIV-infected patients showed that EBV DNA was detected in 15.3% of the women examined, CMV DNA in 13.7%, and HSV-2 DNA in 1.3%. Human papillomavirus was detected in 18.3% of samples.

We analyzed in detail 90 samples positive for HPV DNA. We were interested, first of all, in the presence of co-infection with herpes viruses – EBV, CMV and HSV-2. As the study showed, in 20 (22.5%) cases, HPV was found together with EBV, in 22 (24.7%) samples, HPV was found together with CMV, the combination of HSV-2 and HPV was detected only in 4 cases and amounted to slightly more than 4%. It should be noted that in 8 samples DNA of three viruses was detected - HPV, EBV and CMV. In 54 samples, which amounted to (60%), only HPV was detected.

Thus, it can be noted that the detection rate of herpes viruses (EBV, CMV, HSV-2) with combined HPV infection is significantly higher than the detection rate of the same monoinfections in HIV-infected women in the urogenital tract. It has been proven that the severity of HPV infection depends on the simultaneous presence of different HPV genotypes and the infection of epithelial cells by the virus (the amount of viral DNA).

The viral load (VL) of HPV in the analyzed samples was as follows: In 13 samples, the VL was less than or equal to 3 lg copies of HPV DNA per 10 5 epithelial cells, and in 12 samples it was HPV monoinfection and only in 2 cases was it combined with CMV infection. HPV VL of less than 3 lg copies of HPV DNA in clinical practice is regarded as an insignificant, transient HPV infection. In 29 samples, HPV VL ranged from 3 lg to 5 lg HPV DNA copies per 10 5 epithelial cells. Of these, 12 samples contained only HPV DNA, and in 5, HPV DNA was detected along with herpes nucleic acid. The concentration of HPV within 3 lg-5 lg copies is regarded as clinically significant - the risk of developing dysplasia. In 48 samples, HPV VL was very high - more than 5 lg copies of HPV DNA per 10 5 epithelial cells. 29 samples from this group had combined HPV infection with herpes viruses, and in 19 samples only HPV DNA was detected. An HPV concentration of more than 5 lg copies is considered a high risk for the patient to have dysplasia.

The prevalence of various genotypes among HPV positive patients of the AIDS Center was as follows: type 16 - 25%, type 18 - 10%, type 31 - 22%, type 33 - 10%, type 35 - 17%, type 39 - 7%, type 45 - 8%, 51 type -1%, 52 type - 20%, 56 type - 5%, 58 type - 7%, 59 type -2%. In addition, in 44% more than 1 genotype was detected.

Conclusions. The results obtained indicate the widespread prevalence of combined HPV infection and herpes viruses (EBV, CMV, HSV-2) in the urogenital tract of HIV-infected women. Conducted studies confirm more active replication of HPV in the presence of co-infection with herpes viruses. Against the background of HIV infection, herpes viruses are able to enhance immunosuppression, block cell apoptosis and cause proliferative activity of infected cells, thus significantly facilitating the process of infection with HPV infection, which significantly increases the risk of developing dysplasia and cervical cancer in patients with HIV infection. Conducting a comprehensive study of the urogenital tract for HPV and herpes viruses in women with immunosuppressive conditions is advisable, because has a high preventive value.

Literature

1. Kiselev V.I., Kiselev O.I. Human papilloma viruses in the development of cervical cancer - S.-Pb.-M., 2008.
2. Mazurenko N.N. The role of papilloma viruses in cervical carcinogenesis //Modern Oncology-2009.1.-P.7-10.
3. Gurtsevich V. E., Afanasyeva T. A. Genes of latent Epstein-Barr infection (EBV) and their role in the occurrence of neoplasia // Russian Journal<ВИЧ/СПИД и родственные проблемы>. 1998; T. 2, No. 1: 68-75.
4. Lekstron-Himes J. A., Dale J. K., Kingma D. W. Periodic illness associated with Epstein-Barr virus infection // Clin. Infect.2009. Dis. Jan. 22(1): 22-27.

Human papilloma virus (HPV) or Human papilloma virus (HPV) is the most widespread infection among people, causes diseases of the skin and mucous membranes (warts), is represented by more than 120 types of viruses, and is directly related to benign and malignant diseases. The most common routes of transmission: sexual and household contact.

The first mentions of warts are contained in the treatises of doctors of Ancient Greece back in the 1st century BC. and were called “figs” for their external resemblance.

Papillomaviruses are DNA-containing viruses that are characterized by damage to the basal cells of the epidermis, the deepest layer of the skin or mucous membrane. Cells affected by the virus degenerate, actively divide, and as a result, a papilloma is formed (from the Latin papilla - nipple and Greek oma - tumor).

Currently, thanks to the development of virology, more than 120 types of human papillomaviruses are known. Each of them has a digital designation, which was assigned in the chronological order of their discovery.

Currently, 70 types of papillomavirus are described in sufficient detail. It has been established that HPVs have tissue specificity characteristic of each type. This means that each type affects a specific tissue.

For example, HPV type 1 causes plantar warts, HPV type 2 causes the appearance of common warts on the skin (warts vulgaris), HPV type 3 causes flat warts, etc. (Read about warts on the hands, feet and skin)

As a result of research in 1994, approximately 34 types of HPV were identified, which cause the formation of warts on the mucous membrane and skin of the genital organs, in the perineum and anus. Which are also included in the group genital papillomatous infection with a typical route of transmission through sexual contact. (Read about warts on the genitals or genital warts)

Papilloma viruses are divided according to the degree of likelihood of developing cancer (malignancy), into viruses of high, medium and low risk of oncogenicity. For example, HPV types 6 and 11 can cause genital condylomatosis that is not oncogenic, but can lead to giant condylomas.

At the same time, types 16 and 18 of HPV can lead to the development of cervical cancer, vulvar cancer in women and cause penile cancer in men. HPV infection is a mandatory factor in the development of most cases of cervical cancer, but not sufficient - the participation of associated factors is also necessary: ​​immunodeficiency, smoking, hormonal imbalance and others.

A serious factor for the formation of neoplasms is a concomitant opportunistic infection, for example, herpes simplex virus, trichomonas, mycoplasma, chlamydia, gonococci and other pathogens of sexually transmitted infections.

The combination of HPV infection with two infections is detected on average in 33.3%, with three - in 46.2%, with four - in 20.5% of cases. According to numerous studies, combinations of papillomavirus with genital herpes, cytomegalovirus infection, and trichomoniasis create conditions for potentiating the development of invasive cervical cancer.

The presence of gonorrhea is associated with neoplastic changes in the vulvar area. Chlamydia and Trichomonas contribute to the degeneration of tissue in the cervical area, and can also be a kind of incubator in which the virus can remain for up to several weeks or months. Such a “commonwealth” of infections is dangerous for humans, since the risk of carcinogenesis doubles.

The human papillomavirus is an infection that is transmitted by contact and can be infected both through household and sexual contact. The danger comes from genital forms of the virus, which are transmitted during sexual relations.

Causes of papilloma virus and routes of infection

Papilloma and herpes are viral diseases that have a similar clinical picture and develop for identical reasons. According to statistics, up to 90% of adults are infected with one or both pathologies, while not everyone develops an active form of the disease. How to distinguish herpes simplex (HSV) from human papillomavirus (HPV)?

The main feature by which diseases differ is the method of infection. The first spreads through airborne droplets, the second through skin contact. In this case, the disease must be in an active form. What does it mean?

Most of the time, the causative agent of herpes or papilloma hides in remote places of the human body: HSV-1 (simple) is found in the brain, genital - in the sacrum, and HPV - in the mucous membrane of the genital organs.

MINISTRY OF HEALTH OF THE RF: Papillomavirus is one of the most oncogenic viruses. Papilloma can become melanoma - skin cancer!

Thus, the significant difference between the diseases is that even young children can catch herpes. Papillomavirus is more often spread through sexual contact, since the rashes are localized mainly in the genital area.

Moreover, the presence of one of the pathologies does not in any way affect the infection of the other - HPV does not cause herpes and vice versa. These are two different viruses that manifest themselves for similar reasons - due to weakened immunity, stress, overwork, smoking, etc.

There is a well-known difference between bacteria and viruses.

It consists in the fact that bacterial invasion, as we saw above, is not always easy to stop. However, if we succeed in this, literally not a trace of this incident remains in the body. You don't even develop immunity to bacteria.

At the same time, the virus has the ability to intertwine fragments of its own DNA into the DNA of captured cells. Through this mechanism, the body's immune system learns to recognize viruses and attack them.

Thanks to him, the mother’s immunity is transferred to the child during intrauterine development. In the end, due to the fact that our body accumulates information about past viral infections, we ourselves gain immunity to past diseases.

Nevertheless, based on the behavior of the virus in the body, one can suspect that it has mutagenic potential. The ability to change the DNA of a cell is serious enough to talk about the carcinogenicity of viruses.

After all, a malignant cell is, in fact, a modified cell of the body. Only a cell in which the process of division and cell death is disrupted. She is a mutant. And perhaps it was the changes introduced by the virus to her DNA code that caused her to turn from normal to malignant.

In addition, we know that viruses mutate very often. Every time we get sick with a new strain of influenza, from time to time epidemics of changed chicken pox break out in the world, many people die from diseases that were previously considered harmless.

Thus, viral infections should be recognized in advance as being highly mutagenic. And the fact that it may well be aimed, among other things, at the malignancy of the affected cells. At the moment, it is believed that the particular danger of infection with genital papillomas and herpes is the risk of later developing cervical cancer.

It is expressed by painful rashes on the genitals. There is a risk of transmitting this disease to the newborn, especially during childbirth.

In a newborn, genital herpes can cause serious complications. Therefore, it is especially important to tell your gynecologist about the slightest discomfort, even if you don't think you have genital herpes.

Pregnant women who become infected with this virus should be under close medical supervision. In fact, in the case of a herpes outbreak, there is a serious risk of infection of the child from the mother through the bloodstream if the infection is primary or through the birth canal if there is a new outbreak during pregnancy.

In this case, the child becomes infected during childbirth, but also possibly before birth: the fetus is protected by the amniotic sac, which completely isolates it, but often it cracks at the end of pregnancy and can no longer serve as a protective barrier.

If a pregnant woman suffers from genital herpes, a group of obstetricians and pediatricians discusses the possibility of a cesarean section and further treatment of the newborn before giving birth.

In fact, we already know almost all the most important things about them. These viruses are transmitted sexually. You can get papilloma both at home and during intrauterine development. These diseases are incurable. It is only possible to alleviate the symptoms of exacerbation of herpes and slow down the spread of condylomas.

In 2006, the United States began mass production of two types of the first vaccine against human papillomavirus. One of them is called “Gardasil” and forms immunity against four strains of the virus.

And the second, produced under the name “Cervarix,” immunizes only against two oncogenic and most common strains. These vaccinations and medications are carried out in three visits. And this procedure provides immunity to the declared types of genital warts for the next 6 years.

Strictly speaking, these drugs should be mentioned in the next paragraph - devoted to the treatment of these diseases. But the fact is that at the moment we cannot recommend Gardasil and Cervarix for use.

There are different ways of contracting the virus. All of them are associated with contact between a sick person and a healthy person (bodily contact, shared objects, contact of mucous surfaces during kissing and sexual intercourse), while the possibility of infection is determined by two factors: the activity of the immune system and the ability of the virus to attach to human cells.

As for common warts, the likelihood of their transmission is determined by the state of immunity. They are often localized on the fingers, because it is with our hands that we grasp various objects of common everyday life (door handles in public institutions, in transport).

To become infected with skin types of warts, there must be a break in the skin of another person. The HPV virus enters the blood through wounds, hangnails, cracks and other violations of the integrity of the skin.

Important: the presence of warts indicates low cellular immunity.

Etiology

Papillomaviruses belong to the papovirus family. They are capable of infecting almost all vertebrates. Virions (or virus cells) do not have an envelope; their diameter ranges from 50 to 55 nm. The virus is well preserved at temperatures up to 50 degrees Celsius for half an hour and is resistant to alcohol ethers.

Herpes and papillomatosis: similarities and differences, causes, relationships

One of the most controversial forms of life on Earth is viruses. There are still debates over whether to consider them living organisms or not. And while people are arguing about this, viruses are steadily spreading and infecting humanity.

Among all human viral diseases, urogenital infections create significant problems for patients and doctors, the external manifestations of which do not seem to pose a threat to life, but significantly reduce its quality.

general characteristics

Let's look at two fairly common diseases: urogenital herpes and condylomatosis. Let us immediately note that both diseases are caused by viruses, but they are completely different. They differ from each other in many ways:

1. The structure of the pathogen.
2. The mechanism of reproduction and spread of the virus.
3. External manifestations.
4. Treatment approaches.
5. Forecast.

What unites them is, perhaps, the course of the disease. Both herpes and condylomas are prone to a chronic, relapsing course and periods of exacerbation cause a lot of trouble to the infected person.

Pathogens

This is what doctors call all microorganisms that cause any infections in living beings. What are the similarities and differences between the pathogens that cause condylomas and herpetic rash?

Two very common types of viral infections are transmitted through unprotected sex: HPV and HSV. Some experts are inclined to consider papillomavirus and herpes virus to be synonymous, but in fact they have more differences than similarities.

What types of human papillomavirus can cause cancer?

Human papillomavirus infection, like genital herpes and HIV/AIDS, is a sexually transmitted viral infection. Today, medicine does not have a medicine that can remove papillomavirus from the human body, which gives doctors the right to say that this disease is not curable. However, there are medications and methods that can remove papillomas.

Currently, more than 70 types of human papillomavirus are known.

Viruses 6, 11, 42, 43 and 44 are the cause of genital warts of the vulva, perineum and cervix, as well as respiratory papillomatosis.

Genital warts have been known since ancient times. The healers of Ancient Greece gave it the name “condylomas” or genital warts. They learned to detect human papillomavirus in the late 60s of this century after the discovery of electron microscopy.

Since the same period, there has been an uncontrollable spread of the disease across the planet. In the mid-70s, medical scientists believed that approximately 1.2% of the world's inhabitants were infected with human papillomavirus. The latest data indicate that every 6 earthlings have papillomavirus.

It all starts with sexual contact with a carrier of the virus - a few minutes of sensual pleasure and... after a few months, small, soft, white warts on a thin stalk grow on the delicate and sensitive skin of the female genitalia: labia, vagina, cervix, around the external opening of the urethra or anus (it all depends on ingenuity in intimate fun).

In addition, women experience leucorrhoea - watery discharge from the genital tract, which is characterized by an unpleasant odor.

The stronger sex is less likely to suffer from warts. As a rule, the disease is asymptomatic in men, and only in case of weakened immunity do warts densely litter the trunk and head of the male “piston”, sometimes the testicles and the skin of the perineum.

Some more time passes and the tender and innocent warts grow, turning into formations that resemble the appearance of a rooster's comb or cauliflower. Transforming condylomas greatly complicate the patient’s life: they interfere with walking, and break off during acts of love, causing pain and bleeding, and, to a certain extent, complicating sexual life.

It is then that the patient comes to the doctor, who prescribes pills and “injections” that strengthen the immune system or burns these formations with a laser beam or liquid nitrogen. After such treatment, not a trace of warts remains.

Methods for diagnosing and treating HPV infections: quick and painless relief from annoying diseases. Expert consultations, online appointments.

Complications: if our existence were structured too simply, then, you see, it wouldn’t be worth living! And therefore, the saga with genital warts continues. When warts rip off, bleeding may occur. Patients cannot be sexually active because... they are bothered by warts.

Virus subtypes 16 and 18 can contribute to the malignancy of genital warts. This happens unnoticed, the tumor of the cervix does not show itself for the time being. And our dear, beloved beloved women go to an oncologist with an advanced stage of the disease and often “burn out” from cancer in 1-2 years.

Lyrical digression: it pains me to see how illiterate Russian women are regarding the functioning of their reproductive organs. Let's say I can understand the women of the Caucasus, where religion and culture deliberately limit a woman's sexual knowledge, but ladies from the central regions of Russia?

It is difficult for me, as a representative of the stronger sex, to understand the psychology of a woman who goes to the doctor when she can no longer bear it: a tumor disintegrates or sexual life becomes impossible due to condylomas, the doctor would be happy to help, but he can no longer help.

I don’t understand men who, seeing that their women’s health is not in order, do not even insist that their beloved be examined. There are true and opposite cases when a woman, having discovered some pathology, does not want to be examined in any way, citing the fact that she is afraid of the possible results. How many of you women visit a gynecologist once every six months and undergo the appropriate tests?

American experts testify that during oral sex with a patient with genital warts, the vocal cords and larynx can be affected and respiratory papillomatosis can occur.

Pregnancy: During pregnancy, a woman’s immunity physiologically decreases, which can be a provoking factor for the formation of genital warts in women previously infected with the human papillomavirus.

If a woman has genital warts on the genital tract during pregnancy and childbirth, then during childbirth the child may become infected with the subsequent development of respiratory papillomatosis, i.e. genital warts grow on the vocal cords and in the nasal cavity.

A woman with active manifestations should give birth in a second obstetric (observation) department. Depending on the location and number of condylomas, the doctor may recommend either delivery by cesarean section or vaginal delivery with disinfection of the birth canal with polyvidone iod.

Diagnostics: Scraping from the affected area for human papillomavirus using PCR or cytological examination.

Papillomas on the penis must be distinguished from Hirsuties papillaris genitalis - pearly (pearly) papules of the penis. These epithelial papillae, framing the base of the head, are a normal anatomical formation and do not require removal.

They occur at the time of puberty and by the end of puberty can go away on their own. According to the website http://www.venuro.info/, mother-of-pearl penile pearls are characterized by the presence of closely spaced dense nodules (papules) of the same size (usually several mm) with a shiny matte surface, reminiscent of pearls (hence the name).

Treatment: Destruction of condylomas with laser or liquid nitrogen, treatment that strengthens the immune system. There are special drugs for the treatment of genital warts: Solcoderm from Solco Basel.

The drug is a solution of organic acids and copper nitrate in nitric acid. Designed for outdoor use. Solcoderm has a cauterizing effect. The acids that make up the drug coagulate (coagulate) upon contact with the proteins of papillomatous growths, followed by their mummification.

The second drug is a local immunomodulator - Aldara (imiquimod). Aldara is a biological response modifier that stimulates the secretion of interferons and tumor necrosis factor. Imiquimod is available as a 3% cream.

The above medications are not used during pregnancy.

Prevention:

• Avoiding casual sexual contact and oral sex with strangers;
• Condom use;
• No more than 2 hours after sexual intercourse, irrigate the genitals, pubis and inner thighs with Betadine solution. Women can use Betadine in suppositories immediately after sexual intercourse and toileting the genitals.

In case of condylomatosis, in addition to treatment, constant monitoring by an obstetrician-gynecologist is required: examination once every 6 months, smears for oncocytology once a year.

Ivan Yurievich Kokotkin, obstetrician-gynecologist

The phrase human papillomavirus or HPV occurs quite often and some people believe that infection with this microorganism causes only papillomas to appear on the body.

But not everything is so rosy; infection with HPV sometimes leads to the development of a rather serious disease - cancer. It is possible to guess how the infection will behave in the body, but only by knowing the type of papillomavirus.

Research conducted over the past decades has made it possible to establish that HPV is transmitted only from one person to another, and this can be either a carrier of the infection or a patient with pronounced clinical signs of papillomatosis.

It has been established that papillomavirus is divided into types; there are more than one hundred of them. Depending on the type of virus that has entered the body, all external and internal changes will occur in the future.

The division of HPV into types has made it possible to develop treatment tactics for patients with microorganisms detected through testing.

Photos of different types of papillomas

You need to know that infection with one type of papillomavirus does not guarantee that the body is infected from other subtypes. That is, a person can simultaneously be a carrier of several types of HPV, some of them may not pose any danger, while others increase the likelihood of cancer.

The virus is transmitted in several ways, the main one being sexual. Infection is possible when several people use the same towel, razor, or scissors. The pathogen can be transmitted from a woman giving birth to her child; there is also a risk of self-infection, that is, transfer of the virus from one part of the body to another.

The microorganism is so microscopic that it easily penetrates through the slightest cracks in the skin, abrasions and scratches. According to the latest data, up to 90 percent of the entire population of the planet is infected with different types of the virus.

The virus does not always become active immediately. That is, it can remain in the body for a long time in a “sleeping” state, from which a number of provoking factors bring it out.

Oncogenic classification is a division of virus types that takes into account the likelihood of developing cancer depending on the subtype. In total, the division is used in practical medicine into three groups.

How the virus develops

The period between infection and manifestation of infection can take up to six months. Therefore, it can sometimes be difficult to find out where and from whom the infection was acquired.

After entering the mucous membranes, the virus invades the body’s cells and integrates its DNA into the DNA of a human cell. Then it acquires the ability to reproduce. Infected cells become sources of new viruses that infect neighboring healthy cells (integrate into their DNA and reproduce new viruses).

Viral diseases of the female genital organs. (Herpes simplex virus, papillomavirus, cytomegalovirus). Clinic. Diagnostics. Treatment

Cytomegalovirus is a viral disease that affects the salivary glands, uterus and cervix. Most often, the disease is transmitted by contact - during sexual intercourse and kissing, but sometimes infection can occur through blood transfusion, organ transplantation, pregnancy, childbirth and breastfeeding.

If cytomegalovirus manifests itself in the form of inflammation of the genitourinary system, inflammation of the internal genital organs, erosion of the cervix, vagina, and ovaries are observed. Women complain of pain in the lower abdomen and blue-white vaginal discharge.

Diagnosis of cytomegalovirus is based on DNA analysis, as well as examination of blood, saliva, and cervical discharge. Amniotic fluid is taken from pregnant women for analysis.

Unfortunately, treatment of cytomegalovirus, even with the modern level of medical development, does not completely get rid of the disease. If the disease is asymptomatic and there are no disorders in the immune system, then treatment is not carried out at all.

Human papillomavirus (HPV, or HPV - human papilloma virus) is a widespread virus that causes a variety of diseases in both women and men.

There are now about 100 different types of human papillomavirus, of which 80 types are the most studied. Different types of the virus can cause different diseases (see table of hpv types).

Approximately 30 types cause damage to the female genital organs.

The most dangerous of them are types of papillomavirus with a high cancer risk - i.e. viruses that have the greatest ability to cause cancer of the genital organs, in particular cervical cancer. These viruses include HPV types 16, 18, 31, 33, 35, 39, 45, 51 and 52.

Diagnostics: HPV tests - PCR and Papanicolaou smear (precancerous or cancerous changes in the epithelium).

The most important manifestations of human papillomavirus infection in women are genital and flat condylomas, dysplasia (precancer) and cervical cancer.

Human papillomavirus is the second most common viral infection of the female genital area (after genital herpes).

Papilloma viruses are found in approximately 70% of women. Various manifestations of HPV infection occur in approximately 50% of infected individuals. HPV is transmitted sexually and through household contact with the skin and mucous membranes of an infected person.

In the presence of genital warts, the probability of infection approaches 100%. Using a condom does not always prevent infection, but it does reduce the likelihood of infection occurring when infected.

Genital warts (or, as they are also called, genital warts) are papillary growths of flesh-colored or pink-red color on the skin and mucous membranes of the genital organs. They can be found either individually (in shape they are compared to a cockscomb) or together (in this case they resemble sea kale).

Most often they are located on the skin of the external genitalia, around the anus, the external opening of the urethra, on the mucous membrane of the vagina and cervix. Genital warts are characterized by moderate oncogenic potential (the ability to turn into cancer).

However, they should be removed not only for cosmetic reasons, but also to reduce the risk of developing cervical cancer and prevent infection of your partner(s). Small genital warts are removed using a laser, special chemicals (“cauterization”), liquid nitrogen (cryodestruction) or weak electric current (diathermocoagulation).

Flat condylomas differ from genital condylomas in their shape (they do not protrude above the surface of the mucous membrane) and have a much higher oncogenic potential.

Therefore, for any flat condylomas, colposcopy and biopsy (examination of a piece of tissue under a microscope) are indicated. Most often, flat condylomas are found on the mucous membrane of the cervix and vagina.

If no dysplasia is detected on the biopsy, only a small area of ​​tissue surrounding the condyloma is removed. If dysplasia is detected, a larger area of ​​tissue is removed.

Treatment: For papillomavirus infection of the genital organs, only a doctor can prescribe treatment. In this case, it is necessary to examine and treat the patient’s sexual partner.

· destructive: surgical removal, electrocoagulation, freezing with liquid nitrogen (cryotherapy), laser therapy;

· chemical: the use of concentrated solutions of acids (solcoderm, 80% trichloroacetic acid, nitric acid), phenol and tricresol (pheresol), 5-fluorouracil (5% fluorouracil ointment), etc.

Additionally, immunomodulators are prescribed: recombinant alpha-interferon (laferobion, viferon, alfarekin, genferon), inducers of interferon synthesis, for example, methylglucamine acridone acetate (cycloferon), alloferon (allokin-alpha), etc.

Papillary patterns of the fingers are a marker of athletic abilities: dermatoglyphic signs are formed at 3-5 months of pregnancy and do not change throughout life.

Transverse profiles of embankments and coastal strips: In urban areas, bank protection is designed taking into account technical and economic requirements, but special importance is given to aesthetic ones.

Mechanical retention of earth masses: Mechanical retention of earth masses on a slope is provided by buttress structures of various designs.

Symptoms and signs of genital herpes and papillomavirus

For both of these infections, sexual transmission is the main route. However, it is no secret that papillomas (warts and moles) are usually present on a woman’s body long before the start of sexual activity. So, for now, we will leave the question about all the methods of infection with papilloma open.

But the fact that the main place, so to speak, of dislocation of genital herpes in both sexes is the urethra is the pure truth. In women, it also readily reproduces in the cervical canal.

‘ Genital herpes is similar to ordinary oral herpes. Local redness of the skin, accompanied by a rash on the surface of the lesion. The rash is small and weeping. The blister lasts for a day or two, and then subsides, forming a yellow crust.

The first symptoms of herpes infection appear a week after it occurs. At the beginning of the rash, the woman feels a burning sensation, itching, and swelling of the affected area. Sometimes - with a slight increase in body temperature and mild general malaise.

As the blisters dry, the rash goes away on its own within a few days. The entire process of exacerbation of the disease usually does not last longer than a week. In the presence of drugs, the period of transition/return to