Herpes simplex type 1. Herpes: forms, causes, manifestations in men and women, complications, how to treat

Herpes simplex virus (HSV) infections are quite common in the population. Having first identified it as the cause of febrile blisters or colds, HSV was recognized in the 19th century.

However, the clinical manifestations and consequences of genital herpes were not described until the 1970s, and the epidemiological features of this infection were not delineated to the introduction of accurate serological testing in the 1980s. Despite its long existence among humans, the morbidity associated with HSV has been recognized relatively recently.

Herpes viruses

There are two types of HSV: HSV-1 and HSV-2. HSV-1 is the cause of colds and sores and is often acquired during childhood from close (asexual) contact with family members. In contrast, HSV-2 - the main cause of genital herpes - is almost always transmitted through sexual contact. However, HSV-1 can also cause genital herpes, and the frequency of HSV-1 isolation from this infection has increased.

HSV causes an infection that remains constant throughout the life of the carrier and can probably be transmitted for many years after infection. The impact of HSV infection on health and psychosexual functioning is extremely variable. Serious consequences of infection are observed in newborns, where the final outcome is not positive even with adequate treatment. Persons with weakened conditions, including those with HIV, can also often get HSV.

Although most people do not realize they have this infection, those who experience it have unpleasant recurrent genital masses. The existing association of genital ulcers in general and those caused by HSV-2, including with the transmission of HIV infection, has increased the importance of preventing genital lesions associated with the herpes virus. Unfortunately, the long-term spread of HSV-2 infection suggests that progress in prevention will be slow. As with many other sexually transmitted diseases (STIs), genital lesions associated with the herpes virus affect women disproportionately and in multiple ways.

First, the infection is more common among women, regardless of the level of sexual activity. Second, the disease tends to be clinically serious in women, who are more likely to develop systemic disease and neurologic complications when they first contract the infection. Finally, due to the threat of potential complications during pregnancy and infection of the infant, the consequences of genital herpes affect women more.

Herpes simplex virus type II infection

The prevalence of infection with simple second type virus (HSV-2) increases in direct proportion with age, poverty level and low educational level. According to all studies, the prevalence of this infection is about 1.5 times higher among women than among men. The reasons for this gender mismatch likely lie in anatomy (differences in the genital epithelium between men and women) and behavior (younger women are more likely to have sex with older men, thus increasing the likelihood of having the virus).

In the United States, HSV-2 infection is more common among African Americans than among whites. HSV-2 infection rates remain high among African Americans even after adjusting for sexual behavior, and likely reflect the high underlying prevalence of HSV-2 infection among sexual partners in the African American community. Other behavioral risk factors associated with positive serological reactions to the herpes virus are the number of sexual partners during life and young age at the beginning of sexual activity. In the NHANES study, cocaine use is also correlated with HSV-2 seropositivity.

Since the risk of infection correlates well with the number of sexual partners during life, the detection of antibodies to herpes simplex virus type II has been proposed as a serological marker of sexual activity in various populations. This correlation may be accurate for some populations, but may not be accurate in cells with very high and very low HSV-2 prevalence rates.

For example, the risk of developing infection is evened out in African American women who report having two or more sex partners in their lifetime, while the risk rises sharply among white women. At the other extreme, seropositive rates are so low (3%) among young people in New Zealand aged 21 that no association was found between sexual activity and the risk of HSV-2 infection. In addition, the characteristics of sexual partners can be an important risk factor for contracting herpes simplex virus type II. The choice of sexual partners in relation to the state of serological reactions to HSV-2 has not been actively studied.

One study found that those who seropositively reported the infection were more likely to report looking for sex partners belonging to the demographic group with high risk development of sexually transmitted diseases than those with negative serological reactions to herpes simplex virus type II.

Transmission of herpes simplex virus type 2

As with all sexually transmitted diseases, sexual contact with a person who has genital herpes does not necessarily result in the transmission of herpes simplex virus type II (HSV-2). Gender and previous HSV-1 infection alter the risk of developing HSV-2 infection. Serologically, women are at greatest risk of contracting HSV-2. Other factors that can influence the transmission of HSV-2 include the recurrence rate of a potential source partner, sexual intercourse with obvious lesions, use of barrier contraceptives, and consistent use of antiviral drugs by a partner with herpes. In about 25% of couples who believe they have a different status with respect to genital herpes, serologic tests show that both have HSV-2 infection. This indicates that the infection was transmitted unconsciously or possibly received from previous partners. Couples with different HSV-2 antibody status have an average infection rate of about 12% per year. Transmission efficiency varies widely, however, as some people get HSV-2 after a single intercourse, while other couples do not transmit the virus despite years of unprotected sex. This variability in transmission rates has not been adequately studied.

Herpes simplex virus - the most common reason Genital Ulcers Worldwide: This is well documented in developed countries and is seen in developing countries. The presence of these genital ulcers has been a potential risk factor for HIV infection since the onset of the HIV epidemic. Numerous epidemiological studies confirm the connection between genital ulcers in general and genital herpes, including HIV infection. For example, a prospective cohort study that examined the risk of HIV infection among men with and without genital ulcers found that the former was three times the risk of HIV seroconversion.

In addition, both conventional and nested case-control studies have shown that HSV-2 infection is correlated with HIV infection. Estimates of the relative risk of HIV infection range from 1.2 to 8.5. There is an increased risk of transmission from male to male, male to female and female to male transmission.

It has been suggested that there are two biological mechanisms that are responsible for how the presence of genital herpes can be a risk factor for development. First, infection with HIV is facilitated by mucosal damage that accompanies genital herpes. Secondly, since herpetic formations are associated with an increase in the number of lymphocytes carrying CD4 (through a local inflammatory response), there are more target cells in the genital tract of persons with genital herpes for HIV to attach and penetrate. Both mucosal damage and the presence of an increased number of activated CD4 cells suggest that individuals with genital herpes are at greater risk of contracting HIV.

Genital HSV-1, HSV-2 infection

Studies of individuals with HSV-1 or HSV-2 infection at the same time in the mucous membranes oral cavity and the genital area, have shown that the severity of re-infection depends on the interaction of the type of virus with the site of the anatomical localization of the infection. Thus, relapse rates are higher for genital HSV-2 infection than for oral HSV-1 infection and genital HSV-1 infection, and low for oral HSV-2 infection.

Despite the fact that HSV-1 is an uncommon cause of recurrent genital herpes, it is becoming an increasingly common cause of the first episode of this disease. In the UK, HSV-1 is most commonly found in individuals with primary genital herpes virus infection. Other geographic areas with a high proportion of genital HSV-1 from which data are obtained include Singapore and Japan. In Seattle, HSV-1 causes approximately 30% of primary cases of genital herpes.

The reason for the increased incidence of HSV-1 as a factor in primary genital herpes is not entirely clear. One explanation that is often cited is the common practice of oral-genital sex. For example, one case-control study identified oral sex as a risk factor for infection with the genital herpes virus, more commonly HSV-1. Another explanation for the increasing incidence of HSV-1 as a cause of primary genital herpes is a decrease in rates of HSV-1 infection in childhood. As a consequence, more young people reach adulthood as seronegative and their first exposure to HSV-1 may occur during oral sex.

The assessment of HSV-2 as a risk factor for HIV transmission (as opposed to HIV infection) is even less studied because people who transmit HIV infection are not as extensively researched as those who acquire HIV infection. One report of effective HIV transmission described a man with a history of genital herpes who transmitted HIV to his numerous sexual partners.

Another study (studying married couples) showed a relative risk of 1.9 for HIV infection in women whose husbands had genital herpes. This result confirms that such efficiency of HIV transmission among people with HSV-2 infection occurs through the movement of activated genital lesions caused by herpes.

Among people with HIV infection, this movement may accelerate the local replication of HIV on mucosal surfaces. This assumption is supported by the fact that HIV was sown from genital ulcers (according to studies conducted in Africa), and the detection of HIV virions is confirmed by more than 95% of cases of genital herpes in HIV-infected men. Since the herpes simplex virus is frequently reactivated in many HIV-infected people, the acceleration of local HIV replication at sites of genital lesions may explain how genital ulcers facilitate HIV transmission.

The manifestation of the disease and relapses with herpes simplex virus type II

Among people who are seropositive for HSV-2, only a small number have been diagnosed with genital herpes. For example, in one study, only 9.1% of women and 9.2% of men with HSV-2 antibody reported a history of genital herpes. However, 12.2% of whites knew they had an infection (compared to 3.7% of African Americans). Since there is no evidence that the clinical manifestation of HSV-2 is dependent on race or ethnicity, access to a healthcare system likely plays a role in recognizing infection.

On the other hand, HSV-1 re-infection rates are higher among African Americans, and previous HSV-1 infection can make the clinical diagnosis of HSV-2 infection difficult. The biological characteristics of HSV-2 in individuals who are not aware of the presence of infection are not well defined. However, epidemiological studies show that individuals without clinical manifestations a history of genital herpes is the main source of infection, and preliminary evidence suggests that the virus is activated in virtually all infected.

Many people with genital herpes have unpleasant recurrent genital ulcers long after infection. Typically, relapses are associated with mild physical discomfort, but some patients experience severe or frequent relapses that are clearly detrimental to health. In addition to the physical discomfort of recurrent illness, genital herpes causes significant psychosocial dysfunction. Several studies have shown that genital herpes is associated with isolation and feelings of social stigma. In many patients, these sensations intensify during relapses. Comparison of patients with genital herpes and patients with gonorrhea or dermatological diseases shows that psychosocial dysfunction is more pronounced in people with genital herpes. For most people with genital herpes, the greatest concern is the fear of passing the infection on to their sexual partners. New relationships are often tough because people with herpes must share the infection with others and fear rejection.

Atypical genital herpes

Most of the signs and symptoms of genital herpes affect only a minority of people infected with HSV-2. However, careful studies of HSV-2 seropositive individuals show that there are mostly genital symptoms and signs, but they tend to be mild or atypical, and therefore go unrecognized. For example, after an individualized study session, 50% of HSV-2 seropositive women who had not previously experienced genital herpes admitted to having a typical relapse. It should be noted the manifestations of recurrence of genital herpes, which were a frequent complaint of the genitourinary system in this group of women during the next six months of follow-up.
An undetected HSV-2 infection can cause genital lesions or severe rashes that appear atypically or in an atypical location. Atypical manifestations include cracks, papules on the genitals, or superficial cervical lesions. Lesions that appear in the perianal region are often attributed to anal fissures.

Patients with genital herpes are often diagnosed with recurrent yeast infections, or "jockey's itch" infectious diseases urinary tract, eczema, or pinch. These diagnoses are often supported by an obvious response to therapy, since healing occurs naturally in genital herpes. The presence of type-specific serological research methods facilitates the diagnosis of HSV-2 infection in individuals with atypical manifestations.

Herpes simplex virus can be sown from the genital area during initial infection and relapse, as well as periodically between clinically recognized episodes. During the first and repeated episodes of genital infection, viral contamination tends to last for a shorter time than damage.

With primary infection, the virus can be sown for about two weeks, and with repeated episodes, within two to four days. Studies have shown that herpes simplex virus can also be present in the genital area between clinically apparent relapses.

Viral contamination in the absence of genital lesions is called asymptomatic or subclinical. From an epidemiological point of view, subclinical contamination is important in most cases of both sexual and perinatal transmission of herpes simplex virus and is probably a key element in the prevention of genital herpes. Although genital herpes can be associated with a greater risk of infection during recurrence, asymptomatic transmission is important in most HSV contamination, as it is unlikely that safe sex can take place in the absence of damage.

Genital HSV infection

Cases of genital herpes simplex virus-1 (HSV-1) infection have increased in many parts of the developed world, and in some places they account for 50% of cases of primary genital herpes. The initial manifestations of primary herpes do not differ with genital HSV-1 and HSV-2 infections. However, unlike genital HSV-2 infection, genital HSV-1 infection rarely recurs, therefore, determining the type of virus has prognostic value.

The average time to the first relapse after the onset of genital HSV-1 infection is 310 days. In addition, HSV-1 is rarely sown in the asymptomatic phase. Patients with genital HSV-1 infection can be confident that the course of the disease is likely to be mild. It is not known how often genital HSV-1 infection is acquired through oral sex versus genital contact.

HSV is sometimes sown from the genital area during primary recurrence and infection. Asymptomatic seeding was investigated by teaching patients to take a daily swab of genital secretions. Because viral contamination is rare, short-term studies tend to underestimate the number of people asymptomatic with HSV contamination, as well as the frequency of contamination.

Asymptomatic contamination is common around the time of genital herpes infection. In the first two years of HSV infection, the virus can be isolated from the genital area in 10% on all days and in 6% on days without damage. In the future, the frequency of contamination decreases, albeit slowly. In general, the average frequency of contamination in the subclinical phase in women is approximately 2.4% of the day. However, there is a significant discrepancy: in some women, infrequent dissemination is observed, while in others the virus can be sown up to 25% of the days.

In women, the most common sites of asymptomatic contamination are the perianal region and vulva, followed by the cervix. Men also have asymptomatic seeding in the genital area, mainly on the skin of the genitals and in the perianal region.

In both men and women, seeding is most likely to occur within a week before or after clinical recurrence of herpes simplex infection. The average frequency of contamination in the subclinical phase is 2.4% of days, but a week before relapse the rate of rash is the same as in 10% of days. Since the prodrome can explain some cases of contamination during this period, the signs that determine it are nonspecific in many patients and cannot force them to refrain from sexual intercourse.

Neonatal herpes

In pregnant women with genital infection due to infection, the possibility of transmission to the newborn is of greatest concern. Infection of newborns with herpes simplex virus (HSV) is a rare but very serious illness. The incidence of herpes in newborns varies by region, and the Pacific Northwest and Scandinavian countries have the highest rates in the world.

AT Medical center At Washington State University, neonatal herpes occurs in about one case in 2,200 births. Not surprisingly, the incidence of newborns is lower on the European continent (ie, one case in 35,000 births in the Netherlands), since the prevalence of HSV-2 is also lower.

Interestingly, the incidence rate is also lower in populations in which HSV-2 infection is very common. Such a low incidence rate can be explained by the fact that in these population groups, infection with the virus occurs at a young age, immediately after the onset of sexual activity, and therefore the diagnosis was made at the time of pregnancy. More often, newborns become infected at birth through contact with infected mother's genital secretions.

Approximately 15% of infections are acquired after birth, often due to oral exposure to HSV-1 from close family members. Despite the availability of antiviral therapy, cases of neonatal herpes are associated with high mortality rates, and the majority of those who survive experience deteriorating physical and mental development.

Research explains the risk factors for HSV transmission at birth and suggests prevention. First, most episodes of neonatal transmission occur in women without a history of clinical manifestations of genital herpes. Second, some researchers have found that HSV infection during the last months of pregnancy is associated with a high risk of neonatal transmission.

In a cohort of 15,923 women who were studied at delivery, 56 were cultured with herpes simplex virus and 52 were seropositive. Of the 34 women with herpes simplex virus who previously had antibodies to the same type of virus, one transmitted the infection to her baby. In contrast, of 18 women with the virus who did not have antibodies to the same type of virus, six transmitted the infection to their newborns.

So, recurrence of genital HSV infection is associated with a low risk of occurrence, even if viral contamination occurs during childbirth. In contrast, genital HSV infection shortly before delivery is associated with an extremely high risk (30-50%) of neonatal herpes.

Finally, the risk of transmission also increases with the use of scalp electrodes to examine the fetus, as a puncture of the skin makes it easier for the virus to penetrate. These results suggest that in order to avoid neonatal herpes, it is necessary to prevent genital HSV infection in late pregnancy and to avoid unnecessary use of invasive methods at birth.

Treatment of genital herpes

Although there is no single cure for herpes simplex virus (HSV) infections, effective antiviral therapy is available to alleviate the signs of genital herpes. Unfortunately, modern treatment does not eradicate latent viral infection, and treatment of episodes of active symptoms does not affect the nature of the subsequent activation of the virus. Because therapy is expensive and ineffective, it is underutilized.

- the only widely used antiviral agent, which has been used in the treatment of genital herpes since the 1980s, has been available as oral tablets, injections and topical medications. It is a nucleoside analogue that requires phosphorylation of viral thymidine kinase for activation. So, acyclovir is active only in cells affected by the virus; this feature probably explains the unusually safe profile of this drug.

Acyclovir reduces viral contamination, duration of damage, and alleviates symptoms when used in the first episode of genital herpes. In large clinical trials, it has been verified that this drug prevents the development of neurological complications associated with primary genital herpes.

However, if acyclovir is used to treat recurrent genital herpes, it reduces viral contamination and shortens the duration of the lesions by one to two days. Consequently, the benefit of episodic therapy is negligible for individuals with recurrent injury.

A more effective treatment for recurrent genital herpes simplex virus infection is suppressive therapy, described as a constant daily dose of acyclovir. When taken daily, acyclovir prevents 70% of relapses, and many individuals do not have any recurrence of genital herpes. If relapse occurs while an individual is taking acyclovir, the episode is usually mild and short-lived.

Despite the potential benefits of depressive therapy with acyclovir, it is best taken only in patients with frequent relapses. First, the consent of the patient is required to carry out depressive therapy, and this procedure is expensive. Second, clinical studies have shown the benefit of suppressive therapy only in patients with at least six relapses per year. However, therapy is also likely to be effective for patients with fewer relapses per year.

Regardless of the number of relapses per year, some patients often experience psychological stress during relapses, therefore, they are suitable candidates for depressive therapy. For example, one study has shown improvements in the socio-psychological functioning of patients taking daily acyclovir. However, many clinicians do not offer suppressive therapy to patients who have fewer than six episodes per year.

Drug resistance and safety issues are cited as potential barriers to more frequent use of depressive therapy. However, in immunocompetent patients, continuous use of acyclovir does not lead to acyclovir-resistant strains of the herpes virus. Resistance to acyclovir has been described in individuals with severe immune suppression associated with HIV infection, malignancy, chemotherapy, or bone marrow transplantation.

The clinical manifestations of infection with the herpes virus resistant to acyclovir are rare, but it significantly increases the incidence of herpes. The safety of acyclovir has been evaluated by long-term (up to ten years) studies, and no anomalies have been found (clinically or laboratory) that would be associated with long-term use.

Herpes Prevention

Universal immunization in childhood with an effective HSV-2 vaccine is probably the most effective strategy for controlling genital herpes. This strategy has proven effective against other chronic viral infections, in particular hepatitis B. Unfortunately, an effective vaccine is unlikely to emerge within the next few years. The genital herpes vaccine has been in the spotlight for decades, and several experimental vaccines have been tested.

The results of a study of a drug obtained by the recombination of glycoproteins D and B were encouraging. This drug stimulates the production of neutralizing antibodies, which are equal in quantity or exceed those observed in natural infection. However, the results of clinical trials on efficacy are disappointing, as the vaccine failed to protect susceptible adults against HSV-2 infection.

Other vaccine candidates are also being tested for efficacy: a glycoprotein-based vaccine, and other options, including vaccines based on HSV DNA and genetically attenuated viruses. Meanwhile, the ineffectiveness of previous vaccines sheds light on the complexities of the immune response to HSV and on protective factors.

As with other sexually transmitted diseases, counseling on preventing transmission of infection to sexual partners is an essential part of preventing genital herpes. Unfortunately, the doctors themselves do not really know what recommendations should be given for this prevention.

The use of condoms to prevent transmission of genital herpes is now encouraged, despite minimal evidence of their effectiveness in preventing HSV transmission. Given the (anatomically) wide area of \u200b\u200breactivation of this virus in the genital tract, condoms are probably less protective against HSV than against genital diseases characterized by secretions. Condoms are recommended for sexually active adults because they protect against other sexually transmitted diseases and HIV, but agreement on condom use is low, particularly in stable monogamous couples.

In one study of 107 couples, each with one partner with HSV-2 infection, only four of them used condoms to prevent HSV transmission, and for 15 this was the only way to limit fertility. Other agents that cover most of the genital mucosa, such as germicidal agents and female condoms, may provide better protection than male condoms; however, there is no data to demonstrate their effectiveness in preventing HSV-2 infection.

In some clinics, recommendations for sexually transmitted diseases are developed according to the individual needs of patients. People with new sexual partners are advised to inform them that they have genital herpes. Then each couple can decide how to avoid transmission. Patients are also advised to avoid sexual intercourse during relapses, as the risk of transmission is high.

In the future, patients with genital herpes who are worried about transmitting the virus to their partner are offered depressive therapy. Research shows that antiviral drugs prevent asymptomatic seeding, and suggest that they may be effective in reducing the risk of sexual transmission of genital herpes. A study is ongoing that is evaluating the ability of valaciclovir to interrupt sexual transmission in monogamous couples in which only one partner has HSV-2 infection.

In this study, a partner with genital herpes receives daily suppressive therapy. If a clinical trial demonstrates the effect of antiviral therapy, it will be the first choice for some couples concerned about HSV transmission. However, such a measure is unlikely to generate widespread acceptance.

Any prevention program other than universal vaccination requires identification of people with HSV-2 infection. This selection is achieved using type-specific serological tests. However, it is unclear whether a symptom-free, HSV-2 positive person will change their sexual behavior in order to reduce the likelihood of transmitting infection to their partners.

Knowledge of HIV serological status promoted positive behavioral changes high risk some people. Recently, there is the advantage of early identification of HIV infection, whereas such a procedure was not available until the mid-1980s, when voluntary HIV testing was introduced. Recently, the situation with the detection of HSV is the same, since the infection can be identified in the absence of clinical symptoms, however, the effectiveness of interventions must be proven and made available. The traditional "screening" of HSV-2 infection is not included. However, knowledge of the presence of an infection is likely to contribute to certain behavioral changes.

Prevention of genital herpes during pregnancy. Information support

There is some concern about the psychological impact on an individual of unexpectedly reporting a positive test result for HSV-2 infection, since finding out that a person has HSV-2 infection after passing it on to a partner is also severe trauma. Now in clinics for the treatment of STIs, patients are trying to assure that they are not infected with infections, but exclusively bacterial syndromes. However, HSV-2 infection is probably not one of the most common sexually transmitted diseases in these establishments, and testing for it is still not offered. Patient needs are likely to drive the widespread use of serological tests when they become available.

Serologic tests can also play a role in the treatment of pregnant women. In regions where rates of sexually transmitted bacterial diseases have declined, neonatal HSV infection has become a common cause of morbidity and mortality in newborns. Identifying women at risk through serologic testing and counseling is the only way to reduce the negative effects associated with HSV infection in newborns.

Women with positive serological tests for HSV-2 are convinced that the risk of transmission from it to the newborn is minimal, and they can receive depressive therapy almost until the end of pregnancy. Women at risk of contracting the genital herpes virus during pregnancy are advised to avoid sexual intercourse late in pregnancy (genital and oral-genital). If antiviral therapy is effective in reducing transmission of genital herpes virus, then this provides a potential alternative strategy for preventing HSV-2 transmission during pregnancy.

Numerous information resources available provide peer-to-peer support for people with genital herpes. Since the pathogenesis of the disease is complex and the individual course is too variable, many patients believe that the specialists who provide them with services are able to provide them with up-to-date information about the course of infection and treatment options.

Thanks to sponsorship from the American Public Health Association (ASHA), the Herpes Relief Center was established. The Center publishes the quarterly newsletter The helper, which provides news on method research and discusses many general topics.

ASHA oversees local herpes support groups. Several popular books have been published explaining the nature of genital herpes. There are several sites on the Internet dedicated to the treatment of genital herpes, providing medical information and an opportunity to share experiences.

The rapid expansion of the aforementioned resources confirms research findings showing that people with herpes are often unhappy with health care. So, for many people, getting herpes is a life-changing experience, but most doctors perceive it as a trivial disorder. Because of this difference in perception, it is worth creating alternative sources of information and support for people with herpes.

Or the genitals, not everyone knows about its viral origin. Today we will explain what herpes is, and what dangers it stores in itself.

Herpes refers to viral disease, having a different course, depending on the direct type of pathogen. The most common infection in humans is the herpes simplex virus, one of two known types, each of which causes significant harm. The carriers of the disease are officially considered 90% of the world's population, of which 5% have severe symptoms. Having decided what it is, it is worth familiarizing yourself with the causes and symptoms of the disease.

Causes of occurrence

A sick person becomes a direct carrier of herpes simplex virus 1, as well as type 2. HSV-1 is able to be transmitted with saliva, the contents of the nasopharynx of a person with specific rashes. You can get infected through toys or household items, a kiss, with any method of sexual intercourse. The source of HRH-2 is the carriers of the pathogen, as well as people with genital herpes.

The human herpesvirus types 1 and 2 are able to penetrate with:
• transplantation;
• blood transfusion;
• weakened immunity after a severe and prolonged illness;
• hypothermia;
• stressful situations.

Through an infected placenta, the virus can be transmitted to the fetus. If a pregnant woman is present, during the birth process, the baby will definitely become infected.

Factors provoking infection with recurrent disease:
• overpopulation;
• sexual instability;
• non-observance of personal hygiene, as well as sanitary standards;
• malnutrition;
• body fatigue;
• menses;
• alcohol abuse;
• UV irradiation;
• genetic predisposition;
• stomach upset.

All herpes viruses tolerate ultrasonic radiation, as well as freezing, but die when heated. Microbes are able to maintain their vital activity in saliva for about 30 minutes, on moist tissue - for about 6 hours, in the air - for at least a day. To a person, herpes 1 type penetrates into childhood up to 6 years old. become infected by kissing the carrier of the infection. The virus enters the blood and nerve fibers, settling in the body forever and waiting for a convenient moment for a violent manifestation.

The active phase of the disease begins 7-10 days after infection. It is manifested by itching, as well as a burning sensation in the area of \u200b\u200bthe alleged rash. Then bubble pimples appear, filled with transparent contents. The burst bubbles dry up, and a crust forms on the surface, which disappears without leaving traces.

Although the viruses of both types of infection are separated, they have much in common: they are capable of giving the same type of symptoms and behave identically in the body. The treatment of these varieties is carried out with the same drugs. Misconceptions about different localization are unfounded, since the differences exist only in the frequency of relapses.

Development of type 1 disease

Herpes simplex virus type 1 goes through 4 stages of development:

1. tingling - characterized by a change in the skin, as well as general malaise, redness, itching, burning appears;
2. inflammation - an inconspicuous painful vesicle appears, containing a clear liquid, its size is constantly increasing;
3. ulceration - bursting blisters flow out a colorless liquid containing numerous pathogens, at this moment a person becomes the most infectious;
4. scab formation - upon completion inflammatory process crusts appear, painful and bleeding when damaged.

It takes about 10 days for a herpes rash to completely heal. When treatment for herpes simplex is started late, the infection can weaken the immune system, causing serious complications.

Symptoms

The picture with skin lesions is similar to inflammation on the lips. The defeat of the mucous membranes is accompanied by a constant burning sensation and frequent bursting of bubbles. Additional symptoms may include elevated temperature and headaches.

Main affected areas

Herpes simplex actively affects the nerve zones, appearing in the same places with a relapse, being unable to independently change its location.

However, infection of new sites gives the following results:
• ophthalmic herpes - is formed both on the mucous membrane and on the eyelids;
• facial herpes - accompanied by rashes in various areas, including the nose, ears, cheeks;
• herpetic panaritium - a rash located on the wrists, palms and fingers;
• herpes stomatitis - chose the place of localization of the gums, the insides of the cheeks, tongue and palate.

These are the most common areas affected by herpes type 1. However, the infection can cover the elbows, buttocks, back and head.

Manifestations of the second type of infection

Herpes type 2 is both primary and recurrent, which is expressed by various symptoms. For the first time, the disease can be absolutely asymptomatic, making a person a hidden virus carrier and gradually acquiring a recurrent form. Symptoms of the herpes virus of the second type can manifest themselves both on the surfaces of the genitals and on the thighs, inside the vagina or urethral canal, and on the legs. Anal contact with an infected person can cause damage to the rectum.

Attention! A prolonged course of type 1 infection, exceeding a 30-day period, may indicate low immunity, benign or malignant neoplastic formations, and HIV infection.

The spread of infection in the rest of the areas causes symptoms of the first type. The bubbles formed during the development of the disease burst, flowing out an infectious liquid and transforming into an open wound. Quite often, genital herpes infection is accompanied by general intoxication, with chills, recurrent headaches, severe weakness, and inguinal lymphadenitis. The peculiarities of this type of virus include fairly frequent relapses, repeated at least 1 time throughout the month.

Symptoms

The signs of the second strain of the virus are outwardly difficult to distinguish from the manifestations of the first. The only features of primary infection with genital herpes are:
• general malaise;
• bone soreness;
• chills;
• body aches;
• enlarged lymph nodes;
• the appearance of ulcers is accompanied by pain in the legs and buttocks.

Vaginal herpes can cause constant discomfort and burning.

Attention! The primary form, which does not manifest itself symptomatically, is among the most dangerous. A person, unaware of the presence of a problem, continues to actively engage in sexual activity, which contributes to the spread of the virus and infecting partners. It is at this stage that the herpes virus is especially contagious!

Possible complications

Complications caused by genital infection include:
• radiculomyelopathy;
• encephalitis;
• blindness;
• serous meningitis;
• herpetic proctitis;
• infection respiratory tract and the esophagus.

The infection is considered an adult, therefore it refers to diseases that are sexually transmitted.

Diagnostics

To diagnose herpes types 1 and 2, numerous laboratory tests are performed:

1. Virological tests, as a result of which cell cultures are infected to detect the effect of the virus. Due to this, multinucleated cells with contents are born, which are gradually destroyed.
2. Cytological studies reveal the content of multinucleated cells in the scrapings.
3. Biological methods - by applying contaminated materials to the rabbit's eyes, cause herpetic keratitis. Infected mice develop encephalitis.
4. Enzyme immunoassays allow the determination of antibodies to the herpes simplex virus in the blood. IgM that appeared a week later indicate primary infection or relapse. After a few weeks, IgG antibodies appear in the blood, indicating the vital activity of the herpes simplex virus.
5. PCR can detect the DNA of the pathogen. Using molecular biological technology, it is possible to detect even the smallest particle of the virus in biomaterials.

Pregnancy and the virus

Infected with herpes simplex virus types 1 and 2, a woman may not even know about it. While in a sleeping state, the disease does not manifest itself outwardly, therefore it does not pose a danger to the environment. However, the slightest weakening of the immune system entails a danger to the child.

The consequences of infection for the fetus:

• cerebral paralysis;
• cerebral underdevelopment;
• congenital herpes infections in the body;
• premature birth or spontaneous miscarriage.

If a baby is infected with herpes simplex during childbirth, complications may be as follows:

• damage to the eyes;
• rash in the mouth and on the skin;
• enznphalitis (inflammation of the brain of the head);
• herpic infection, leading to the death of about 80% of newborns.

To reduce the risk, reproductive specialists, as well as gynecologists, advise to be tested for the herpes simplex virus during pregnancy planning. Research is carried out on two main indicators:

• anti IgG - indicate that antibodies are present in the body, and the infection was transferred earlier;
• anti IgM - indicates the activity of the virus.

Decoding analyzes looks like this:

• when no infection is found in the body, IgG antibodies to the herpes simplex virus will be negative, which makes pregnancy planning possible;
• with active activity of the infection, antibodies will be positive, which will require immediate therapy;
• if IgM antibodies were detected, but IgG were not found, it means that herpetic infection is in the most active stage and it is worth forgetting about planning a pregnancy for now;
• when studies have shown the opposite result, pregnancy can be planned, since the herpes simplex virus exists in a dormant state.

The presence of IgM antibodies is not conducive to conceiving a baby. Therefore, when planning a pregnancy, you should take care of timely treatment.

If during the months of pregnancy, strains of types 1 and 2 enter the stage of active life, it is immediately prescribed. Medications are prescribed carefully, observing the reaction of the patient's body. At the end of therapy, additional studies are carried out to confirm or deny the herpes simplex virus IgG. From the moment the baby was born, he received in-depth antiviral therapy.

The possibility of transmitting the virus to the baby

Based on the timing of pregnancy, at which the infection occurred, the risk for the baby is calculated. The herpes simplex virus that enters the woman's body before reaching the 20-week period will not harm the fetus. However, if treatment is not timely, the most dire consequences are predicted (miscarriage or frozen pregnancy). Much more dangerous is infection in the third trimester. The threat of transmission of infection exceeds 30%. If during childbirth the genitals of a woman are covered with rashes, the threat of infection of the baby is 90%.

Genital herpes and childbirth

The greatest danger to the unborn baby is genital herpes, the symptoms of which appeared or worsened before childbirth. In this situation, antiviral therapy with Acyclovir begins 4 weeks before the expected delivery. If, at the beginning of labor, the genitals are covered with rashes, the use of a Caesarean section is recommended, which will significantly reduce the risk of infection of the infant.

The effectiveness of drug therapy

If herpes simplex was confirmed by the diagnosis, treatment can eliminate numerous problems:

• eliminate the symptoms of the disease;
• stop the further development of the infection;
• to get rid of subsequent relapses.

This problem can be solved by a specific treatment regimen, which includes innovative antiviral drugs that have an immunomodulatory effect. They are produced in the following form:

• injection solutions;
• pills and tablets taken orally;
• vaginal or rectal suppositories;
• gels and ointments for external use.

These drugs are used to treat various strains of herpes. Most often, complex treatment is practiced, including, in addition to antiviral drugs, drugs that strengthen the cells of the body. And with severe burning and itching of the affected areas with the herpes simplex virus, antihistamine therapy is provided.

Folk method

To get rid of the problem, lotions of freshly squeezed celandine juice are often used. Compresses are made from grated garlic, apples and potatoes. Effective results can be achieved by treating the rash with freshly squeezed juice of onions, alder leaves, wormwood, aspen, and figs.

Attention! Traditional methods allow you to get rid of only the visual manifestations of the infection, but do not help to deactivate it, stopping further development.

When external signs disappear, treatment is prescribed aimed at increasing immunity, preventing relapse and restoring the body. Given that the herpes simplex virus is actively developing with a decrease in immunity, strengthening the protective functions is of primary importance.

How to avoid infection

If it is laboratory established that you do not have herpes simplex antibodies at all, only compliance with the following recommendations will allow you to avoid infection:

• you should not share your drink or food with anyone;
• do not finish drinking or finishing food behind others;
• always use individual dishes designed for you, this is especially true when symptoms of herpes appear in households;
5 (100%) 2 votes

The herpes virus is extremely dangerous to humans. Today more than 100 herpes viruses have been studied, 8 types of which have been isolated from humans. They all cause a variety of diseases, collectively called herpes infection. The culprit of the herpes disease is human herpes simplex virus types 1 and 2. The genitals are most common. It is also common, which is caused by the herpes simplex virus type 3. These diseases are characterized by the rash of grouped vesicles located on the mucous membranes and skin.

Number of cases herpes infection growing steadily. Scientists have proven that 90% of the world's population is infected with herpes simplex viruses (one or more serotypes). 1/3 of the infected population suffers from recurrent forms of the disease. Up to 20% of adults are affected. The reason for the increase in cases of the disease is early sexual activity.

Figure: 1. In the photo, the herpes virus.

Once in the human body (more often in childhood), viruses persist (stay) in it for life, causing diseases that differ in a variety of clinical manifestations. All types of viruses are very similar, which makes it impossible to distinguish them even with a powerful electron microscope. The type of pathogen can be distinguished only by the presence of specific antibodies in the patient's body.

Herpetic infections are highly contagious (infectious), including intrauterine infection. In immunodeficiency states, they appear in a patient one of the first and are markers for HIV infection.

Viruses at a temperature of 37.5 ° C retain their viability for only 20 hours. In the environment, they are stored for up to 2 hours on coins, door handles, and water taps. Up to 3 hours - on plastic and wood products.

The atypical picture of the disease and the resistance of pathogens to antiviral therapy are the features of the modern course of herpes infection.

How the herpes virus is transmitted

Airborne droplets, direct contact with an infected or sick person through blood, saliva, semen, mucous secretions, through his household items and hygiene are the main ways of infection with herpes viruses.

• The herpes virus is transmitted through intercourse, blood transfusions, organ transplants, and kissing. Contact with infection most often occurs in childhood - up to 5 years. The pathogens are transmitted to the child through the placenta and during childbirth.
• Shingles, chickenpox and other viruses are transmitted by airborne droplets.
• Cytomegaloviruses enter the body with saliva (often with kissing), genital secretions (sexual intercourse), breast milk, through non-sterile syringes, donor blood transfusions, donor organ transplantation and the use of sperm and eggs.

The development of herpes infection is inhibited by the protective antibody titer. In adults, it reaches 90%. The development of the disease in children is inhibited by passive maternal immunity.

Figure: 2. In the photo, the Varicella zoster virus (left). In the photo on the right - viruses of the 6th type.

Figure: 3. In the photo on the left, immature herpes simplex virions. On the right is a mature virus. Its distinctive feature is its thick shell.

The herpes virus is not alone!

The herpes virus family ( Herpesviridae) has more than 80 microorganisms, 8 of which are dangerous to humans.

1 TO α-herpes viruses include viruses of 1, 2 and 3 types that cause herpes and shingles. They affect different types of cells and persist for a long time in the paravertebral ganglia. Their distinctive feature is their rapid reproduction in target cells.

Human herpes simplex virus type 1 (Herpes simplex virus 1) most often affects the mucous membranes of the mouth, eyes, skin of the face and upper half of the body.

Human herpes simplex virus type 2 (Herpes simplex virus 2) most often affects the skin and mucous membranes of the genitals, the skin of the buttocks and lower extremities.

Human herpes virus type 3 causes diseases such as chickenpox and (Herpes zoster).

The herpes simplex virus has a tropism for nerve cells. Being a weak inducer of interferon, it persists in the human body for life and is the cause of recurrent relapses of the disease. With a decrease in immunity, the disease acquires a generalized course.

2. β-herpes viruses, affecting cells, lead to an increase in their size (cytomegaly), cause immunosuppressive conditions.

Human herpes virus type 5 (Cytomegalovirus) Is the causative agent.

Human herpesvirus 6 and 7 causes exanthema of newborns, which manifests itself high temperature body and the subsequent appearance of a macular papular rash. It is assumed that these microorganisms are the cause of the development of acute hepatitis, chronic fatigue syndrome and decreased (depression) immunity.

3. γ-herpes viruses focused on T- and B-lymphocytes. Pathogens stay in these cells for a long time, causing sarcomas and lymphomas.

Herpes simplex virus type 4 (Epstein-Barr) is the cause of infectious mononucleosis, Burkitt's lymphoma, nasopharyngeal carcinoma, hairy leukoplakia of the tongue, B-cell lymphoma, chronic fatigue syndrome and decreased immunity.

Herpes virus type 8 is a cause in HIV-negative, HIV-infected people and AIDS patients.

Herpes simplex virus

The culprit of the herpes disease is human herpes simplex virus types 1 and 2. Their path in the body is complex and requires a little explanation.

1. When transmitting herpes simplex viruses from a sick person or a virus carrier, pathogens are fixed on target cells, then penetrate through the cell membrane into the cell, where they multiply. Reproduction begins within two hours after infection of the cells, reaching a maximum after 8 hours. The higher the level of metabolism in the cell, the faster viruses multiply. A high level of metabolism is noted in the cells of the epithelium, mucous membranes, blood cells, lymphocytes.

2. After 18 hours, the first generation of herpes simplex viruses already begins to enter the intercellular space, biological fluids, circulatory and lymphatic systems, where they are located for 1 - 4 hours. It is during this period that the patient experiences acute intoxication.

Figure: 4. In the photo on the left, the exit of a virus particle from the cell. The photo on the right shows new viruses in the intercellular space.

3. After 4 hours of free stay, viruses begin to adsorb on new cells and then penetrate into their cytoplasm for subsequent replication (reproduction). Each generation of pathogens lives on average for 3 days. The faster the reproduction process goes, the larger the affected area. During this period, characteristic rashes appear on the skin and mucous membranes.

Figure: 5. The photo shows characteristic rashes with herpes. Against the background of redness, bubbles with clear liquid, after opening which erosion (damage) remains, covered with crusts. A week later, complete epithelialization of the damaged areas of the skin and mucous membranes is noted.

4. If, as a result of treatment, the complete destruction of viruses has not occurred, then the rest of them penetrates along the nerve fibers into the paravertebral ganglia. From that moment on, the cell will constantly produce a small amount of viral particles, and the person will become a carrier of herpes for life. Antibodies appear in the patient's blood.

Figure: 6. Schematic representation of a virus inside a nerve cell.

Herpes simplex signs and symptoms

Signs and symptoms of herpes simplex during the period of primary manifestation

1. Precedes the period of rashes in 80% of cases prodromal period... During this period, viruses multiply in target cells.

2. Intoxication phenomena appear at the time of the release of the first generation viruses into the extracellular space, biological fluids, circulatory and lymphatic systems. The main signs and symptoms of herpes during this period are manifested in the form of an intoxication syndrome, which is characterized by headache, fever, chills, myalgias, an increase in peripheral lymph nodes, weakness and sleep disturbance.

3. The appearance of a rash marks the period of introduction of new generation viruses into new cells of mucous membranes and skin for subsequent replication of viral particles. The faster viruses multiply, the larger the affected area. During this period, characteristic rashes appear on the skin and mucous membranes.

A vesicular rash (a rash with fluid-filled blisters) is the main symptom of herpes simplex. It appears against the background of redness of the skin. The bubbles quickly open, leaving in place areas of damage (erosion), which eventually epithelize.

The rash appears most often in the area of \u200b\u200bthe red border of the lips, wings of the nose, genitals, gluteal region. The mucous membrane of the mouth is often affected, causing diseases such as gingivitis, stomatitis, glossitis, and herpes sore throat.

The acute period lasts from 8-10 to 18-22 days. The severity of clinical manifestations fades away after a week. Then the damaged epithelium begins to slough off.

Rashes are single and up to a strong degree of severity, which depends on the state of the patient's immunity. Antibodies in the patient's body with the primary manifestation of herpes are absent. With a relapse of the disease, antibodies to the virus are always determined.

Figure: 7. In the photo, shingles. Vesicular eruptions along the axons of the nerve cells of the paravertebral ganglia, which are a reservoir of viruses.

3. Pain symptom with herpes manifests itself both during the rash, and independently of them during the relapse of the disease. With the localization of rashes on the face, pain occurs along the branches trigeminal nerve... In the case of genital herpes, pains are localized along the branches of the paravertebral ganglia of the lumbar spine. A painful symptom in women is often the only manifestation of genital herpes occurring with damage to the vagina, cervix, etc.

In men, pain often occurs in the perineum and external genital area. Pain caused by irritation of parasympathetic fibers manifests itself as a burning sensation. It is this symptom that is characteristic of the manifestation of herpes.

Relapses of herpes and herpes infection

In 20% of patients, herpes infection recurs due to the state of the human immune system, virulence, pathogenicity and type of viruses. Relapses of the disease destroy the patient's physical health, disrupt the function of vital organs and adversely affect mental health.

Chemotherapy and HIV infection negatively affect the state of the immune system.

In most cases, the cause of the recurrence of the disease cannot be identified. Patients with recurrent herpes infections are often perceived as a chronic disease. With herpes simplex, the disease has a short clinical period. In a patient, after a week, complete epithelialization of damaged areas of the skin and mucous membranes is noted.

Immunity inhibits the development of the disease. A good immune system prevents the spread of viruses in the patient's body and the first encounter with an infection ends with a complete cure. With immunosuppression, viruses enter the paravertebral ganglia of the autonomic nervous system and, subsequently, will cause relapses of the disease.

Clinical forms of diseases caused by herpes simplex virus type I

Herpes simplex virus type I infects:

• skin: red border of lips, skin of the face, eyelids, hands, is often the cause of herpetic eczema;
• the oral mucosa, causing herpetic gingivitis, glossitis, stomatitis and herpes sore throat;
• eyes, causing inflammation of the outer membrane of the eye (conjunctivitis), the edge of the eyelid (blepharitis), the cornea of \u200b\u200bthe eye (keratitis), the iris and ciliary body of the eyeball (iridocyclitis), the choroid and retina (chorioretinitis), the vessels of the uveal tract (uveitis), the outer layer of blood vessels (perivasculitis) and optic neuritis.

Figure: 8. The photo shows herpes on the lips and nose.

Figure: 9. In the photo herpes on the face.

Figure: 10. In the photo there is herpes in the mouth.

Figure: 11. The photo shows herpes sore throat.

Figure: 12. On the photo herpes in the mouth - stomatitis and gingivitis.

Figure: 13. The photo shows herpetic conjunctivitis (left) and keratitis (right).

Clinical forms of diseases caused by herpes simplex virus type II

Herpes simplex virus type II infects:

• skin and mucous membranes of the genitals (penis, urethra, external genital organs of a woman, cervical canal, endometrium and perineum),
• skin of the buttocks and lower limbs,
• the lining of the brain and its substance (meningoencephalitis),
• is the cause of congenital herpes and the neonatal period.

Figure: 14. The photo shows genital herpes in men.

Figure: 15. The photo shows genital herpes in women.

Figure: 16. In the photo there is a herpes of the genital organs of a woman.

Figure: 17. The photo shows congenital herpes.

Clinical forms of diseases caused by the human herpes virus type 3

Human herpes virus type 3 ( Varicella zoster) causes chickenpox and herpes zoster ( Herpes zoster).

Figure: 18. In the photo, chickenpox in a child and a pregnant woman.

Figure: 19. The photo shows shingles. rashes along the intercostal nerves.

Figure: 20. In the photo, herpes on the face. Damage to the skin of the face, eyelids and forehead. Rash along the branches of the trigeminal nerve.

Figure: 21. The photo shows shingles (rare forms).

Clinical forms of diseases caused by the herpes virus type 4 and 8

Herpes viruses of types 4 and 8 multiply in blood cells - T and B lymphocytes, which are immunocompetent cells. A decrease in the number of these cells leads to the development of secondary immunodeficiency. In such patients, acute respiratory infections are often noted, efficiency decreases, long worries subfebrile temperature body, lymph nodes increase, psychasthenia develops.

Herpes virus type 4 () is the cause of infectious mononucleosis, Burkitt's lymphoma, nasopharyngeal carcinoma, hairy leukoplakia of the tongue, B-cell lymphoma, chronic fatigue syndrome and decreased immunity.

Herpes virus type 8 is the cause of Kaposi's sarcoma in HIV-negative, HIV-infected people and AIDS patients.

Figure: 22. Mononuclear cells in the photo are B-lymphocyte cells, where Epstein-Barr viruses have penetrated and multiply. With massive reproduction, viruses destroy the cell membrane and enter the bloodstream. If their number is small, then they reside for a long time in the lymphocytes of the salivary glands, nose and crypts of the tonsils. Released into the external environment with saliva, they become the cause of infection in healthy people.

Figure: 23. The photo shows enlarged lymph nodes with infectious mononucleosis.

Why are herpes and herpes infection dangerous?

• Herpes simplex viruses and cytomegaloviruses negatively affect human reproductive function, leading to the development of serious diseases of expectant mothers, fetuses, newborns and young children.
• Mortality in herpetic neuroinfection is 20%, the incidence of disability is 50%.
• Half of patients with ophthalmic herpes (herpes of the eyes) develop cataracts or glaucoma.
• In AIDS, diseases caused by the herpes simplex virus, cytomegalovirus and Epstein-Barr virus often occur.
• A lot of scientific research proves the role of cytomegalovirus, type 8 viruses and epstein-Barr viruses in the development of a number of neoplasms.

Diagnosis of herpes

Diagnosis of herpes is based on the detection of the virus in the light of an electron microscope and in storage cells with their subsequent identification, detection of antibodies and DNA fragments of viruses in biological material.

Figure: 24. Herpes virus. The photo was taken under the light of an electron microscope.

Millions of people around the world suffer from a variety of diseases caused by the herpes virus. Herpetic infection has various forms of manifestation. The course of the disease often becomes chronic and has different transmission routes. Herpes and herpes infections are difficult to treat. Viruses persisting in the body for a long time lead to a weakening of the immune system, therefore there is no complete cure for herpes viral infections.

Almost a third of the world's population is affected by herpes infection and 50% of them have recurrences of the disease every year, since immunity against this viral infection no. Scientific data show that by the age of 5 years, the infection with the herpes virus reaches 60%, and by the age of 15, almost 90%. Most people are life-long virus carriers. The overwhelming number of outcomes of primary infection (85-99%) is represented by asymptomatic (latent) infection, due to which patients do not receive timely medical care in order to prevent the formation of a chronic recurrent form of the disease. At the same time, there is evidence of the formation of a chronic herpes infection in the majority of people with a primary visit to a doctor for herpes simplex.

Herpes simplex virus (Herpessimplex) belongs to the group of herpetic DNA viruses. There are HSV type 1 (H. labialis), which affects the mucous membranes of the eyes, mouth, red border of the lips, skin and mucous membranes of the wings of the nose, skin of the face, etc., as well as HSV type 2 (H. genitalis), which affects the mucous membranes and the skin of the genitals. The recurrent form of herpes infection caused by HSV develops in 15-25% of those infected. The recurrent form of GI is exhibited with repeated symptoms of the disease within a year. Often, a recurrent form is established when the frequency of relapses during the year is more than 6-10 with characteristic symptoms of the disease.

Features of herpes infection caused by HSV:

1) Life-long persistence of HSV in the body of the infected person, which indicates the absence of the formation of sterile immunity (that is, antibodies are present, and the pathogen does not leave the body). HSV, even with a latent infection, is present in the body intracellularly.
2) The influence of HSV on the immunity of the patient (the formation of secondary immunodeficiency), which does not appear immediately. Over the years, a person's resistance to common colds and skin pathogens decreases.
3) Oncogenicity of HSV. Herpes simplex virus type 2 (genital) has been associated with cervical cancer.
4) Teratogenicity and influence on the course of pregnancy. Herpes simplex, in particular genital, plays a predominant role in the etiology of spontaneous abortion and premature birth, in the violation of embryo and organogenesis, congenital pathology of newborns.
5) The tendency to form a chronic form of the disease in almost all patients.
The chronic form of herpes simplex is dangerous for its relapses (exacerbations), which significantly affect the patient's quality of life.

HSV manifestations

Features of the formation of the immune response in herpes infection caused by HSV.

It is the "special relationship" between the herpes simplex virus and the human body that is both the basis for the formation of antiviral immunity, and the reason for the lack of complete elimination of the virus from the body, and contribute to serious violations of human immunity. When HSV enters the body, several "steps" or phases of immune defense begin to work.

Scheme of the immune response in herpes

1) Early immune response phase - the so-called primary innate defense - cells of the monocytic-macrophage link, dendritic cells, natural killers (a group of lymphocytes, the surface of which is coated with antiherpetic antibodies IgM, G and tuned to destroy the freely circulating virions of viruses), the complement system. This phase begins to work from the first days when the body meets the virus. The result is a massive migration of inflammatory cells to the focus, the synthesis of a- and b-interferons, which contributes to the formation of immunity to the virus of target cells, as well as, as a result, the destruction of already infected cells.

The scheme of work of interferons

2) Late defense phase follows the first phase and is characterized by the presentation of the virus itself by macrophage cells to T- and B-lymphocytes, which as a result are transformed into antibody-producing plasma cells. The extracellular virus binds by means of antibodies. In the same phase, macrophages and lymphocytes synthesize proinflammatory mediators (interleukin 1 and 2, tumor necrosis factor and others), which completes the inflammatory response.

A type-specific immune response is formed 14-28 days after the initial encounter with HSV, regardless of the form of the disease (with typical manifestations or asymptomatic). Reactivation of a chronic infection inevitably leads to a re-release of antigen into the blood, which leads to a multicomponent immune response, that is, a re-production of antibodies.

The result of immune disorders in the often recurrent form of chronic herpes infection is a decrease in the total number of T- and B-lymphocytes, a decrease in their functional activity, changes in the interferon system, macrophage cell link.

Treatment of frequently recurrent forms of herpes infection caused by HSV.

Treatment of patients with chronic herpes infection is a rather difficult task due to the ability to persist for life and a significant decrease as a result of this immune defense of the patient's body. One of the most frequent questions of patients: "Doctor, is it possible to completely get rid of the herpes simplex virus?" - remains unanswered. The main goal and expected outcome of therapeutic measures is to achieve the stage of long-term remission, that is, to reduce the frequency of recurrences of herpes during the year to a minimum and lengthen the period of "relapse-free" calm. Moreover, the patient must understand that the virus does not leave the body, but goes into a "dormant" intracellular state.

The basic principles of treatment of frequently recurrent forms of herpes infection [Moscow City Antiherpetic Center]:

1) Relapse relief (activation of chronic infection) - antiviral and immunomodulatory therapy in short courses, taking into account the data of the immunogram and the level of interferons in the body (interferon status) with local treatment. The course is 5-10 days.
2) Anti-relapse therapy - the use of herpes vaccine, prolonged antiviral drug regimens and long-term immunomodulator regimens. The course is 30-60-90 days or more.
3) Supportive therapy during dispensary observation (adaptogens, revaccination of herpes vaccine and other methods).

The success of treatment largely depends on an integrated approach to therapy, a combination of immunomodulators with different mechanisms of action and the effective use of a specific treatment.

Treatment of herpes infection consists of several interrelated areas.

The first is etiotropic or antiviral therapy, which is administered internally and locally directly during the period of clinical manifestations of herpes. The purpose of antiviral therapy is the actual virostatic effect (disruption of viral DNA synthesis, disruption of the assembly process of viral particles, inhibition of virus reproduction and, ultimately, disruption of the interaction of human cells and herpes simplex virus). The drugs of choice for oral administration are acyclovir (zovirax, acyclovir-acri), valacyclovir (valtrex, valvir, valtsikon, wirdel), famciclovir (famvir).

There are several reception schemes:

1) a short scheme for 5-10 days of primary manifestations or activation of chronic infection; doses of acyclovir 1000-1200 mg / day for 5-3 doses, valtrex 1000 mg / day in 2 doses, famvir 500 mg / day in 2 doses;
2) prolonged (suppressive) scheme of daily intake in courses of several (6-12) months; dosages of acyclovir 800 mg / day, valtrex 500-1000 mg / day, famvir 500 mg / day. The prolonged regimen is preferred for patients with frequent relapses more than 6-9 times a year with an efficacy of up to 80%.

For local therapy are used: 3-5-7.5% cream, ointments and gels acyclovir, zovirax, panavir, herpferon, virosept, penciclovir, 1% fenistilpentsivir, 2-4% tebrofen, virmerts, viferon, epigenlabial, panthenol spray, infagel , 5% iviquimod and others. Local therapy is used from the first symptoms of the disease, and to prevent relapse within 1 month after the symptoms disappear. The use of local hormone therapy is not recommended due to the possibility of a protracted recurrent process. When symptoms of ophthalmic herpes (herpetic keratitis and keratoconjunctivitis) occur, eye drops are used: Lokferon, Ophthalmoferon, Interlock, Reaferon in the form of drops, others.

The second direction in the treatment of the herpes form, and in particular its often recurrent form, is immunotherapy. The aim of immunotherapy is to correct various kinds of violations of the specific and nonspecific links of human immunity and, as a result, expected to be achieved, to reduce relapses to a minimum and increase the time of quiet interrecurrent remission.

Any means of immunotherapy should be selected and prescribed by a doctor, drugs have side effects and contraindications!

Herpes immunotherapy can be performed in 2 forms: nonspecific and specific.

1. Non-specific immunotherapy is widely targeted and used for many diseases, including herpes simplex virus. Includes immunoglobulins, interferons and inducers of endogenous interferon, as well as drugs that stimulate cellular and humoral immunity (the process of phagocytosis, T- and B-cell links of immunity).

1.1 Immunoglobulins are prescribed both with a replacement purpose due to the content of antibodies in them, as well as with a direct immunomodulatory purpose (improvement of phagocytosis processes, the ability to change the production of interleukins, activate subpopulations of T-lymphocytes, and others). For recurrent herpes, normal human immunoglobulin containing antibodies to the herpes virus can be prescribed. The drug is injected intramuscularly in a single dose of 0.15-0.2 ml per 1 kg of human body weight once a day in 2-3 days. The course of treatment is 4-5 injections.
In more severe cases of herpes infection (damage to the central nervous system and internal organs, as well as severe immunodeficiency), replacement therapy with intravenous forms of immunoglobulins with an increased content of antiherpetic antibodies (sandoglobulin, Switzerland) or an intravenous solution of domestically produced immunoglobulin is performed.

1.2 Interferons belong to the factors of natural immunity. Interferon synthesis occurs
in any organism in response to viruses, bacteria and other pathogens entering it. Interferons are factors of nonspecific protection of the body, combine antiviral, antiproliferative, immunomodulatory effects, in particular, their properties have been proven to stimulate phagocytosis, increase the activity of natural killer cells, and thereby directly participate in the elimination of the pathogen. Three types of interferons have been identified: α - interferon (leukocyte), β - interferon (fibroblast), γ - interferon (immune, synthesized by T-lymphocytes). γ-interferon has the lowest antiviral protection, but high immunomodulatory properties.
In chronic recurrent herpes infection, α-interferons (viferon, kipferon), as well as γ-interferon (ingaron) are mainly used.

Viferon - refers to α-2b-interferons, contains antioxidants, it is known in 4 doses in the form of rectal suppositories. Viferon 1 (150 thousand IU), Viferon 2 (500 thousand IU), Viferon 3 (1,000,000 IU), Viferon 4 (3,000,000 IU). Viferon increases the level of secretory IgA, normalizes the IgE level, has an immunomodulatory effect on T- and B-lymphocytes, and also restores the impaired function of the production of endogenous α-2b interferon. This is a drug for substitution therapy, that is, ready-made α-2b-interferon is delivered to the tissues; due to this, with prolonged use (more than 2 weeks), the production of its own endogenous interferon begins to be inhibited. This must be taken into account when prescribing long courses of the drug for recurrent herpes infection, namely, the withdrawal of the drug should be carried out gradually. In case of recurrent herpeseviferon, it is recommended to prescribe in the prodromal period (before the expected clinical manifestations) or in the first hours and days after the first symptoms of recurrent infection (burning, itching, redness, the appearance of vesicles - characteristic herpetic elements).
Adults are prescribed Viferon-3 (1 million IU) 1 suppository rectally 2 times a day every 12 hours every day for a course of 10 days, followed by supportive therapy to prevent subsequent relapses. For this purpose, the drug is prescribed 1 suppository 2 times a day, 2 times a week for 10 days (that is, within 5 weeks). Further, prophylactic interferon-stabilizing courses are prescribed: Viferon-2 (500 thousand IU), 1 suppository 2 times a day every day for 5 days every month (that is, after 4 weeks) in a general course up to a year from the start of therapy.
There is a "lightweight" scheme for patients with recurrent herpes for 12 weeks: viferon-3, 1 suppository 3 times a day after 8 hours - 1 week; then 1 candle 2 times a day after 12 hours 1 week; then 1 candle 1 time per day every day for 2 weeks; then Viferon-2 1 suppository 1 time per day 3 times a week every other day for 2 weeks; then 1 candle 1 time per day 2 times a week for 3 weeks; then 1 candle 1 time per day 1 time per week for 3 weeks. Total - course admission for 3 months [RK Galeeva, KSMA, Kazan].

Kipferon is a combination of α-2 interferon and KIP (complex immunoglobulin preparation containing immunoglobulins A, G, M) at a dosage of 500 thousand IU + 60 mg of the corresponding components. It has an immunomodulatory effect on the cellular and humoral links of immunity. It exists in the form of suppositories used both intravaginally and rectally (depending on the disease and its severity). Adults are prescribed 1-2 million IU (2-4 candles) per day with 1-2 candles taken 2 times a day after 12 hours for 10-14 days daily. Perhaps the appointment of repeated courses.

Ingaron - refers to γ-interferons. It is found in 4 doses - 100 thousand IU, 500 thousand IU, 1 million IU, 2 million IU, and is prescribed parenterally during the period of activation of chronic infection. The main difference is the effect of ingaron, a significant increase in the presentation of herpes-infected cells and their recognition by T-lymphocytes, respectively, as well as blocking the replication of herpes simplex virus DNA and the assembly of viral particles. It is prescribed 500 thousand IU subcutaneously every other day with a course of 5 injections.

1.3 Endogenous interferon inducers - already from the name it is clear that the main action of the drugs is to stimulate the production of the human body's own interferon, which is necessary to combat the herpes virus in particular.

Amiksin (analogue of lavomax) - inductor in the body of all types of interferons - α, β, γ. A feature of the drug is long-term circulation of therapeutic concentration in the blood (up to 8 weeks). In addition to the induction of interferons, amixin promotes an increase in the formation of specific antibodies (IgM, IgG), normalizes the ratio of helper cells (T-helpers) to T-suppressors, and has a direct antiviral effect. Interferon is produced sequentially, first in the intestine, then in the liver and in the FEC (blood corpuscles), and a high level of interferons in the blood is reached within 24 hours after taking amiksin. Scheme: 1-2 tablets (125-250 mg) in the first 2 days of therapy, then every other day 1 tablet for a course of up to 4 weeks (course dose of 10-20 tablets). Further, maintenance therapy 125 mg (1 tab) 1 time per week for 2 months,

Cycloferon is an inducer of predominantly early α-interferon in tissues and organs. It activates macrophages, T- and B-lymphocytes, restores the ratio of T-helpers / T-suppressors. While taking cycloferon, a high level of endogenous interferon is maintained for 3 days. In addition to the immunomodulatory effect, its antiviral activity is expressed: early dates affects the reproduction of the virus, lowers the virulence of "daughter viruses", thereby forming defective viral particles that are eliminated. In case of herpes infection, the drug is taken once a day for adults and children over 12 years old, 450-600 mg (3-4 tablets) according to the scheme: on the 1st, 2nd, 4,6,8,11,14,17,20,23 days. Heading dose of the drug is 40 tablets. Treatment begins with the first symptoms of the disease. With a recurrent form, the course can be repeated after 3-6 months. Parenteral administration: 250 mg (1 ampoule of 2 ml) 1 time per day according to the "basic scheme" 10 injections: on the 1st, 2nd, 4, 6, 8,11,14, 17,10, 23 days. With a frequently relapsing form, you can continue the administration 1 time in 3 days for 4 weeks.

Neovir - as well as cycloferon, stimulates the production of endogenous alpha-interferon, and it is also called the "superinducer" of interferons, since it leads to the synthesis of high concentrations of endogenous interferon-alpha. It normalizes the balance of CD4 / CD8 lymphocytes, activates the monocytic-macrophage defense system. It is applied intramuscularly during the period of activation of the infection 250-500 mg (1-2 ml) 1 time per day after 24 hours in the amount of 3 injections, then 3 more injections in the same dose and frequency after 48 hours. A single dose can also be calculated at the rate of 4-6 mg / kg of the patient's body weight. The general course is 5-7 injections. In the inter-relapse period, supportive therapy is indicated to consolidate therapeutic effect prescribed: 250 mg (1 injection) once a week for 1 month. With a frequently recurrent form of the disease, such maintenance courses can be repeated several times with an interval of 4-5 weeks.
Plant inducers of endogenous interferon:

Panavir - a purified extract of the shoots of the Solanumtuberosum plant - is a natural immunomodulator with antiviral action. Promotes the production of endogenous α- and γ-interferons. Available in 4 forms (injections, ointment, rectal and vaginal suppositories) 200 mcg each. When a chronic infection is activated, 200 μg (1 ampoule or vial) is prescribed intravenously with a jet once a day after 48-24 hours with a course of 2 injections; with a frequently recurrent form, this course can be repeated after 4 weeks. You can also use suppositories: rectally 1 suppository 1 time per day after 48-24 hours in a course of 2 days, intravaginally 1 suppository 1 time per day every day for 5 days.

Ridostin is a preparation based on the RNA of the yeast Sacchromycescerevisiae. The drug stimulates the production of interferon, activates the process of phagocytosis, natural killer cells and others. The drug is administered at 8 mg (1 ampoule) intramuscularly 1 time in 3 days with a course of 3 injections. For the prevention of relapses, 4 injections are administered with an interval of 2 days, then the courses can be repeated after 2-3 months.
Alpizarin is a herbal preparation with a combined antiviral and immunomodulatory effect: stimulation of the production of γ-interferon, activity of phagocytosis, the process of antibody formation. It is prescribed 100-200 mg (1-2 tablets) 3-4 times a day from 5 to 14 days with subsequent prevention of relapses: repeat 10-14 days of the course 1 month after the end of the main one.

1.4 Drugs that stimulate phagocytosis, as well as T- and B-cell links of immunity (drugs are shown after a thorough examination of the immune system - immunograms).

a) Endgenic origin

Taktivin (Timalin) are an extract of the thymus of cattle, it is prescribed for a significant violation of the T-cell link of human immunity, that is, a significant immunodeficiency. They normalize the quantitative composition of immunity cells - T- and B-lymphocytes, activate cellular immunity, the processes of phagocytosis. If we talk about herpes infection, then the drug can be recommended for recurrent ophthalmic herpes. Taktivin is prescribed at a dose of 1 mcg / m2 / day subcutaneously once a day, the course is 14 days (7 injections every other day). The courses can be repeated no earlier than in 4-6 months. Prevention of subsequent relapses boils down to the following: during the expected period of relapse, a course is carried out consisting of 5 injections every other day at a dose of 25-50 μg with an interval of 3-6 months.

Immunofan is a preparation containing amino acid residues of thymopoietin. The drug activates the antioxidant system of the body, activates the processes of phagocytosis, restores the links of cellular and humoral immunity, enhances and accelerates the processes of antibody formation. It is prescribed in 2 forms: intramuscularly or subcutaneously, 1 ml (50 mcg) 1 time per day every day for 15-20 days. In case of a frequently recurrent form, the course can be repeated no earlier than after 4 weeks.

b) Exogenous origin (plant and animal immunomodulators)

Licopid (glucosaminylmuramyl dipeptide) - tablet form 1 and 10 mg. The drug enhances the activity of phagocytosis cells, proiferative activity B- and T-lymphocytes, activates and accelerates the formation of specific antibodies. In chronic recurrent herpes, 1 tablet (10 mg) is prescribed orally 1-2 times a day for 6 days during the period of infection activation. For herpetic stomatitis, lycopid is prescribed 1 tablet (1 mg) 1 time per day sublingually (under the tongue) for 10 days at easy course... With a recurrent form of stomatitis, 1 tablet (10 mg) 1 time per day under the tongue for 10 days.

Derinat is an immunomodulator of animal origin. Affects the processes of cellular and humoral immunity, in particular, stimulates B- and T-lymphocytes, cells of the monocytic-macrophage link, activates natural killer cells, and accordingly accelerates the elimination of the pathogen, stimulates regenerative processes. It is applied intramuscularly 5 ml (75 mg) 1 time / day according to the scheme: 5 injections after 24 hours, then 5 injections after 72 hours.

c) Synthetic immunomodulators:
Polyoxidonium is an immunomodulator of domestic production, promotes the activation of the processes of phagocytosis, natural killers, and also stimulates the processes of antibody production.
With a frequently recurrent form of chronic herpes infection, there is

1) a short regimen of polyoxidonium administration: 6 mg / m every other day with a course of 5 injections or for 10 days and
2) prolonged regimen for 45 days: 6 mg i / m daily for 5 days, then 6 mg i / m every other day for 5 injections for 10 days, then 6 mg i / m 2 times a week for 1 month.

Both the short and the beginning of the prolonged regimen are quite effective in the complex therapy of relapse relief, but it is the prolonged regimen that significantly shortens the duration of the relapse period, and also reduces the frequency of their occurrence in the long-term period. The overwhelming majority of patients on the prolonged regimen noted the prolongation of the remission period [AE Shulzhenko, IN Zuykova, Institute of Immunology, IMBA, Moscow].

Isoprinosine is a modern immunomodulator with a nonspecific antiviral effect. It normalizes the functional activity of lymphocytes of different classes, increases monocyte-macrophage activity, stimulates the activity of cytotoxic T-lymphocytes, natural killers, normalizes the ratio of T-helpers / T-suppressors, stimulates the production of immunoglobulins, endogenous interferon, cytokines. It is prescribed in a dose of 6-8 tablets / day, 500 mg each (3-4 g / day) in 3-4 doses orally for 5-10 days, then in the inter-relapse period 1 tab (500 mg) 2 times a day within 30 days.

Immunomax - affects humoral and cellular immunity. Activates the process of phagocytosis, natural killer cells, promotes the production of cytokines, stimulates the production of antibodies. It is prescribed 100-200 U intramuscularly 1 time a day according to the scheme in 1, 2, 3, 8, 9, 10 days with a course of 6 injections.

Tamerite is a synthetic immunomodulator with antioxidant and anti-inflammatory effects. The drug improves the functional activity of cells of the monocytic-macrophage link, prevents the overproduction of pro-inflammatory mediators (TNF, IL and others), activates neutrophils, and stimulates reparative processes. It is prescribed 100 mg (1 bottle) once a day for 5-10 days, followed by a switch to maintenance therapy, 100 mg once every 3 days, with a course of up to 15-30 intramuscular injections.

Galavit is a drug with an effect similar to tamerit, often used in gynecological practice in the form of intramuscular injections and rectal suppositories. In chronic recurrent herpes, 100 mg is prescribed daily 1 time per day for 5 days, followed by a switch to injections of 100 mg 1 time per day every other day in the amount of 15 injections. Another scheme of galavit involves the appointment of rectal suppositories: 1 suppository at night for 5 days every day, then 1 suppository at night every other day with 15 injections.

2. Specific immunotherapy.
Specific immunotherapy is designed to directly stimulate specific immune responses against the herpes simplex virus, that is, the activation of all links of the body's specific antiviral defense. Such therapy is prescribed no earlier than at the end of the primary course of exacerbation relief chronic illnessand preferably after completing it. As specific means are used: antiherpetic vaccine and a fairly new method of therapy with dendritic cells.

2.1 Herpes vaccine
Therapy for herpes with a recombinant multivalent herpes vaccine is carried out only during remission and no earlier than 5 days after the acute manifestations of herpes subside. The vaccine contains both types of herpes simplex virus killed by formalin, stimulates cellular mechanisms resistance or resistance of the body to herpes simplex viruses of types 1 and 2. A single dose of 0.2 ml, which is injected intradermally into the inner surface of the forearm. A course of 5 injections is carried out after 7 days, and with a frequently recurrent form, after 10 days. Revaccination (5 injections of a repeated course) is carried out for patients suffering from a frequently recurrent form of herpes with a regularity of 1 time in 6-8 months, and between courses of the vaccine, therapy should be supplemented with non-specific immunotherapy. The latest clinical use of the vaccine allows us to speak about a rapid onset of recovery, a reduction in the duration of subsequent relapses, and an extension of the period of remission, but it does not allow us to speak unambiguously about the prevention of relapse of the disease. In this regard, the search for alternative methods of specific therapy continues.

2.2 Vaccination method using generated DCs (dendritic cells) [patent RU 2514034
on the basis of the FGBU "NN Blokhin Russian Oncology Center" RAMS].
Dentritic cells (DC) - These are the main antigen-presenting cells for T-lymphocytes of the human immune system, which are of bone marrow origin. It is these cells that are assigned the initial role in triggering targeted immunological responses in response to the ingress of a pathogen (virus). DCs are capable of capturing various antigens through phagocytosis and expressing them on their surface.

The aim of the method is to reduce the frequency of relapses by 3 times compared to the initial state and lengthen the period of remission in the often recurrent form of herpes.

The task of this method of therapy is to develop a new effective method of vaccination of herpes infection, carried out both in the acute period of the disease and in the stage of remission.

The method of therapy is as follows: monocytes are isolated from the patient's blood, from which, in the presence of interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor - GM-CSF-, antigen-presenting “immature” DCs are obtained; DCs are "loaded" with a suspension of herpes simplex virus vaccine antigens of types 1 and 2 and under the action of special inducers of differentiation DCs become "mature", all these processes generally take 6-7 days. This suspension of DC (the so-called IL4-DC) is cryopreserved. The resulting specific vaccine is administered to the patient.

Scheme of administration: the vaccine is injected intradermally at 4-6 different points along the lymphatic collectors (outer surface of the shoulder, umbilical region, groin area, scapular region), the course consists of 3-4 injections, the dose gradually increases from 1-2 * 106 DC to 8 * 106 DC (the second injection requires a 2-fold increase in the dose, with the 3rd injection - 4 times). The interval between the introduction is from 2 to 4 weeks.

A fundamentally new method of therapy was developed at the FGBU "NIIKI" of the Siberian Branch of the Russian Academy of Medical Sciences.

2.3 Immunotherapy with dendritic cells generated from the patient's monocytesinterferon-α ["Method of immunotherapy of chronic often recurrent herpesvirus infection" patent RU 2485962 on the basis of the Federal State Budgetary Institution "Research Institute of Clinical Immunology" of the Siberian Branch of the Russian Academy of Medical Sciences (FGBU "NIIKI" SB RAMS)]

Purpose: treatment of a chronic, often recurrent form of GI, in which there is always a decrease in the number of antigen-presenting DCs, as well as a violation of their functional activity.

Objectives: a significant reduction in the number of relapses to a minimum, as well as the severity of clinical manifestations during a possible activation of the infection, and as a result of the formation of a persistent relapse-free period of remission in chronic herpes infection.

The need for this method: the use of GM-CSF for DC generation in combination with IL-4 is not exhaustive in this problem, since IL4-DCs have a high ability to capture antigen, but low stimulatory activity for T-lymphocytes; Also, the obtained IL4-DCs have a low migration ability and are quickly transformed back into monocytes, which results in the possibility of loss of specific antigen-presenting properties. For this reason, a new method for generating DC has been developed.

Brief essence of the method: creation of an alternative method of DC generation, in which IL-4 is replaced by interferon-α (IFN-DC), then IFN-DC is "loaded" with recombinant antigens of the herpes simplex virus. The trained DCs at a dose of 5 * 106 are cryopreserved. IFN-DCs are able to generate much faster, a high ability to capture antigen has been proven, are quite stable, have a high migration activity, induce adequate cellular and humoral immunity, and have direct cytotoxic activity.

The indication for the method is the often recurrent form of GI with a recurrence rate of 6 or more per year, which is resistant to standard treatment methods (antiviral, immunomodulators).

Treatment regimen: conduct 2 courses of DC vaccinations "induction" and "maintenance". The "induction" course includes 4-6 subcutaneous injections into the upper third of the shoulder at a dose of 5 * 106 DC with an interval of 2 weeks. After 3 months after completion, a "supporting" course is carried out: 3-6 subcutaneous injections at a dose of 5 * 106 DC with an interval of 1 month. At the same time, interleukin-2 is prescribed as an adjuvant (roncoleukin), 0.25 mg subcutaneously (this is necessary to enhance the T-cell immune response).

Summarizing all of the above, we can talk about the variety of drugs and methods of treatment for chronic herpes infection. Treatment regimens are selected strictly individually, prescribed by the attending doctor, taking into account the basic principles of herpes therapy. An example of a treatment regimen for a frequently recurrent form of herpes infection (Russian Medical Academy of Postgraduate Education) is the following:

1) relief of exacerbation ( antiviral drug and an immunomodulator - for example, an interferon inducer, local therapy for 5-10 days);
2) anti-relapse therapy (vaccination, treatment with dendritic cells and in the intervals between courses);
3) supportive therapy (continuation of the immunomodulator with long courses, preferably the same as in the first stage).

Infectious disease doctor N.I. Bykova