Herpes simplex (herpes infection): causes and pathogenesis
Last reviewed: 23.04.2024
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Causes of simple herpes (herpetic infection)
Herpes simplex (herpetic infection) is caused by herpes simplex virus type 1 and 2 (human herpesvirus type 1 and 2), the Herpesviridae family, the subfamily Alphaherpesviruses, the genus Simplexvirus.
The genome of the herpes simplex virus is represented by double-stranded linear DNA, a molecular weight of about 100 mDa. Capsid of the correct form, consists of 162 capsomers. Virus replication and the assembly of nucleocapsids occur in the nucleus of the infected cell. The virus has a pronounced cytopathic effect, causing the death of the affected cells, but the penetration of the herpes simplex virus into certain cells (in particular, neurons) is not accompanied by viral replication and cell death. The cell has a depressing effect on the viral genome, leading it to a latent state, when the existence of the virus is compatible with its normal activity. After a while, the activation of the viral genome may occur, followed by replication of the virus, in some cases, herpetic eruptions may reappear, indicating that the latent form of infection has been reactivated and the infection has become manifest. The genomes of the herpes simplex virus-1 and herpes simplex virus-2 are 50% homologous. Both viruses can cause damage to the skin, internal organs, nervous system, genitals. However, the herpes simplex virus-2 causes lesions of the genitals much more often. There is evidence of the possibility of a mutation of the herpes simplex virus with the acquisition of new antigenic properties.
Herpes simplex virus is resistant to drying, freezing, at a temperature of 50-52 ° C, it is inactivated within 30 minutes. The lipoprotein coat of the virus dissolves under the influence of alcohols and acids.
Usual disinfectants have no significant effect on the herpes simplex virus. Ultraviolet irradiation rapidly inactivates the virus.
The pathogenesis of herpes simplex (herpetic infection)
The virus of herpes simplex penetrates into the human body through the mucous membranes, damaged skin (in the cells of the cornermal epithelium of the skin there are no receptors to the virus). Reproduction of the virus in epithelial cells leads to their death with the formation of foci of necrosis and vesicles. From the primary focus of the herpes simplex virus through retrograde axonal transport migrates into sensory ganglions: HSV-1 predominantly in the ganglion of the trigeminal nerve. HSV-2 - in the lumbar ganglia. In cells of sensory ganglia, virus replication is suppressed, and it persists in them for life. Primary infection is accompanied by the formation of humoral immunity, the intensity of which is supported by periodic activation of the virus and its penetration into the mucous membranes of the oropharynx (VPG-1) and genital organs (HSV-2). In some cases, the reactivation of the virus is accompanied by clinical manifestations in the form of a bubble rash (relapse of herpetic infection). It is possible and hematogenous spread of the virus, as evidenced by the emergence of generalized rashes, damage to the central nervous system and internal organs, as well as the detection of the virus in the blood by PCR. Relapses of herpes infection are associated with a decrease in the level of specific immunity under the influence of nonspecific factors (excessive insolation, hypothermia, infectious diseases, stress).
As a rule, one strain is isolated from one patient of the herpes simplex virus, but in patients with immunodeficiency several strains of the same subtype of the virus can be isolated.
The immune status of the organism largely determines the probability of the development of the disease, the severity of the course, the risk of latent infection and the persistence of the virus, the frequency of subsequent relapses. The state of both humoral and cellular immunity matters. Disease in people with impaired cellular immunity is much more difficult.
Herpetic infection (simple herpes) can cause immunodeficiency. Proof of this is the ability of the virus to reproduce in T and B lymphocytes, which leads to a decrease in their functional activity.
Epidemiology of herpes simplex (herpetic infection)
Herpes infection is ubiquitous. Antibodies to the herpes simplex virus are found in more than 90% of the population over the age of 40. The epidemiology of herpetic infection caused by HSV-1 and HSV-2 viruses is different. Primary infection of HSV-1 occurs in the first years of life (from 6 months to 3 years), most often manifested by vesicular stomatitis.
Antibodies to the herpes simplex virus-2 detect, as a rule, in persons who have reached puberty. The presence of antibodies and their titre correlate with sexual activity. At 30% of persons. Having antibodies to the herpes simplex virus-2, in the anamnesis there are indications to the transferred or current infection of the genital organs, accompanied by rashes.
The source of the herpes simplex virus-1 is a person during the reactivation of herpetic infection with the release of the virus into the environment. Asymptomatic salivary seizure of herpes simplex virus 1 was observed in 2-9% of adults and in 5-8% of children. Source of the herpes simplex virus-2 - patients with genital herpes and healthy faces, in the secret of the mucous membrane of the genital organs which contains the herpes simplex virus-2.
The mechanisms of transmission of HSV-1 and HSV-2 are also different. A number of authors attribute the herpes simplex virus-1 to infection with the aerosol mechanism of transmission of the pathogen. However, although infection with the herpes simplex virus-1 occurs in childhood, unlike other children's infections for HSV-1 infection, foci (for example, in children's institutions) and seasonality are not typical. The main substrates of the virus are saliva, the secret of the mucous membrane of the oropharynx, the contents of the herpetic vesicles, that is, the transmission of the virus occurs through direct or indirect (toys, dishes, other salivary objects) contact. The defeat of the respiratory tract, the presence of catarrhal phenomena providing an airborne pathway for the transmission of the pathogen, are of little significance.
The main mechanism of transmission of the herpes simplex virus-2 is also contact, but it is mainly sexually transmitted. Since the transmission of the herpes simplex virus-1 is also possible sexually (oral-genital contacts), herpetic infection is classified as sexually transmitted diseases. HSV can be found in saliva and the genital tract in clinically healthy individuals. However, in the presence of active manifestations of infection, the frequency of virus isolation increases several times, and the virus titre in the affected tissues is 10-1000 times or more. Transplacental transmission of the virus is possible in the presence of a pregnant woman with a recurrence of herpetic infection accompanied by viremia. However, fetal infection often occurs when passing through the birth canal.
Transmission of the virus is possible with blood transfusion and organ transplantation. The susceptibility is high. As a result of the transferred herpetic infection, non-sterile immunity is formed, which, due to a variety of endo- and exogenous causes, can be disrupted.
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