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Herpes simplex (herpetic infection) - Causes and pathogenesis
Last reviewed: 04.07.2025
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Causes of Herpes Simplex (Herpes Infection)
Herpes simplex (herpes infection) is caused by herpes simplex viruses types 1 and 2 (human herpes virus types 1 and 2), family Herpesviridae, subfamily Alphaherpesviruses, genus Simplexvirus.
The herpes simplex virus genome is represented by double-stranded linear DNA, the molecular weight is about 100 mDa. The capsid is of regular shape, consisting of 162 capsomeres. Replication of the virus and assembly of nucleocapsids occur in the nucleus of the infected cell. The virus has a pronounced cytopathic effect, causing the death of affected cells, but penetration of the herpes simplex virus into some cells (in particular, neurons) is not accompanied by replication of the virus and cell death. The cell has an inhibitory effect on the viral genome, bringing it to a latent state, when the existence of the virus is compatible with its normal activity. After some time, activation of the viral genome with subsequent replication of the virus may occur, in some cases herpetic eruptions may reappear, which indicates reactivation and transition of the latent form of infection to the manifest one. The genomes of herpes simplex virus-1 and herpes simplex virus-2 are 50% homologous. Both viruses can cause lesions of the skin, internal organs, nervous system, and genitals. However, herpes simplex virus-2 causes genital lesions much more often. There is evidence that the herpes simplex virus can mutate and acquire new antigenic properties.
The herpes simplex virus is resistant to drying, freezing, and is inactivated within 30 minutes at a temperature of 50-52 °C. The lipoprotein envelope of the virus dissolves under the influence of alcohols and acids.
Conventional disinfectants do not have a significant effect on the herpes simplex virus. Ultraviolet radiation quickly inactivates the virus.
Pathogenesis of herpes simplex (herpes infection)
The herpes simplex virus enters the human body through mucous membranes and damaged skin (there are no receptors for the virus in the cells of the keratinizing epithelium of the skin). Reproduction of the virus in epithelial cells leads to their death with the formation of foci of necrosis and vesicles. From the primary focus, the herpes simplex virus migrates by retrograde axonal transport to the sensory ganglia: HSV-1 mainly to the ganglion of the trigeminal nerve. HSV-2 - to the lumbar ganglia. In the cells of the 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 maintained by periodic activation of the virus and its penetration into the mucous membranes of the oropharynx (HSV-1) and genitals (HSV-2). In some cases, reactivation of the virus is accompanied by clinical manifestations in the form of vesicular rashes (relapse of herpes infection). Hematogenous spread of the virus is also possible, as evidenced by the appearance of generalized rashes, damage to the central nervous system and internal organs, as well as detection of the virus in the blood by the PCR method. Relapses of herpes infection are associated with a decrease in the level of specific immunity under the influence of non-specific factors (excessive insolation, hypothermia, infectious diseases, stress).
As a rule, one strain of the herpes simplex virus is isolated from one patient, but in patients with immunodeficiency, several strains of the same subtype of the virus can be isolated.
The immune status of the body largely determines the probability of developing the disease, the severity of the disease, the risk of developing a latent infection and persistence of the virus, and the frequency of subsequent relapses. The state of both humoral and cellular immunity is important. The disease is much more severe in people with impaired cellular immunity.
Herpes infection (herpes simplex) can cause immunodeficiency states. Evidence of this is the ability of the virus to multiply in T- and B-lymphocytes, which leads to a decrease in their functional activity.
Epidemiology of herpes simplex (herpes infection)
Herpes infection is widespread. Antibodies to the herpes simplex virus are found in more than 90% of the population over 40 years of age. The epidemiology of herpes infection caused by HSV-1 and HSV-2 viruses is different. Primary infection with HSV-1 occurs in the first years of life (from 6 months to 3 years), most often manifesting itself as vesicular stomatitis.
Antibodies to the herpes simplex virus-2 are usually found in people who have reached puberty. The presence of antibodies and their titer correlate with sexual activity. In 30% of people with antibodies to the herpes simplex virus-2, there are indications in the anamnesis of a past or current infection of the genitals, accompanied by rashes.
The source of the herpes simplex virus-1 is a person during the reactivation of a herpes infection with the release of the virus into the environment. Asymptomatic release of the herpes simplex virus-1 with saliva is noted in 2-9% of adults and 5-8% of children. The source of the herpes simplex virus-2 is patients with genital herpes and healthy individuals whose genital mucosal secretions contain the herpes simplex virus-2.
The mechanisms of transmission of HSV-1 and HSV-2 are also different. A number of authors classify the herpes simplex virus-1 as an infection with an aerosol mechanism of pathogen transmission. However, although infection with the herpes simplex virus-1 occurs in childhood, unlike other childhood droplet infections, focality (for example, in children's institutions) and seasonality are not characteristic of HSV-1 infection. The main substrates of the virus are saliva, secretion of the mucous membrane of the oropharynx, the contents of herpetic vesicles, that is, transmission of the virus occurs by direct or indirect (toys, dishes, other saliva-covered objects) contact. Damage to the respiratory tract, the presence of catarrhal phenomena that ensure the airborne 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 realized mainly through sexual contact. Since the transmission of the herpes simplex virus-1 is also possible through sexual contact (oral-genital contacts), herpes infection is classified as a sexually transmitted disease. HSV can be detected in saliva and the genital tract of clinically healthy individuals. However, in the presence of active manifestations of infection, the frequency of virus excretion increases several times, and the titer of the virus in the affected tissues - by 10-1000 times or more. Transplacental transmission of the virus is possible if a pregnant woman has a relapse of herpes infection, accompanied by viremia. However, more often, infection of the fetus occurs during passage through the birth canal.
The virus can be transmitted by blood transfusion and organ transplantation. Susceptibility is high. As a result of a herpes infection, non-sterile immunity is formed, which can be disrupted due to various endo- and exogenous causes.
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