Herpes simplex virus
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Infection caused by the herpes simplex virus can have several clinical forms, but is most often asymptomatic. The usual clinical manifestations are vesicular eruptions on the skin and mucous membranes. Sometimes there may be severe keratitis, meningoencephalitis or disseminated disease of the newborn. Herpes simplex virus is pathogenic for many species of animals - mice, rats, hamsters, guinea pigs, rabbits, dogs, monkeys, which usually cause fever and encephalitis (with intracerebral infection), and rabbits also have keratoconjunctivitis.
Since the virus has a dermoneyroterropic effect, in surviving animals and infected people it can persist for a long time in a latent state in the brain, epithelial cells, trigeminal ganglia and other nerves in the form of double-stranded circular DNA forms.
The virus reproduces well in the chorion-allantoic membrane of chick embryos, where in 2-3 days. After infection it forms convex white plaques visible to the naked eye. In drug-prints of them, giant cells with intranuclear inclusions are visible. The virus multiplies easily in almost all widely used cell cultures, forming plaques in monolayers. In infected cells, body-inclusions are formed, giant multinucleated cells appear that are further necrotic (cytopathic effect). Especially suitable for infection is the primary culture of rabbit kidney cells.
[Pathogenesis and symptoms of herpes simplex
When infected with a virus, its primary reproduction occurs in the epithelium of the mucous membrane of the mouth, pharynx or genital organs. Further, the virus enters the blood (a generalized infection) by the lymphogenous pathway and, after passing through the blood-brain barrier, can cause meningitis or encephalitis. When generalized herpes infection in newborns, death occurs, which leads to multiple small-scale necrosis and inflammatory foci in the internal organs. In case of recovery, the condition of the virus carrier is established, which changes throughout life and manifests itself in transitory herpetic attacks, which can be provoked by various agents (solar radiation, fever, stress, spicy food, etc.).
Herpes simplex virus type 1 can cause the development of the following clinical forms of the disease:
- acute herpetic (aphthous) stomatitis develops more often in primary infected children, incubation period 3-5 days, mucosal lesions heal 2-3 weeks later .;
- herpetic eczema (a Kaposi rash similar to a rash with chicken pox) is accompanied by fever and blistering rashes on most of the body surface, sometimes a lethal outcome is observed;
- keratoconjunctivitis; with frequent relapses, irreversible corneal opacity and blindness can be observed;
- meningoencephalitis; lethality is quite high, in case of recovery - persistent residual neurologic changes;
- Herpes labialis (labialis) - the most common form; on the border of the mucous membrane and the skin on the lips appear clusters of merging vesicles, turning into ulcers that heal without scars.
Herpes simplex virus type 2 causes two main clinical forms of the disease: genital herpes (characterized by a bubble-ulcerative rash on the skin and mucous of the genitals, frequent relapses) and herpes of newborns (the child becomes infected at birth from a sick mother, manifestation - from erased forms to generalization with lethal outcome). There may be a different location of the rashes (wounds, fingers at dentists, etc.). Transplacental infection of the fetus with the herpes simplex virus is rare and causes the development of congenital malformations.
Immunity with simple herpes
The child of the first 6 months. Life has, as a rule, antibodies to the virus, acquired passively from the mother. Further, they are lost, the child is most susceptible to herpetic infection at the age of 6 months. Up to 2 years. In the blood of the sick, antibodies that neutralize the virus are detected, as well as specific IgA on the mucous membranes, but they do not interfere with the persistence of the virus and the development of a latent infection.
Epidemiology of Type 1 and 2 Viruses
There are data that up to 70-90% of people are infected with the herpes simplex virus type 1 and that it is present in the human body more constantly than any other virus. Primary infection occurs in the early period of life. After the disappearance of maternal antibodies, the infection occurs in the form of vesicular or aphthous stomatitis. The virus is no longer removed from the body, since it is not available to the action of antibodies. Herpes simplex virus type 1 is transmitted by direct contact through saliva or through dishes contaminated with the saliva of the carrier. The source of infection of children is usually one of the parents with an active form of herpes.
Herpes simplex virus type 2 is transmitted sexually or during labor from a sick mother. It spreads like a typical venereal disease. The source of infection is only a person.
Laboratory diagnosis of herpes simplex
Diagnosis of herpes simplex can use viroscope, virologic and serological methods. The material for the study is scrapings from the cornea, the contents of bubbles, saliva, etc. Scrubs and swabs taken from the base of fresh herpetic eruptions and stained by Romanovsky-Yemza after immediate fixation in absolute alcohol contain giant multinucleated cells with intranuclear inclusions (Caudry's body) .
To isolate the virus, cell cultures, chicken embryos and laboratory animals are used. In infected cell cultures, plaques and a characteristic cytopathic effect are detected, in chick embryos, plaques are detected when infected with the chorallantoic membrane, and plaques formed by the herpes simplex virus type 2 are larger than plaques formed by type 1 virus. When infecting newborn mice in the brain, the symptoms of encephalitis develop 2 -6th day. It is very sensitive and specific for the herpes virus to infect the scarified cornea of the rabbit. The final identification is performed in a neutralization reaction in mice, chick embryos or cell cultures using standard antiherpetic immune sera of animals, as well as in the immunofluorescence (RIF) reaction.
With serodiagnosis it is important to decide whether this is a primary disease or exacerbation of a chronic infection. Therefore, paired sera are used, which are examined with the help of DSC, RIF and IFM.
Treatment of herpes simplex
The specific treatment of herpes simplex is based on the use of chemotherapy drugs - modified nucleosides that suppress the replication of the virus, but have toxicity and contribute to the emergence of resistant strains of the virus (adeninarabinoside, 5-iodine-2-deoxyuridine, acyclovir, etc.). Inductors of interferon are effective, especially in case of acute course of the disease.