Herpes simplex virus (HSV) is an etiological agent of 2 widespread diseases in humans: orofacial infection, the so called “cold sores”, and genital herpes (GH). There are two closely related species of HSV, HSV-1 and HSV-2. Both are large enveloped viruses containing double-stranded DNA. HSV infection occurs worldwide. Estimated prevalence of the HSV-1 infection is highest in Africa (87%) and lowest in the Americas (40-50%). The prevalence of HSV-2 infection is much lower: in Africa-31.5%, in Americas-14.4%.
HSV infects its host at mucosal or epithelial surfaces and causes primary infection of the epithelium. Then the virus enters sensory neurons and is transported by retrograde flow along axons that connect the point of entry into the body to nuclei of sensory neurons. Viral multiplication occurs in a small number of sensory neurons; the viral genome then remains in a latent state for the life of the host. HSV causes benign vesicular and ulcerative lesions in immunocompetent adults and may cause severe systemic disease in neonates and immunosuppressed hosts. HSV can be transmitted to child under primary or recurrent herpes, both in the presence or absence of symptoms. However, under recurrent herpes, the risk of transmission to a newborn is low even if open sores are present at the time of birth (the risk is 3/100). On the contrary, the risk is considerably higher if the primary infection is acquired in the third trimester, and especially in the last 6 weeks of pregnancy (the risk increases to around 50%).
Immune response plays a vital role in maintaining the latent state and in rapidly eliminating reactivated virus. IgG antibodies appear after primary HSV infections 2 weeks after onset of clinical lesions, and the titer increases until 3-4 weeks after clinical symptoms. Later, the IgG antibody titers to HSV usually remain stable even after clinical recurrent infections.
Infected newborns have been found to produce IgM specific for HSV within 1 to 3 weeks after onset of infection. These antibodies continue to increase during the first 2 months and may be detectable for as long as 1 year, but sometimes rises in titers of IgM can be demonstrated later, after recurrences.
The widespread methods in the diagnostics of herpes are virus isolation in cell culture or PCR detection of HSV DNA. Serologic assays could determine whether there is a recurrent or new infection. In new infections, IgG is still negative in acute phase whereas in recurrent infections IgG is positive.
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