Diagnosis of herpes simplex virus infections.

Abstract

Herpes simplex virus (HSV) infections of humans have been recognized since ancient times. Two biologically distinct serotypes, HSV type 1 (HSV-1) and HSV type 2 (HSV-2) were identified (Rawls, 1985) and the serological techniques with various specificity and sensitivity were developed to identify HSV infections in order to understand epidemiology and pathogenesis of these infections in human host (Wentworth et al., 1971; Corey et al., 1983; Whitley, 1990). The prevalence of HSV1 infections increases gradually from childhood, reaching up to 80–90% in adult age. However HSV-2 infections are sexually acquired, so its incidence begins to increase in adolescence (Whitley, Johnson et al., 1989). The prevalence rates for HSV-2 infections range from about 20–60% in various countries. In general, primary HSV-1 and HSV-2 infections are entirely asymptomatic. As with most herpesvirus family members initial infections with HSV-1 and HSV-2 results in establishment of viral latency. Under certain circumstances both viruses are reactivated from the latent state and cause symptomatic infections. The classical manifestation of primary HSV-1 infection is called herpes gingivostomatitis. Gingivostomatitis is characterized with painful vesicular lesions of the oral mucosa, particularly of gingiva with a high temperature and submandibular lymphadenopathy. Conjunctivitis, keratitis, herpetic whitlow and sporadic acute necrotizing encephalitis are the other clinical manifestations of HSV-1 infection. Encephalitis occurs in older children and adults with high mortality if not treated (Whitley, 1988). HSV-2 infections are manifested as herpes genitalis and infection is characterized by the appearance of extensive, bilaterally located ulcers in genitalia accompanied by fever, inguinal lymphadenopathy and dysuria (Corey et al., 1983). Approximately 85% of primary symptomatic HSV genital infections are caused by HSV-2. HSV-1 only contributes 15% of the primary genital infections. However, most of the recurrent genital infections are due to HSV-2 (Gleaves et al., 1985). Most primary infections with HSV-1 and HSV2 do not manifest characteristic clinical disease and are almost entirely asymptomatic and followed by latent infection of neuronal cells in the trigeminal and dorsal root ganglia. HSV-1 and HSV-2 are classified in the alphaherpesvirus subfamily of herpesviruses (Roizman and Batterson, 1985). All herpesviruses are morphologically similar. They have icosahedral capsids containing 162 capsomers enclosing a core structure containing double-stranded linear viral DNA. Complete virion mature by budding off through the nuclear membrane acquiring phospholipid-rich viral envelope. The space between viral capsid and envelope is called viral tegument