Abstract
Eight viruses are included in the herpesvirus group: herpes simplex virus (HSV) (types 1 and 2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesviruses 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8). All of the herpesvirus have icosahedral symmetry, are surrounded by a lipid-containing envelope derived from the host cell membrane, and have a double strand of linear DNA ranging from 125 kb (VZV) to 230 kb (CMV). After primary infection, herpesvirus DNA becomes latent in an episomal form in specific target cells; reactivation and active virus infection generally occur with immune deficit or suppression of the host (1). Infections with herpesviruses generally occur early in life. Apparent clinical manifestations in children are recognized with dermal lesions of HSV (stomatitis), VZV (chickenpox), HHV-6, and perhaps HHV-7 (roseola). Reactivated CMV and EBV infections in immunocompromised patients are recognized most often as causes—pneumonia, hepatitis, gastroenteritis, encephalitis, and lymphoproliferative disorders (EBV) in organ transplant recipients and in individuals with AIDS. HHV-8 has been recently detected in affected skin tissue (Kaposi’s sarcoma) and from body cavity-based lymphomas from AIDS patients with human immunodeficiency vrus (HIV) infection (1).
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Espy, M.J., Shawn Mitchell, P., Persing, D.H., Smith, T.F. (1998). Herpesviruses. In: Stephenson, J.R., Warnes, A. (eds) Diagnostic Virology Protocols. Methods in Molecular Medicine™, vol 12. Springer, Totowa, NJ. https://doi.org/10.1385/0-89603-479-8:89
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DOI: https://doi.org/10.1385/0-89603-479-8:89
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