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Human herpesvirus 6 (HSV-6) was first isolated from the peripheral blood of patient with AIDS in the year 1986. HSV-6 like EBV and CMV is lymphotrophic and ubiquitous. This virus is believed to persist chronically in salivary gland tissue in some of the adults. The virus is spread by the saliva, which is the main source of infection. Like other herpesviruses, HSV-6 causes a latent infection in T cells and monocytes. The replication of the virus in CD41 T lymphocytes is controlled by CMI. The reac-tivation of the virus occurs in immunocompromised patients (patients with AIDS or other immunosuppression disorders). HSV-6 causes roseola infantum, a febrile infection that affects young children. The virus may also cause mononucleosis syn-drome and lymphadenopathy.
Human herpesvirus 7 (HSV-7) was first isolated from periph-eral CD4 cells of healthy persons in 1990. HSV-7 like HSV-6 has also been isolated from saliva of healthy adults and has been implicated as one of the causative agents of rubeola infantum and febrile seizures in children. The virus has also been associated with acute hemiplegia of childhood, hepatitis, and respiratory tract infections.
Human herpesvirus 8 (HSV-8) is associated with Kaposi’s sar-coma and also with body cavity lymphoma and Castleman disease. DNA sequences of HSV-8 have been identified in patients with Kaposi’s sarcoma. This virus, also known as KS-associated herpesvirus, is believed to be important in causing and/or maintaining lesions in Kaposi’s sarcoma. The lesion in Kaposi’s sarcoma begins as red purple or dusky area that enlarges into a plaque and progresses subsequently into a tumorous growth. T-is condition is observed most commonly in immunosuppressed patients but also occurs in children, although rarely.
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