Kaposi’s Sarcoma-Associated Herpesvirus
Kaposi’s Sarcoma-Associated Herpesvirus
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DOI:
10.1128/9781555815981.ch25
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发表时间:
2009
期刊:
影响因子:
--
通讯作者:
P. Moore;Yuan Chang
中科院分区:
文献类型:
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作者:
P. Moore;Yuan Chang
Kaposi’s sarcoma-associated herpesvirus (KSHV), also called human herpesvirus 8 (HHV-8), is a large double-stranded DNA herpesvirus that causes Kaposi’s sarcoma (KS) as well as some malignant and hyperplastic lymphoid disorders. KSHV also resides as a latent virus in infected cells. In contrast to lytic replication, latent viral gene expression provides proliferation and survival factors that inhibit premature cell death. Initiation of lytic replication begins with a highly choreographed cascade of gene expression that determines the sequence of events leading to linear genome replication, virion synthesis, genome packaging, and egress of the virus from the infected cell. Although the incidence of AIDS-associated KS declined 70 to 90% after the introduction of effective antiretroviral therapy, these drugs do not inhibit KSHV infection, and a second emergence of KS among persons with low HIV loads and high CD4+ cell counts has been reported. Although KSHV is poorly transmissible through transfusion, transfusion transmission can occur and may cause silent transmission and disease. Studies of AIDS patient cohorts show that KS can develop within weeks or months of primary infection, and in one case, an HIV-positive man developed transient angiolymphoid hyperplasia with microscopic foci of KS spindle cells immediately after infection. The majority of Castleman’s disease is of the hyaline-vascular variant, which presents as solitary lymph node hyperplasia typically in the mediastinum or retroperitoneum. Among AIDS patients, the most effective control measure for KS is effective antiretroviral therapy. The rate of new KS diagnoses is markedly lower among persons on highly effective antiretroviral therapy.