Haque Muzammel, Ueda Keiji, Nakano Kazushi, Hirata Yuko, Parravicini Carlo, Corbellino Mario, Yamanishi Koichi
Department of Microbiology, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan1.
Department of Pathology2 and Institute of Infectious Diseases3, University of Milan, 'L. Sacco' Hospital, Milan, Italy.
J Gen Virol. 2001 May;82(Pt 5):1175-1180. doi: 10.1099/0022-1317-82-5-1175.
The expression of major histocompatibility complex class I (MHC-I) molecules at the cell surface was down-regulated in BC-3 cells infected with Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 at early times after treatment with 12-O-tetradecanoylphorbol acetate (TPA), and in HeLa cells transfected with the K5 gene of KSHV. However, an immunoprecipitation study on these cells with anti-MHC-I monoclonal antibody revealed that there was no significant reduction in the synthesis of MHC-I molecules. A pulse-chase analysis followed by endoglycosidase H digestion also demonstrated the stability and transport of MHC-I molecules from the endoplasmic reticulum to at least the medial-GOLGI: K5 antigen was clearly detected by immunohistological examination of samples from Kaposi's sarcoma, primary effusion lymphoma and Castleman's disease. These results suggest that the down-regulation of MHC-I molecules by K5 gene expression during reactivation may be important for evading immunological surveillance in the host.
在用12 - O - 十四酰佛波醇 - 13 - 乙酸酯（TPA）处理后的早期，感染卡波西肉瘤相关疱疹病毒（KSHV）/人疱疹病毒8的BC - 3细胞以及转染了KSHV的K5基因的HeLa细胞中，细胞表面主要组织相容性复合体I类（MHC - I）分子的表达下调。然而，用抗MHC - I单克隆抗体对这些细胞进行免疫沉淀研究发现，MHC - I分子的合成没有显著减少。脉冲追踪分析后进行内切糖苷酶H消化也证明了MHC - I分子从内质网到至少内侧高尔基体的稳定性和转运：通过对卡波西肉瘤、原发性渗出性淋巴瘤和卡斯特曼病样本的免疫组织学检查可以清楚地检测到K5抗原。这些结果表明，在病毒激活过程中，K5基因表达导致的MHC - I分子下调可能对逃避宿主的免疫监视很重要。
