Robek M D, Wong F H, Ratner L
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Virol. 1998 May;72(5):4458-62. doi: 10.1128/JVI.72.5.4458-4462.1998.
Human T-cell leukemia virus type 1 (HTLV-1) infects and transforms CD4+ T-lymphocytes both in vivo and in vitro. Although the Tax protein of HTLV-1 has been strongly implicated as a transforming agent, other virally encoded proteins may also play a role in the transformation process. In addition to the rex and tax genes, the pX region of the HTLV-1 genome contains two open reading frames (pX-I and pX-II) which encode the putative viral accessory proteins known as p12I, p30II, and p13II. Mutations in the ACH molecular clone of HTLV-1 that are predicted to abrogate the expression of p12I, p13II and p30II were constructed. These mutations had no effect on viral replication or the immortalization of primary lymphocytes. Although these proteins are dispensable for viral replication and immortalization in vitro, it remains possible that they alter infection in vivo.
人类嗜T淋巴细胞病毒1型（HTLV-1）在体内和体外均可感染并转化CD4 + T淋巴细胞。尽管HTLV-1的Tax蛋白被强烈认为是一种转化因子，但其他病毒编码的蛋白可能也在转化过程中发挥作用。除rex和tax基因外，HTLV-1基因组的pX区域包含两个开放阅读框（pX-I和pX-II），它们编码被称为p12I、p30II和p13II的假定病毒辅助蛋白。构建了HTLV-1的ACH分子克隆中的突变，预计这些突变会消除p12I、p13II和p30II的表达。这些突变对病毒复制或原代淋巴细胞的永生化没有影响。尽管这些蛋白在体外对于病毒复制和永生化并非必需，但它们仍有可能改变体内感染情况。
