Regulation of Latency in the Human T Cell Leukemia Virus, HTLV-1

التفاصيل البيبلوغرافية
العنوان: Regulation of Latency in the Human T Cell Leukemia Virus, HTLV-1
المؤلفون: Bangham, Charles R.M., Miura, Michi, Kulkarni, Anurag, Matsuoka, Masao
المصدر: Annual Review of Virology; September 2019, Vol. 6 Issue: 1 p365-385, 21p
مستخلص: The human T cell leukemia virus persists in vivo in 103to 106clones of T lymphocytes that appear to survive for the lifetime of the host. The plus strand of the provirus is typically transcriptionally silent in freshly isolated lymphocytes, but the strong, persistently activated cytotoxic T lymphocyte (CTL) response to the viral antigens indicates that the virus is not constantly latent in vivo. There is now evidence that the plus strand is transcribed in intense intermittent bursts that are triggered by cellular stress, modulated by hypoxia and glycolysis, and inhibited by polycomb repressive complex 1 (PRC1). The minus-strand gene hbzis transcribed at a lower, more constant level but is silent in a proportion of infected cells at a given time. Viral genes in the sense and antisense strands of the provirus play different respective roles in latency and de novo infection: Expression of the plus-strand gene taxis essential for de novo infection, whereas hbzappears to facilitate survival of the infected T cell clone in vivo.
قاعدة البيانات: Supplemental Index
الوصف
تدمد:2327056X
23270578
DOI:10.1146/annurev-virology-092818-015501