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


Division of Infectious Diseases, Department of Medicine, Imperial College London, London W2 1PG, United Kingdom; email: [Email]


The human T cell leukemia virus persists in vivo in 103 to 106 clones 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 hbz is 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 tax is essential for de novo infection, whereas hbz appears to facilitate survival of the infected T cell clone in vivo.


cell stress,epigenetics,gene burst,latency,reservoir,retrovirus,

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