Transcriptional and Epigenetic Regulatory Mechanisms Affecting HTLV-1 Provirus.

Viruses

International Research Center for Medical Sciences, Center for AIDS Research, Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto 860-0811, Japan.

Published: June 2016

AI Article Synopsis

  • - HTLV-1 is a retrovirus linked to serious conditions like adult T-cell leukemia and myelopathy, integrating into the DNA of host cells and replicating alongside them.
  • - During chronic infection, HTLV-1 can create numerous infected cell clones which proliferate in various body tissues, evading the immune system while expressing viral proteins that help them survive.
  • - The article discusses how the regulation of HTLV-1 gene expression is crucial for understanding its persistent infection and associated diseases, highlighting the balance between viral expression and host immune response.

Article Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus associated with human diseases, such as adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/Tropic spastic paraparesis (HAM/TSP). As a retrovirus, its life cycle includes a step where HTLV-1 is integrated into the host genomic DNA and forms proviral DNA. In the chronic phase of the infection, HTLV‑1 is known to proliferate as a provirus via the mitotic division of the infected host cells. There are generally tens of thousands of infected clones within an infected individual. They exist not only in peripheral blood, but also in various lymphoid organs. Viral proteins encoded in HTLV-1 genome play a role in the proliferation and survival of the infected cells. As is the case with other chronic viral infections, HTLV-1 gene expression induces the activation of the host immunity against the virus. Thus, the transcription from HTLV-1 provirus needs to be controlled in order to evade the host immune surveillance. There should be a dynamic and complex regulation in vivo, where an equilibrium between viral antigen expression and host immune surveillance is achieved. The mechanisms regulating viral gene expression from the provirus are a key to understanding the persistent/latent infection with HTLV-1 and its pathogenesis. In this article, we would like to review our current understanding on this topic.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926191PMC
http://dx.doi.org/10.3390/v8060171DOI Listing

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