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HHV Latency Associated Transcript (HHV LAT) is a length of RNA which accumulates in cells hosting long-term, or ''latent'', Human Herpes Virus (HHV) infections. The LAT RNA is produced by genetic transcription from a certain region of the viral DNA. LAT regulates the viral genome and interferes with the normal activities of the infected host cell. Herpes virus may establish lifelong infection during which a ''reservoir'' virus population survives in host nerve cells for long periods of time. Such long-term Herpes infection requires a mode of cellular infection known as ''latent'' infection. During the latent infection, the metabolism of the host cell is disrupted. While the infected cell would ordinarily undergo an organized death or be removed by the immune system, the consequences of LAT production interfere with these normal processes. Latency is distinguished from ''lytic'' infection; in lytic infection many Herpes virus particles are produced and then burst or ''lyse'' the host cell. Lytic infection is sometimes known as "productive" infection. Latent cells harbor the virus for long time periods, then occasionally convert to productive infection which may lead to a ''recurrence'' of symptomatic Herpes symptoms. During latency, most of the Herpes DNA is inactive, with the exception of LAT, which accumulates within infected cells. The region of HHV DNA which encodes LAT is known as LAT-DNA. After splicing, LAT is a 2.0-kilobase transcript (or intron) produced from the 8.3-kb LAT-DNA. The DNA region containing LAT-DNA is known as the ''Latency Associated Transcript Region''.〔 (Free full-text article: ()) 〕 Apoptosis is the process of normal cell death. In order to maintain a reservoir of latently infected host cells, Herpes virus interferes with apoptosis. HSV-1 LAT expression was once thought to produce interfering ''micro-RNA'' (miRNA) which suppress production of Human apoptosis-pathway proteins such as TGF-β1 and SMAD3,〔 (Full-text: ()) 〕 but these findings were retracted by the researchers in January 2008.〔Gartner JJ, Sethupathy P, Hatzigeorgiou AG, Fraser NW (Jan 31 2008). Retraction in ''Nature'' 451 (7178):600.〕 HHV-8 LAT expression similarly produces miRNAs which suppress production of Thrombospondin-1 protein involved in apoptosis and angiogenesis.〔 〕 Expression of LAT also reduces the production of other proteins involved in the apoptosis mechanism, including proteins caspase-8 and caspase-9.〔 〕 LAT expression regulates the activity of the Herpes genome during latent infection. LAT expression results in the suppression of Herpes lytic genes.〔 (Free full-text: ()) 〕 Genetic studies of the LAT-DNA have identified a portion known as a ''chromatin insulator'' which forms a boundary between activated LAT-DNA and the inactive lytic viral DNA.〔 〕 ==LAT regulates the expression of lytic genes== HHV Infected Cell Polypeptide 0 (ICP0) gene is expressed very early during lytic infection, and for this reason is called an ''immediate-early'' Herpes gene. In 1991, Farrell and colleagues report that the 2.0-kb LAT intron terminates at the 5' end with a 750-base antisense RNA complement for the ICP0 gene.〔 In 2005, Qing-Yin Wang and colleagues from Harvard Medical School concluded, using assays comparing LAT-negative vs. LAT-positive virus strains, that expression of LAT in neurons represses the expression of several lytic gene products, including ICP4 and Thymidine Kinase. LAT expression results in changes to Histones, thus converting portions of viral DNA into a non-productive form known as heterochromatin.〔 Simian varicella virus (SVV) is a ''Varicellovirus'' (a Genus of Subfamily ''Alphaherpesvirinae'') which expresses an HHV LAT homolog known as SVV LAT, and an HHV ICP0 analog known as SVV-ORF61 (Open Reading Frame). SVV LAT is encoded such that it contains an antisense copy of SVV-ORF61 and that expression of SVV LAT during latency downregulates expression of ORF61 and other immediate-early SVV gene products. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「HHV Latency Associated Transcript」の詳細全文を読む スポンサード リンク
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