HHV Latency Associated Transcript

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.[1]

The LAT mainly performs two functions: it suppresses apoptosis so that latently infected host cells stay alive for the reservoir,[2] and suppresses the expression of lytic genes during latent infection.[3]

  1. ^ Farrell MJ, Dobson AT, Feldman LT (1991-02-01). "Herpes simplex virus latency-associated transcript is a stable intron". Proceedings of the National Academy of Sciences. 88 (3): 790–794. Bibcode:1991PNAS...88..790F. doi:10.1073/pnas.88.3.790. PMC 50899. PMID 1846963.
  2. ^ Henderson G, Peng W, Jin L, Perng GC, Nesburn AB, Wechsler SL, Jones C (December 2002). "Regulation of caspase 8- and caspase 9-induced apoptosis by the herpes simplex virus type 1 latency-associated transcript". Journal of Neurovirology. 8 (2): 103–111. doi:10.1080/13550280290101085. PMID 12491160.
  3. ^ Wang QY, Zhou C, Johnson KE, Colgrove RC, Coen DM, Knipe DM (1 Nov 2005). "Herpesviral latency-associated transcript gene promotes assembly of heterochromatin on viral lytic-gene promoters in latent infection". Proceedings of the National Academy of Sciences. 102 (44): 16055–16059. Bibcode:2005PNAS..10216055W. doi:10.1073/pnas.0505850102. PMC 1266038. PMID 16247011.