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Pregled bibliografske jedinice broj: 715116

MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs


Umbach, J.L.; Kramer, M.F.; Jurak, Igor; Karnowski, H.W.; Coen, D.M.; Cullen, B.R.
MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs // Nature, 454 (2008), 7205; 780-783 doi:10.1038/nature07103 (međunarodna recenzija, članak, znanstveni)


Naslov
MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs

Autori
Umbach, J.L. ; Kramer, M.F. ; Jurak, Igor ; Karnowski, H.W. ; Coen, D.M. ; Cullen, B.R.

Izvornik
Nature (0028-0836) 454 (2008), 7205; 780-783

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
MiRNA; HSV

Sažetak
Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT). Here we show that LAT functions as a primary microRNA (miRNA) precursor that encodes four distinct miRNAs in HSV-1 infected cells. One of these miRNAs, miR-H2-3p, is transcribed in an antisense orientation to ICP0-a viral immediate-early transcriptional activator that is important for productive HSV-1 replication and thought to have a role in reactivation from latency. We show that miR-H2-3p is able to reduce ICP0 protein expression, but does not significantly affect ICP0 messenger RNA levels. We also identified a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previously unknown transcript distinct from LAT. miR-H6 shows extended seed complementarity to the mRNA encoding a second HSV-1 transcription factor, ICP4, and inhibits expression of ICP4, which is required for expression of most HSV-1 genes during productive infection. These results may explain the reported ability of LAT to promote latency. Thus, HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression.

Izvorni jezik
Engleski

Znanstvena područja
Biologija



POVEZANOST RADA


Ustanove
Sveučilište u Rijeci - Odjel za biotehnologiju

Autor s matičnim brojem:
Igor Jurak, (229960)

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • MEDLINE


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