Journal
JOURNAL OF VIROLOGY
Volume 88, Issue 10, Pages 5524-5532Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00481-14
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Funding
- National Institute of Allergy and Infectious Diseases [RAI101080A]
- American Cancer Society [PF-10-164-01-MPC]
- Swiss National Science Foundation [200021-124936]
- Swiss National Science Foundation (SNF) [200021_124936] Funding Source: Swiss National Science Foundation (SNF)
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Reactivation of human cytomegalovirus (HCMV) is a significant cause of disease and death in immunocompromised patients, underscoring the need to understand how latency is controlled. Here we demonstrate that HCMV has evolved to utilize cellular microRNAs (miRNAs) in cells that promote latency to regulate expression of a viral protein critical for viral reactivation. Our data reveal that hsa- miR-200 miRNA family members target the UL122 (immediate early protein 2) 3' untranslated region, resulting in repression of this viral protein. Utilizing recombinant viruses that mutate the miRNA-binding site compared to the sequence of the wild-type virus results in lytic rather than latent infections in ex vivo infections of primary CD34(+) cells. Cells permissive for lytic replication demonstrate low levels of these miRNAs. We propose that cellular miRNA regulation of HCMV is critical for maintenance of viral latency.
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