Linked Life Data

17440050

Source:http://linkedlifedata.com/resource/pubmed/id/17440050

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pubmed-article:17440050pubmed:abstractTextLatency enables human cytomegalovirus (HCMV) to persist in the hematopoietic cells of infected individuals indefinitely and prevents clearance of the pathogen. Despite its critical importance to the viral infectious cycle, viral mechanisms that contribute to latency have not been identified. We compared the ability of low-passage clinical and laboratory-adapted strains of HCMV to establish a latent infection in primary human CD34(+) cells. The low-passage strains, Toledo and FIX, established an infection with the hallmarks of latency, whereas the laboratory strains, AD169 and Towne, replicated producing progeny virus. We hypothesized that ULb' region of the genome, which is unique to low-passage strains, may encode a latency-promoting activity. We created and analyzed recombinant viruses lacking segments or individual open reading frames (ORFs) in the ULb' region. One 5-kb segment, and more specifically the UL138 ORF, was required for HCMV to establish and/or maintain a latent infection in hematopoietic progenitor cells infected in vitro. This is the first functional demonstration of a virus-coded sequence required for HCMV latency. Importantly, UL138 RNA was expressed in CD34(+) cells and monocytes from HCMV-seropositive, healthy individuals. UL138 might be a target for antivirals against latent virus.lld:pubmed
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pubmed-article:17440050pubmed:authorpubmed-author:SinclairJohnJlld:pubmed
pubmed-article:17440050pubmed:authorpubmed-author:HighKevinKlld:pubmed
pubmed-article:17440050pubmed:authorpubmed-author:GoodrumFelici...lld:pubmed
pubmed-article:17440050pubmed:authorpubmed-author:ReevesMatthew...lld:pubmed
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pubmed-article:17440050pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:17440050pubmed:year2007lld:pubmed
pubmed-article:17440050pubmed:articleTitleHuman cytomegalovirus sequences expressed in latently infected individuals promote a latent infection in vitro.lld:pubmed
pubmed-article:17440050pubmed:affiliationDepartment of Immunobiology, BIO5 Institute, University of Arizona, Tucson, AZ 85711, USA. fgoodrum@email.arizona.edulld:pubmed
pubmed-article:17440050pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17440050pubmed:publicationTypeClinical Triallld:pubmed
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