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Molecular changes associated with replication of simian immunodeficiency virus in human cells.
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Molecular changes associated with replication of simian immunodeficiency virus in human cells.

Author: T Kodama Affiliation: New England Regional Primate Research Center, Harvard Medical School, Southborough, MA.; DP Burns; Kestler HW 3rd; MD Daniel; RC Desrosiers
Edition/Format: Article Article : English
Publication:Journal of medical primatology, 1990; 19(3-4): 431-7
Database:From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Summary:
The SIVmac239 infectious clone does not have a premature stop codon in its transmembrane protein (TMP) region and it produces full-length (41 kilodalton, kDa) TMP in macaque peripheral blood lymphocytes (PBL) in vitro and in vivo. However, viruses with truncated forms of TMP (28kDa) are selected during propagation in human cell types; truncated forms arise from point mutations, CAG (glutamine) to TAG (stop), in the  Read more...
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Details

Document Type: Article
All Authors / Contributors: T Kodama Affiliation: New England Regional Primate Research Center, Harvard Medical School, Southborough, MA.; DP Burns; Kestler HW 3rd; MD Daniel; RC Desrosiers
ISSN:0047-2565
Language Note: English
Unique Identifier: 117615888
Awards:

Abstract:

The SIVmac239 infectious clone does not have a premature stop codon in its transmembrane protein (TMP) region and it produces full-length (41 kilodalton, kDa) TMP in macaque peripheral blood lymphocytes (PBL) in vitro and in vivo. However, viruses with truncated forms of TMP (28kDa) are selected during propagation in human cell types; truncated forms arise from point mutations, CAG (glutamine) to TAG (stop), in the viral genome. These results document molecular changes associated with adaptation of SIVmac for growth in human cells.

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