Source:http://linkedlifedata.com/resource/pubmed/id/10364501
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1999-7-23
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pubmed:abstractText |
During 14 months of infection of a pig-tailed macaque, the acutely lethal simian immunodeficiency virus SIVsmmPBj14 (SIV-PBj14) evolved from the minimally pathogenic strain SIVsmm9. The virus isolated at 8 months (SIV-PBj8) exhibited properties of both SIVsmm9 and SIV-PBj14, indicating that a phenotypic transition occurred between 6 and 10 months. To assess the influence that this new composition of biologic properties might have on pathogenicity, three pig-tailed macaques were inoculated intravenously with SIV-PBj8. Although no animals developed the severe acute disease syndrome typical of SIV-PBj14, all had high levels of viremia and died of AIDS at 4, 10. 5, and 32 months. Characterization of the SIV-PBj8-derived quasispecies that evolved in these macaques showed that at 4 days after inoculation, viruses from all three animals exhibited in vitro properties different from those of the inoculum. By 4 months, the initial phenotypic profiles had changed, with the quasispecies in plasma from the animal (J90232) that died at this time most closely resembling SIV-PBj14, not SIV-PBj8. Phylogenetic trees of the gp41/Nef region of viruses in 4-month plasma from J90232 revealed three distinct populations with high bootstrap values: one group branched with SIVsmm9, one with SIV-PBj14, and one with SIV-PBj8 (ratio of clones, 5:9:5). Nucleotide sequence analysis suggested that some members of the original SIV-PBj8 quasispecies may have been evolving toward a SIV-PBj14-like genotype at the time macaque J90232 died. The use of SIV-PBj8, which was more pathogenic than SIVsmm9, but less pathogenic than SIV-PBj14, may provide the optimal genetic background on which to identify the minimal, multigenic determinants of the SIV-PBj14 phenotype. The results of our studies on SIV-PBj14 indicate that in some, but not all, cases of primate lentivirus infection more pathogenic variants evolve, selectively proliferate, and more than likely contribute to disease progression.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0042-6822
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1999 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
259
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
166-75
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10364501-Animals,
pubmed-meshheading:10364501-Evolution, Molecular,
pubmed-meshheading:10364501-Genome, Viral,
pubmed-meshheading:10364501-Macaca,
pubmed-meshheading:10364501-Simian Acquired Immunodeficiency Syndrome,
pubmed-meshheading:10364501-Simian immunodeficiency virus,
pubmed-meshheading:10364501-Viral Envelope Proteins,
pubmed-meshheading:10364501-Virulence
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pubmed:year |
1999
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pubmed:articleTitle |
Pathogenicity and comparative evolution in vivo of the transitional quasispecies SIVsmmPBj8.
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pubmed:affiliation |
Department of Microbiology, University of Alabama School of Medicine, Birmingham, Alabama 35294, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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