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dc.contributor.author Lim, SY
dc.contributor.author Chan, T
dc.contributor.author Gelman, RS
dc.contributor.author Whitney, JB
dc.contributor.author O'Brien, KL
dc.contributor.author Barouch, DH
dc.contributor.author Goldstein, DB
dc.contributor.author Haynes, BF
dc.contributor.author Letvin, NL
dc.date.accessioned 2011-06-21T17:31:21Z
dc.date.issued 2010
dc.identifier.citation PLoS genetics, 2010, 6 (6), pp. e1000997 - ?
dc.identifier.issn 1553-7404
dc.identifier.uri http://hdl.handle.net/10161/4474
dc.description.abstract CCL3 is a ligand for the HIV-1 co-receptor CCR5. There have recently been conflicting reports in the literature concerning whether CCL3-like gene (CCL3L) copy number variation (CNV) is associated with resistance to HIV-1 acquisition and with both viral load and disease progression following infection with HIV-1. An association has also been reported between CCL3L CNV and clinical sequelae of the simian immunodeficiency virus (SIV) infection in vivo in rhesus monkeys. The present study was initiated to explore the possibility of an association of CCL3L CNV with the control of virus replication and AIDS progression in a carefully defined cohort of SIVmac251-infected, Indian-origin rhesus monkeys. Although we demonstrated extensive variation in copy number of CCL3L in this cohort of monkeys, CCL3L CNV was not significantly associated with either peak or set-point plasma SIV RNA levels in these monkeys when MHC class I allele Mamu-A*01 was included in the models or progression to AIDS in these monkeys. With 66 monkeys in the study, there was adequate power for these tests if the correlation of CCL3L and either peak or set-point plasma SIV RNA levels was 0.34 or 0.36, respectively. These findings call into question the premise that CCL3L CNV is important in HIV/SIV pathogenesis.
dc.format.extent e1000997 - ?
dc.language.iso en_US en_US
dc.relation.ispartof PLoS genetics
dc.relation.isversionof 10.1371/journal.pgen.1000997
dc.title Contributions of Mamu-A*01 status and TRIM5 allele expression, but not CCL3L copy number variation, to the control of SIVmac251 replication in Indian-origin rhesus monkeys.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2010-6-0 en_US
duke.description.endpage e1000997 en_US
duke.description.issue 6 en_US
duke.description.startpage e1000997 en_US
duke.description.volume 6 en_US
dc.relation.journal Plos Genetics en_US
pubs.issue 6
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Immunology
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Molecular Genetics and Microbiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Duke Human Vaccine Institute
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Cancer Institute
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Clinical Research Institute
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Human Vaccine Institute
pubs.organisational-group /Duke/University Institutes and Centers
pubs.organisational-group /Duke/University Institutes and Centers/Global Health Institute
pubs.volume 6

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