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dc.contributor.author Schmitz, JE
dc.contributor.author Zahn, RC
dc.contributor.author Brown, CR
dc.contributor.author Rett, MD
dc.contributor.author Li, M
dc.contributor.author Tang, H
dc.contributor.author Pryputniewicz, S
dc.contributor.author Byrum, RA
dc.contributor.author Kaur, A
dc.contributor.author Montefiori, DC
dc.contributor.author Allan, JS
dc.contributor.author Goldstein, S
dc.contributor.author Hirsch, VM
dc.coverage.spatial United States
dc.date.accessioned 2011-06-21T17:32:21Z
dc.date.issued 2009-12
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20011508
dc.identifier.citation PLoS Pathog, 2009, 5 (12), pp. e1000691 - ?
dc.identifier.uri http://hdl.handle.net/10161/4591
dc.description.abstract African green monkeys (AGM) and other natural hosts for simian immunodeficiency virus (SIV) do not develop an AIDS-like disease following SIV infection. To evaluate differences in the role of SIV-specific adaptive immune responses between natural and nonnatural hosts, we used SIV(agmVer90) to infect vervet AGM and pigtailed macaques (PTM). This infection results in robust viral replication in both vervet AGM and pigtailed macaques (PTM) but only induces AIDS in the latter species. We delayed the development of adaptive immune responses through combined administration of anti-CD8 and anti-CD20 lymphocyte-depleting antibodies during primary infection of PTM (n = 4) and AGM (n = 4), and compared these animals to historical controls infected with the same virus. Lymphocyte depletion resulted in a 1-log increase in primary viremia and a 4-log increase in post-acute viremia in PTM. Three of the four PTM had to be euthanized within 6 weeks of inoculation due to massive CMV reactivation and disease. In contrast, all four lymphocyte-depleted AGM remained healthy. The lymphocyte-depleted AGM showed only a trend toward a prolongation in peak viremia but the groups were indistinguishable during chronic infection. These data show that adaptive immune responses are critical for controlling disease progression in pathogenic SIV infection in PTM. However, the maintenance of a disease-free course of SIV infection in AGM likely depends on a number of mechanisms including non-adaptive immune mechanisms.
dc.format.extent e1000691 - ?
dc.language eng
dc.language.iso en_US en_US
dc.relation.ispartof PLoS Pathog
dc.relation.isversionof 10.1371/journal.ppat.1000691
dc.subject Adaptive Immunity
dc.subject Animals
dc.subject Antigens, CD20
dc.subject B-Lymphocyte Subsets
dc.subject Blotting, Western
dc.subject CD8-Positive T-Lymphocytes
dc.subject Cercopithecus aethiops
dc.subject Immunohistochemistry
dc.subject Immunophenotyping
dc.subject In Situ Hybridization
dc.subject Lymphocyte Depletion
dc.subject Macaca nemestrina
dc.subject Reverse Transcriptase Polymerase Chain Reaction
dc.subject Simian Acquired Immunodeficiency Syndrome
dc.subject Simian Immunodeficiency Virus
dc.subject Viremia
dc.title Inhibition of adaptive immune responses leads to a fatal clinical outcome in SIV-infected pigtailed macaques but not vervet African green monkeys.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2009-12-0 en_US
duke.description.endpage e1000691 en_US
duke.description.issue 12 en_US
duke.description.startpage e1000691 en_US
duke.description.volume 5 en_US
dc.relation.journal Plos Pathogens en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20011508
pubs.issue 12
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Surgery
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Surgery/Surgery, Surgical Sciences Section for AIDS Research & Development
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Human Vaccine Institute
pubs.publication-status Published
pubs.volume 5
dc.identifier.eissn 1553-7374

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