Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response
Identifieur interne : 002E22 ( Main/Exploration ); précédent : 002E21; suivant : 002E23Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response
Auteurs : Jean D. Boyer [États-Unis] ; Sanjeev Kumar [États-Unis] ; Tara Robinson [États-Unis] ; Rose Parkinson [États-Unis] ; Ling Wu [États-Unis] ; Mark Lewis [États-Unis] ; David I. Watkins [États-Unis] ; David B. Weiner [États-Unis]Source :
- Journal of Medical Primatology [ 0047-2565 ] ; 2006-08.
Abstract
In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.
Url:
DOI: 10.1111/j.1600-0684.2006.00179.x
Affiliations:
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Boyer</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author><author><name sortKey="Kumar, Sanjeev" sort="Kumar, Sanjeev" uniqKey="Kumar S" first="Sanjeev" last="Kumar">Sanjeev Kumar</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author><author><name sortKey="Robinson, Tara" sort="Robinson, Tara" uniqKey="Robinson T" first="Tara" last="Robinson">Tara Robinson</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author><author><name sortKey="Parkinson, Rose" sort="Parkinson, Rose" uniqKey="Parkinson R" first="Rose" last="Parkinson">Rose Parkinson</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Ling" sort="Wu, Ling" uniqKey="Wu L" first="Ling" last="Wu">Ling Wu</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author><author><name sortKey="Lewis, Mark" sort="Lewis, Mark" uniqKey="Lewis M" first="Mark" last="Lewis">Mark Lewis</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Bioqual, Frederick, MD</wicri:regionArea><wicri:noRegion>MD</wicri:noRegion></affiliation></author><author><name sortKey="Watkins, David I" sort="Watkins, David I" uniqKey="Watkins D" first="David I." last="Watkins">David I. Watkins</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Wisconsin National Primate Research Center and Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI</wicri:regionArea><wicri:noRegion>WI</wicri:noRegion></affiliation></author><author><name sortKey="Weiner, David B" sort="Weiner, David B" uniqKey="Weiner D" first="David B." last="Weiner">David B. Weiner</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA</wicri:regionArea><wicri:noRegion>PA</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Primatology</title><title level="j" type="alt">JOURNAL OF MEDICAL PRIMATOLOGY</title><idno type="ISSN">0047-2565</idno><idno type="eISSN">1600-0684</idno><imprint><biblScope unit="vol">35</biblScope><biblScope unit="issue">4‐5</biblScope><biblScope unit="page" from="202">202</biblScope><biblScope unit="page" to="209">209</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-08">2006-08</date></imprint><idno type="ISSN">0047-2565</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0047-2565</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Boyer, Jean D" sort="Boyer, Jean D" uniqKey="Boyer J" first="Jean D." last="Boyer">Jean D. Boyer</name></noRegion><name sortKey="Kumar, Sanjeev" sort="Kumar, Sanjeev" uniqKey="Kumar S" first="Sanjeev" last="Kumar">Sanjeev Kumar</name><name sortKey="Lewis, Mark" sort="Lewis, Mark" uniqKey="Lewis M" first="Mark" last="Lewis">Mark Lewis</name><name sortKey="Parkinson, Rose" sort="Parkinson, Rose" uniqKey="Parkinson R" first="Rose" last="Parkinson">Rose Parkinson</name><name sortKey="Robinson, Tara" sort="Robinson, Tara" uniqKey="Robinson T" first="Tara" last="Robinson">Tara Robinson</name><name sortKey="Watkins, David I" sort="Watkins, David I" uniqKey="Watkins D" first="David I." last="Watkins">David I. Watkins</name><name sortKey="Weiner, David B" sort="Weiner, David B" uniqKey="Weiner D" first="David B." last="Weiner">David B. Weiner</name><name sortKey="Wu, Ling" sort="Wu, Ling" uniqKey="Wu L" first="Ling" last="Wu">Ling Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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