Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2005-7-4
pubmed:abstractText
Because most studies of AIDS pathogenesis in nonhuman primates have been performed in Indian-origin rhesus macaques (Macaca mulatta), little is known about lentiviral pathogenicity and control of virus replication following infection of alternative macaque species. Here, we report the consequences of simian-human immunodeficiency virus SHIV-89.6P and SIVmac251 infection in cynomolgus (Macaca fascicularis) and rhesus macaques of Chinese origin. Compared to the pathogenicity of the same viruses in Indian rhesus macaques, both cynomolgus and Chinese rhesus macaques showed lower levels of plasma virus. By 9 to 10 months after infection, both viruses became undetectable in plasma more frequently in cynomolgus than in either Chinese or Indian rhesus macaques. Furthermore, after SHIV-89.6P infection, CD4+ T-cell numbers declined less and survival was longer in cynomolgus and Chinese rhesus macaques than in Indian rhesus macaques. This attenuated pathogenicity was associated with gamma interferon ELISPOT responses to Gag and Env that were generated earlier and of higher frequency in cynomolgus than in Indian rhesus macaques. Cynomolgus macaques also developed higher titer neutralizing antibodies against SHIV-89.6 at 10 and 20 weeks postinoculation than Indian rhesus macaques. These studies demonstrate that the pathogenicity of nonhuman primate lentiviruses varies markedly based on the species or geographic origin of the macaques infected and suggest that the cellular immune responses may contribute to the control of pathogenicity in cynomolgus macaques. While cynomolgus and Chinese rhesus macaques provide alternative animal models of lentiviral infection, the lower levels of viremia in cynomolgus macaques limit the usefulness of infection of this species for vaccine trials that utilize viral load as an experimental endpoint.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-10588548, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-11309631, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-11679158, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-11875482, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-11899095, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-12093882, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-12131186, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-12390539, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-15134366, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-15297611, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-15575373, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-407808, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-8178433, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-8794335, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-8806570, http://linkedlifedata.com/resource/pubmed/commentcorrection/15994781-9311879
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-538X
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8878-85
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Pathogenicity of simian-human immunodeficiency virus SHIV-89.6P and SIVmac is attenuated in cynomolgus macaques and associated with early T-lymphocyte responses.
pubmed:affiliation
Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. kreimann@bidmc.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural