scholarly journals Chronic Δ9-Tetrahydrocannabinol Administration May Not Attenuate Simian Immunodeficiency Virus Disease Progression in Female Rhesus Macaques

2014 ◽  
Vol 30 (12) ◽  
pp. 1216-1225 ◽  
Author(s):  
Angela M. Amedee ◽  
Whitney A. Nichols ◽  
Nicole J. LeCapitaine ◽  
Curtis Vande Stouwe ◽  
Leslie L. Birke ◽  
...  
Keyword(s):  
Disease Progression ◽  
Simian Immunodeficiency Virus ◽  
Virus Disease ◽  
Rhesus Macaques ◽  
Immunodeficiency Virus ◽  
Female Rhesus ◽  
Female Rhesus Macaques

scholarly journals Control of Simian Immunodeficiency Virus SIVmac239 Is Not Predicted by Inheritance of Mamu-B*17-Containing Haplotypes

2006 ◽  
Vol 81 (1) ◽  
pp. 406-410 ◽  
Author(s):  
Jason A. Wojcechowskyj ◽  
Levi J. Yant ◽  
Roger W. Wiseman ◽  
Shelby L. O'Connor ◽  
David H. O'Connor
Keyword(s):  
Human Immunodeficiency Virus ◽  
Disease Progression ◽  
Simian Immunodeficiency Virus ◽  
Virus Disease ◽  
Rhesus Macaques ◽  
Host Genetics ◽  
Mhc Genes ◽  
Histocompatibility Complex ◽  
Identical By Descent ◽  
Immunodeficiency Virus

ABSTRACT It is well established that host genetics, especially major histocompatibility complex (MHC) genes, are important determinants of human immunodeficiency virus disease progression. Studies with simian immunodeficiency virus (SIV)-infected Indian rhesus macaques have associated Mamu-B*17 with control of virus replication. Using microsatellite haplotyping of the 5-Mb MHC region, we compared disease progression among SIVmac239-infected Indian rhesus macaques that possess Mamu-B*17-containing MHC haplotypes that are identical by descent. We discovered that SIV-infected animals possessing identical Mamu-B*17-containing haplotypes had widely divergent disease courses. Our results demonstrate that the inheritance of a particular Mamu-B*17-containing haplotype is not sufficient to predict SIV disease outcome.

scholarly journals The Effects of Chronic Binge Alcohol on the Genital Microenvironment of Simian Immunodeficiency Virus-Infected Female Rhesus Macaques

2014 ◽  
Vol 30 (8) ◽  
pp. 783-791 ◽  
Author(s):  
Nisha Loganantharaj ◽  
Whitney A. Nichols ◽  
Gregory J. Bagby ◽  
Julia Volaufova ◽  
Jason Dufour ◽  
...  
Keyword(s):  
Simian Immunodeficiency Virus ◽  
Rhesus Macaques ◽  
Infected Female ◽  
Immunodeficiency Virus ◽  
Female Rhesus ◽  
Female Rhesus Macaques

scholarly journals Simian Immunodeficiency Virus Disease Course Is Predicted by the Extent of Virus Replication during Primary Infection

1999 ◽  
Vol 73 (6) ◽  
pp. 4829-4839 ◽  
Author(s):  
Silvija I. Staprans ◽  
Peter J. Dailey ◽  
Ann Rosenthal ◽  
Chris Horton ◽  
Robert M. Grant ◽  
...  
Keyword(s):  
Disease Progression ◽  
Simian Immunodeficiency Virus ◽  
Virus Replication ◽  
Virus Disease ◽  
Rhesus Macaques ◽  
Host Responses ◽  
Disease Course ◽  
Peak Viremia ◽  
Immunodeficiency Virus ◽  
High Level

ABSTRACT To elucidate the relationship between early viral infection events and immunodeficiency virus disease progression, quantitative-competitive and branched-DNA methods of simian immunodeficiency virus (SIV) RNA quantitation were cross-validated and used to measure viremia following infection of rhesus macaques with the pathogenic SIVmac251 virus isolate. Excellent correlation between the methods suggests that both accurately approximate SIV copy number. Plasma viremia was evident 4 days postinfection, and rapid viral expansion led to peak viremia levels of 107 to 109 SIV RNA copies/ml by days 8 to 17. Limited resolution of primary viremia was accompanied by relatively short, though variable, times to the development of AIDS (81 to 630 days). The persistent high-level viremia observed following intravenous inoculation of SIVmac251 explains the aggressive disease course in this model. Survival analyses demonstrated that the disease course is established 8 to 17 days postinfection, when peak viremia is observed. The most significant predictor of disease progression was the extent of viral decline following peak viremia; larger decrements in viremia were associated with both lower steady-state viremia (P = 0.0005) and a reduced hazard of AIDS (P = 0.004). The data also unexpectedly suggested that following SIVmac251 infection, animals with the highest peak viremia were better able to control virus replication rather than more rapidly developing disease. Analysis of early viral replication dynamics should help define host responses that protect from disease progression and should provide quantitative measures to assess the extent to which protective responses may be induced by prophylactic vaccination.

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