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.

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 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 Vaccine-induced immune responses against both Gag and Env improve control of simian immunodeficiency virus replication in rectally challenged rhesus macaques

2017 ◽  
Vol 13 (7) ◽  
pp. e1006529 ◽  
Author(s):  
Mauricio A. Martins ◽  
Young C. Shin ◽  
Lucas Gonzalez-Nieto ◽  
Aline Domingues ◽  
Martin J. Gutman ◽  
...  
Keyword(s):  
Immune Responses ◽  
Simian Immunodeficiency Virus ◽  
Virus Replication ◽  
Rhesus Macaques ◽  
Immunodeficiency Virus

scholarly journals Contribution of Peaks of Virus Load to Simian Immunodeficiency Virus Pathogenesis

2002 ◽  
Vol 76 (5) ◽  
pp. 2573-2578 ◽  
Author(s):  
Roland R. Regoes ◽  
Silvija I. Staprans ◽  
Mark B. Feinberg ◽  
Sebastian Bonhoeffer
Keyword(s):  
Disease Progression ◽  
Simian Immunodeficiency Virus ◽  
Rhesus Macaques ◽  
Equivalent Model ◽  
Time Range ◽  
Survival Times ◽  
Set Point ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
Viral Load Data

ABSTRACT The mechanisms causing AIDS and subsequently death in human immunodeficiency virus type 1 infection are not yet fully understood. Nonetheless, correlates of accelerated progression to disease based on immunological and virological markers have been identified. The best correlate identified to date is the baseline virus load or the so-called viral set point. By focusing on a virus load measurement from a restricted time range, however, we ignore valuable information contained in the long-term profile of the virus load. Here, we investigate the relationship between virus load and survival with the aid of a statistical model. The model takes into consideration the virus load at every stage of the disease. In particular, we aim to determine the effect of peaks of virus load on disease progression. We fit our model to unique sequential viral load data of 12 simian immunodeficiency virus mac251-infected rhesus macaques which contain frequent measurements throughout the entire course of the infection until the development of simian AIDS. Our model enables us to predict the survival times of the animals more accurately than an equivalent model which considers the viral set point only. Furthermore, we find that peaks of the virus load contribute less to disease progression than phases of low virus load with the same amount of viral turnover. Our analysis implies that the total viral turnover is not the best correlate of survival. As a consequence, the direct cytopathic effects of virus replication may, by themselves, have less of an impact on disease progression than previously thought.

scholarly journals Specific passage of simian immunodeficiency virus fromend-stage disease results in accelerated progression to AIDS in rhesus macaques

1999 ◽  
Vol 80 (12) ◽  
pp. 3089-3097 ◽  
Author(s):  
Lennart Holterman ◽  
Henk Niphuis ◽  
Peter J. F. ten Haaft ◽  
Jaap Goudsmit ◽  
Gary Baskin ◽  
...  
Keyword(s):  
Simian Immunodeficiency Virus ◽  
Late Stage ◽  
Rhesus Macaques ◽  
Disease Course ◽  
Rapid Disease Progression ◽  
Stage Disease ◽  
Immunodeficiency Virus ◽  
End Stage ◽  
Subsequent Passage

To determine whether passage of late-stage variants of simian immunodeficiency virus (SIV) would lead to a more virulent infection and rapid disease progression, a study was designed to examine the effects of selective transmission of SIV from late-stage cases of AIDS in Macaca mulatta. In a uniform group of 10 age-matched animals from the same genetic breeding stock infected with SIVB670, it took 7 months before one of the ten animals developed AIDS. Passage of virus taken from this animal immediately prior to death resulted in death of the recipient due to AIDS within 4 months. Again, subsequent passage of virus taken late in disease resulted in an accelerated disease course, with AIDS developing within 2·5 and 1·8 months in two recipients. The fourth passage of virus taken late in disease from the most rapid progressor (1·8 months) resulted in AIDS developing in this recipient within 1 month of infection. During each consecutive passage in vivo, the loss of memory T cells became more acute. Evidence that the virus became more virulent with selective passage of late-stage variants was provided by the markedly increased levels of both plasma antigen and viral RNA. Subsequent in vivo passage from end-stage AIDS selected for a strain of SIV capable of causing the acute development of AIDS as rapidly as 1 month post-infection. The pathology of acute AIDS in these cases closely resembled that seen after a chronic disease course.

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