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Home Viral load and viral diversity as factors during the pathogenesis of SIV-infected rhesus macaques

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Viral load and viral diversity as factors during the pathogenesis of SIV-infected rhesus macaques

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Disclaimer	Access requires a license to the Dissertations and Theses (ProQuest) database.
Link to File	http://libproxy.tulane.edu:2048/login?url=http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:9816780
Title	Viral load and viral diversity as factors during the pathogenesis of SIV-infected rhesus macaques
Author	Simpson, Laura Ann
School	Tulane University
Academic Field	Biology, Molecular Biology, Microbiology
Abstract	Quantitation of plasma virus loads by reverse transcriptase quantitative competitive polymerase chain reaction (RT QC-PCR) and p26 antigen capture assay were performed periodically over 357 days in 22 rhesus macaques intravenously inoculated with SIVdeltaB670 to assess the relationship of virus load to the rate of progression to AIDS. Monkeys were divided into those that died prior to 360 days p.i. (rapid progressors) and those which survived longer (slow progressors) based on the mean survival time. The primary viremic episode ($$56 days p.i.) were evaluated independently. During the primary viremic episode, both rapid and slow progressors had an early increase (day 7) in antigenemia and viremia followed by a decline (day 28); this decline was more pronounced in slow progressors. The majority of rapid progressors had recurrent antigenemia as compared to slow progressors and rapid progressors had a peak in RNA copy number earlier than the slow progressors during persistent infection. Cox proportional hazard model using 1n (RNA copy number x 10$\sp4$/ml) showed day 28 as having a relationship with the hazard of death (p = 0.10). This model also showed that the inclusion of p26 antigen levels for all animals as a time dependent variable was highly significant (p $<$ 0.05) and for the 1n (RNA copy number x 10$\sp4$/ml) it was of borderline significance (p = 0.07) Genetic diversity of SIV was examined in eleven SIVdeltaB670 infected rhesus macaques using heteroduplex mobility assay (HMA) on PCR products from plasma and PBMC samples. Although there were several different patterns noticeable early in infection, 10 out of 11 monkeys showed a substantial increase in genetic diversity prior to the onset of clinical symptoms. The only animal which did not show this shift to greater genetic diversity was free of clinical symptoms for the duration of the study These data indicate that the ability of an SIV-infected animal to maintain low virus loads after the primary viremic episode and suppress a variety of viral variants is important for survival
Language	eng
Advisor(s)	Murphey, Michael
Degree Date	1997
Degree	Ph.D
Publisher	Tulane University
Publication Date	1997
Source	Source: 156 p., Dissertation Abstracts International, Volume: 58-11, Section: B, page: 5808
Identifier	See 'reference url' on the navigation bar.
Rights	Copyright is in accordance with U.S. Copyright law
Contact Information	digitallibrary@tulane.edu
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Viral load and viral diversity as factors during the pathogenesis of SIV-infected rhesus macaques

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