CD8_and_SIV

CD8_and_SIV - JOURNAL OF VIROLOGY, Aug. 2007, p. 88278832...

Info iconThis preview shows pages 1–2. Sign up to view the full content.

View Full Document Right Arrow Icon
J OURNAL OF VIROLOGY, Aug. 2007, p. 8827–8832 Vol. 81, No. 16 0022-538X/07/$08.00 1 0 doi:10.1128/JVI.00895-07 Copyright © 2007, American Society for Microbiology. All Rights Reserved. Mamu-B*08 -Positive Macaques Control Simian Immunode±ciency Virus Replication £ John T. Loffredo, 1 Jess Maxwell, 1 Ying Qi, 2 Chrystal E. Glidden, 1 Gretta J. Borchardt, 1 Taeko Soma, 1 Alex T. Bean, 1 Dominic R. Beal, 1 Nancy A. Wilson, 1 William M. Rehrauer, 3 Jeffrey D. Lifson, 4 Mary Carrington, 2 and David I. Watkins 1,3 * Wisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, Wisconsin 53715 1 ; Laboratory of Genomic Diversity, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland 21702 2 ; Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53715 3 ; and AIDS Vaccine Program/Basic Research Program, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland 02172 4 Received 26 April 2007/Accepted 20 May 2007 Certain major histocompatibility complex (MHC) class I alleles are associated with the control of human immunodeFciency virus and simian immunodeFciency virus (SIV) replication. We have designed sequence-speciFc primers for detection of the rhesus macaque MHC class I allele Mamu-B*08 by PCR and screened a cohort of SIV-infected macaques for this allele. Analysis of 196 SIV mac 239-infected Indian rhesus macaques revealed that Mamu-B*08 was signiFcantly overrepresented in elite controllers; 38% of elite controllers were Mamu-B*08 positive compared to 3% of progressors ( P 5 0.00001). Mamu-B*08 was also associated with a 7.34-fold decrease in chronic phase viremia ( P 5 0.002). Mamu-B*08 -positive macaques may, therefore, provide a good model to understand the correlates of MHC class I allele-associated immune protection and viral containment in human elite controllers. Certain HLA class I alleles strongly in²uence whether individ- uals become slow or rapid progressors after human immunode- ±ciency virus (HIV) infection (8, 18–20, 28, 30, 32, 39). Long-term nonprogressor/elite controller (EC) cohorts are enriched for HLA-B27 and HLA-B57 . Numerous studies have implicated these molecules in the presentation of epitopes that elicit effective HIV-speci±c CD8 1 T-lymphocyte responses (2, 3, 13, 17, 21, 22, 24, 31, 32). Unfortunately, there are many dif±culties associated with understanding the basis for these HLA associations in HIV- infected people, including inoculum variability, allelic diversity, and access to acute-phase samples. Studying simian immunode- ±ciency virus (SIV)-infected rhesus macaques that control viral replication may shed some light on why certain HLA-B27 - and HLA-B57 -positive humans control HIV infection. Although certain major histocompatibility complex (MHC) class I alleles, including Mamu-A*01 and Mamu-B*17 , are as- sociated with slow disease progression in SIV-infected ma- caques (33–35, 38, 41, 42), independently, the presence of these alleles is not predictive for disease outcome. In the case of Mamu-B*17 , only one-fourth of Mamu-B*17 -positive ma- caques become ECs, controlling SIV replication below 1,000 viral RNA (vRNA) copies/ml of plasma during the chronic phase of SIV infection (41). Even
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
Image of page 2
This is the end of the preview. Sign up to access the rest of the document.

This note was uploaded on 11/01/2010 for the course A B taught by Professor C during the Spring '10 term at HKU.

Page1 / 6

CD8_and_SIV - JOURNAL OF VIROLOGY, Aug. 2007, p. 88278832...

This preview shows document pages 1 - 2. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online