Impact of Pre-adapted HIV Transmission View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-05-16

AUTHORS

Jonathan M Carlson, Victor Y Du, Nico Pfeifer, Anju Bansal, Vincent Y F Tan, Karen Power, Chanson J Brumme, Anat Kreimer, Charles E DeZiel, Nicolo Fusi, Malinda Schaefer, Mark A Brockman, Jill Gilmour, Matt A Price, William Kilembe, Richard Haubrich, Mina John, Simon Mallal, Roger Shapiro, John Frater, P Richard Harrigan, Thumbi Ndung'u, Susan Allen, David Heckerman, John Sidney, Todd M Allen, Philip J R Goulder, Zabrina L Brumme, Eric Hunter, Paul A Goepfert

ABSTRACT

Human leukocyte antigen class I (HLA)-restricted CD8(+) T lymphocyte (CTL) responses are crucial to HIV-1 control. Although HIV can evade these responses, the longer-term impact of viral escape mutants remains unclear, as these variants can also reduce intrinsic viral fitness. To address this, we here developed a metric to determine the degree of HIV adaptation to an HLA profile. We demonstrate that transmission of viruses that are pre-adapted to the HLA molecules expressed in the recipient is associated with impaired immunogenicity, elevated viral load and accelerated CD4(+) T cell decline. Furthermore, the extent of pre-adaptation among circulating viruses explains much of the variation in outcomes attributed to the expression of certain HLA alleles. Thus, viral pre-adaptation exploits 'holes' in the immune response. Accounting for these holes may be key for vaccine strategies seeking to elicit functional responses from viral variants, and to HIV cure strategies that require broad CTL responses to achieve successful eradication of HIV reservoirs. More... »

PAGES

606-613

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  • Journal

    TITLE

    Nature Medicine

    ISSUE

    6

    VOLUME

    22

    Author Affiliations

  • Microsoft Research, Redmond, Washington, USA.
  • Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
  • Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA.
  • British Columbia Centre for Excellence in HIV/AIDS, Vancouver, British Columbia, Canada.
  • Emory Vaccine Center, Yerkes National Primate Research Center, Emory University, Atlanta, Georgia, USA.
  • Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada.
  • Imperial College of Science, Technology and Medicine, London, UK.
  • Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California, USA.
  • Rwanda-Zambia HIV Research Group, Zambia-Emory HIV Research Project, Lusaka, Zambia.
  • Gilead Sciences, Foster City, California, USA.
  • Department of Clinical Immunology, Royal Perth Hospital, Perth, Western Australia, Australia.
  • Center for Translational Immunology and Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
  • Harvard T.H. Chan School of Public Health, Harvard University, Boston, Massachusetts, USA.
  • Institute for Emerging Infections, Oxford Martin School, University of Oxford, Oxford, UK.
  • Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
  • Max Planck Institute for Infection Biology, Berlin, Germany.
  • Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA.
  • Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
  • Department of Paediatrics, University of Oxford, Oxford, UK.
  • Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, USA.
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.4100

    DOI

    http://dx.doi.org/10.1038/nm.4100

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1048672101

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27183217


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