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Improved health and survival of FIV-infected cats is associated with the presence of autoantibodies to the primary receptor, CD134

Academic Article
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Overview

authors

  • Grant, C. K.
  • Fink, E. A.
  • Sundstrom, M.
  • Torbett, Bruce
  • Elder, John

publication date

  • 2009

journal

  • Proceedings of the National Academy of Sciences of the United States of America  Journal

abstract

  • We analyzed antibody responses in sera from feline immunodeficiency virus (FIV)-infected and uninfected cats. A strong antiviral response to the viral surface glycoprotein (SU) was noted in both natural and experimental infections. In addition, 143 of 226 FIV-infected animals (63%) also expressed antibodies to the primary binding receptor, CD134, whereas cats infected with other feline RNA viruses, including calicivirus, coronavirus, herpesvirus, and feline leukemia virus, did not. Both affinity-purified anti-CD134 and anti-SU antibodies blocked FIV infection ex vivo. FACS analyses revealed that the anti-CD134 antibodies bound to a cryptic epitope on the receptor that was only exposed when SU bound to CD134. Anti-CD134 binding caused displacement of SU from the surface of the cell and inhibition of infection. The presence of antibodies to CD134 correlated with lower virus loads and a better overall health status in FIV(+) cats, whereas anti-SU antibodies were present independent of health status. The findings are consistent with a role for antireceptor antibodies in protection from virus spread and disease progression.

subject areas

  • Animals
  • Autoantibodies
  • Cats
  • Cell Line
  • Feline Acquired Immunodeficiency Syndrome
  • Humans
  • Immunodeficiency Virus, Feline
  • Receptors, OX40
  • Survival Rate
  • T-Lymphocytes
  • Viral Load
  • Virus Internalization
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Research

keywords

  • FIV
  • antireceptor antibody
  • autoantibody
  • lentivirus
  • virus neutralization
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Identity

PubMed Central ID

  • PMC2775039

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.0911307106

PubMed ID

  • 19901342
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Additional Document Info

start page

  • 19980

end page

  • 19985

volume

  • 106

issue

  • 47

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