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Expanded host cell tropism and cytopathic properties of feline immunodeficiency virus strain ppr subsequent to passage through interleukin-2-independent t cells

Academic Article
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Overview

authors

  • Lerner, D. L.
  • Elder, John

publication date

  • February 2000

journal

  • Journal of Virology  Journal

abstract

  • A cytopathic variant of feline immunodeficiency virus (FIV) strain PPR emerged after passage of wild-type virus on an interleukin-2-independent cell line. The virus, termed FIV-PPRglial, displayed a phenotype markedly different from the parental virus, including the ability to productively infect previously refractory cell lines, induction of large syncytia, and accelerated kinetic properties. A chimeric molecular clone, FIV-PPRchim42, containing the FIV-PPRglial envelope within the backbone of FIV-PPR, exhibited all the characteristics of the FIV-PPRglial phenotype, demonstrating that the viral envelope was responsible for the acquired traits. Subsequent molecular characterization revealed that the FIV-PPRglial envelope contained five amino acid substitutions relative to wild-type FIV-PPR. Mutagenic analyses further demonstrated that the acquired phenotype was minimally attributable to a combination of three mutations, specifically, a glutamine-to-proline change within the second constant domain of the surface protein (SU); a threonine-to-proline change within the V4 loop, also in the SU; and a premature stop codon in the cytoplasmic tail of the transmembrane protein. All three changes were required to produce the FIV-PPRglial phenotype. Cotransfection studies with mutant viruses in combination with each other and with FIV-PPR indicated that the truncated cytoplasmic tail was responsible for the induction of syncytium formation. Receptor usage analyses were pursued, and distinctions were observed between FIV-PPR and FIV-PPRglial. In vitro infections with FIV-PPR, FIV-PPRglial, and FIV-34TF10 on two adherent cell lines were ablated in the presence of SDF1alpha, the natural ligand for CXCR4. In contrast, viral infection of T cells was not limited to CXCR4 usage, and inhibition studies indicate the potential involvement of a CC chemokine receptor.

subject areas

  • Amino Acid Sequence
  • Animals
  • Cats
  • Cell Line
  • Chemokine CCL4
  • Chemokine CCL5
  • Cytopathogenic Effect, Viral
  • Giant Cells
  • Immunodeficiency Virus, Feline
  • Interleukin-2
  • Macrophage Inflammatory Proteins
  • Molecular Sequence Data
  • Mutation
  • T-Lymphocytes
  • Transfection
  • Tropism
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Identity

International Standard Serial Number (ISSN)

  • 0022-538X

Digital Object Identifier (DOI)

  • 10.1128/jvi.74.4.1854-1863.2000

PubMed ID

  • 10644358
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Additional Document Info

start page

  • 1854

end page

  • 1863

volume

  • 74

issue

  • 4

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