ArticleJournal of virology1991
Viral genetic determinants of T-cell killing and immunodeficiency disease induction by the feline leukemia virus FeLV-FAIDS.
Article in Journal of virology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 92 citations in OpenAlex.
- Exploring the link between viruses and cancer in companion animals: a comprehensive and comparative analysis.Infectious agents and cancer · 2023Review
- Infectious Causes of Neoplasia in the Domestic Cat.Veterinary sciences · 2022Review
- Reduced Folate Carrier: an Entry Receptor for a Novel Feline Leukemia Virus Variant.Journal of virology · 2019Article
- A Retrospective Examination of Feline Leukemia Subgroup Characterization: Viral Interference Assays to Deep Sequencing.Viruses · 2018Review
- Novel Feline Leukemia Virus Interference Group Based on the env Gene.Journal of virology · 2016Article
- Article
- The surface glycoprotein of a natural feline leukemia virus subgroup A variant, FeLV-945, as a determinant of disease outcome.Veterinary immunology and immunopathology · 2011Article
- Viral determinants of FeLV infection and pathogenesis: lessons learned from analysis of a natural cohort.Viruses · 2011Review
- The receptors for gibbon ape leukemia virus and amphotropic murine leukemia virus are not downregulated in productively infected cells.Retrovirology · 2011Article
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- Identification of a feline leukemia virus variant that can use THTR1, FLVCR1, and FLVCR2 for infection.Journal of virology · 2009Article
- Identification of residues outside of the receptor binding domain that influence the infectivity and tropism of porcine endogenous retrovirus.Journal of virology · 2008Article
- Advances in understanding molecular determinants in FeLV pathology.Veterinary immunology and immunopathology · 2008Review
- Up-regulation of a cellular protein at the translational level by a retrovirus.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Expression of murine leukemia virus envelope protein is sufficient for the induction of apoptosis.Journal of virology · 2008Article
- Genetic characterization of feline leukemia virus from Florida panthers.Emerging infectious diseases · 2008Article
- Article
- Induction of endoplasmic reticulum stress in thymic lymphocytes by the envelope precursor polyprotein of a murine leukemia virus during the preleukemic period.Journal of virology · 2007Article
- Feline leukemia virus T entry is dependent on both expression levels and specific interactions between cofactor and receptor.Virology · 2007Article
- Importance of receptor usage, Fli1 activation, and mouse strain for the stem cell specificity of 10A1 murine leukemia virus leukemogenicity.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Within the fatal immunodeficiency disease-inducing strain of feline leukemia virus, FeLV-FAIDS, are viruses which range in pathogenicity from minimally (clone 61E is the prototype) to acutely pathogenic, most of the latter of which are also replication defective (clone 61C is the prototype). Mixtures of 61E and 61C virus and chimeras generated between them, but not 61E alone, killed feline T cells. T-cell killing depended on changes within a 7-amino-acid region near the C terminus of the gp70 env gene or was achieved independently by changes within a 109-amino-acid region encompassing the N terminus of gp70. The carboxy-terminal change was also sufficient for induction of fatal immunodeficiency disease in cats. Other changes within the 61C gp70 gene enhanced T-cell killing, as did changes in the long terminal repeat, the latter of which also enhanced virus replication. T-cell killing correlated with high levels of intracellular unintegrated and proviral DNA, all of which were blocked by treatment of infected cells with sera from 61C-immune cats or with a neutralizing monoclonal antibody. These findings indicate that T-cell killing is a consequence of superinfection and that the mutations in env critical to pathogenicity of the immunosuppressive variant result in a failure to establish superinfection interference in infected cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.