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Science 19 February 1988:
Vol. 239. no. 4842, pp. 906 - 910
DOI: 10.1126/science.2893454

Articles

Science, Vol 239, Issue 4842, 906-910
Copyright © 1988 by American Association for the Advancement of Science


articles

Molecular cloning of a feline leukemia virus that induces fatal immunodeficiency disease in cats

J Overbaugh, PR Donahue, SL Quackenbush, EA Hoover, and JI Mullins

Department of Cancer Biology, Harvard School of Public Health, Boston, MA 02115.

A replication-defective variant of feline leukemia virus was molecularly cloned directly from infected tissue and found to induce a rapid and fatal immunodeficiency syndrome in cats. Studies with cloned viruses also showed that subtle mutational changes would convert a minimally pathogenic virus into one that would induce an acute form of immunodeficiency. The data suggest that acutely pathogenic viruses may be selected against by current methods for isolation of the human and simian immunodeficiency viruses.


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Unique Long Terminal Repeat and Surface Glycoprotein Gene Sequences of Feline Leukemia Virus as Determinants of Disease Outcome.
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Subtle Mutational Changes in the SU Protein of a Natural Feline Leukemia Virus Subgroup A Isolate Alter Disease Spectrum.
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Host Range and Receptor Binding Properties of Vectors Bearing Feline Leukemia Virus Subgroup B Envelopes Can Be Modulated by Envelope Sequences outside of the Receptor Binding Domain.
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Genetic and Biochemical Analyses of Receptor and Cofactor Determinants for T-Cell-Tropic Feline Leukemia Virus Infection.
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Selection Forces and Constraints on Retroviral Sequence Variation.
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A Putative Cell Surface Receptor for Anemia-Inducing Feline Leukemia Virus Subgroup C Is a Member of a Transporter Superfamily.
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J. Virol. 73, 6500-6505
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S. K. Ghosh and D. V. Faller (1999)
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Pathogenicity Induced by Feline Leukemia Virus, Rickard Strain, Subgroup A Plasmid DNA (pFRA).
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In Vivo Evolution of a Novel, Syncytium-Inducing and Cytopathic Feline Leukemia Virus Variant.
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Evolution of a Simian Immunodeficiency Virus Pathogen.
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High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR.
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Amplimers with 3'-terminal phosphorothioate linkages resist degradation by vent polymerase and reduce Taq polymerase mispriming..
C M de Noronha and J I Mullins (1992)
Genome Res. 2, 131-136
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West African HIV-2-related human retrovirus with attenuated cytopathicity.
L. Kong, S. Lee, J. Kappes, J. Parkin, D Decker, J. Hoxie, B. Hahn, and G. Shaw (1988)
Science 240, 1525-1529
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