Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
MOLECULAR ASPECTS OF FELINE LEUKEMIA VIRUS PATHOGENESIS
Retrovirus Biology and Human Disease. Gallo RC and Wong-Staal F, eds. New York, Marcel Dekker, p. 87-116, 1990.. Unique Identifier : AIDSLINE ICDB/91676221 Mullins JI; Hoover EA; Dept. of Cancer Biology, Harvard Univ. Sch. of Public Health,; Boston MA
Abstract:
Feline leukemia viruses (FeLV) are naturally occurring, contagious type C retroviruses (oncovirus subfamily) of domestic cats. Up to 50% of free-roaming, urban domestic cats probably become infected at some point in their lifetime. Molecular analyses of FeLV genomes, their gene products, and the genetic mechanisms underlying the development of FeLV-associated diseases have been conducted in several laboratories over the past decade, utilizing both naturally occurring and experimentally induced infections. The divergent mechanisms of disease induction in viremic cats are beginning to be understood. Genetic analysis of several naturally occurring FeLV isolates is reviewed under the following headings: genome organization and gene products, structure and origin of endogenous FeLV-related sequences, origin of FeLV subgroups and their prevalence in natural infections, viral genetic determinants of FeLV host range in vitro, infectivity and pathogenicity of FeLV subgroups, variable regions and conservation of backbone structure in deduced FeLV and murine gp70 proteins, identification of FeLV neutralization epitopes, immunodeficiency-disease-inducing FeLV variant, and genetic events associated with FeLV-induced proliferative disease. FeLV has provided substantial insight into the mechanisms of retrovirus-induced pathogenesis. These include the first evidence that horizontally transmitted retroviruses are an important cause of naturally occurring leukemia, identification of a large number of viral oncogenes, and early evidence that retrovirus infection can result in antiproliferative diseases of the lymphoreticular system. More recent studies have shown that FeLV genome variants can confer disease, specifically due to changes within an otherwise highly conserved extracellular glycoprotein (gp70) gene. Each of the three FeLV subgroups has a consistent pattern of disease specificity (FeLV-C induces fatal anemia), or structure (FeLV-B originates from recombination of FeLV-A and endogenous FeLV-related sequences), or both (FeLV-A gp70 sequences are highly conserved and these viruses display minimal pathogenicity). The widespread prevalence of FeLV infection in domestic cats and the resulting importance of FeLV as a pathogen, as well as the recent emergence of an FeLV model for AIDS, will continue to focus research on mechanisms of disease induction by FeLV and the development of antiviral strategies and vaccines. (145 Refs)
Keywords: Animal Base Sequence/GENETICS Cat Diseases/*MICROBIOLOGY Cats Cell Transformation, Viral/GENETICS Cloning, Molecular Feline Acquired Immunodeficiency Syndrome/MICROBIOLOGY Gene Expression Regulation, Viral/*PHYSIOLOGY Genes, Viral/GENETICS Immunodeficiency Virus, Feline/GENETICS Leukemia/MICROBIOLOGY/*VETERINARY Leukemia Virus, Feline/*GENETICS/PATHOGENICITY Repetitive Sequences, Nucleic Acid/*GENETICS MONOGRAPH REVIEW
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
