title: Pathogenicity of a subgroup C feline leukemia virus (FeLV) is augmented when administered in association with certain FeLV recombinants.
abstract: There is evidence to suggest that infectious feline leukemia viruses (FeLVs) may be altered biologically because of homologous recombination with non-infectious endogenous FeLV (enFeLV) sequences in the infected cells. To evaluate the role of such recombination events in FeLV pathogenesis, a molecular clone of subgroup C FeLV, Sarma strain (FSC), was tested for induction of aplastic anemia in the absence or presence of mixtures of recombinants between FSC and an enFeLV element. In the recombinants, FSC sequences in the viral surface glycoprotein (SU) protein were variably replaced by the corresponding sequences of the enFeLV. The results showed that the virus mixtures varied in their infectivity to neonatal specific pathogen-free cats. One group of mixtures, although exhibiting relatively reduced infectivity, represented the most acute disease-inducing agents. The presence of recombinants in this mixture significantly accelerated the development of erythrocyte aplasia compared to cats infected with FSC alone. In addition, infected cells appeared to be distributed differently in various hematopoietic organs with respect to infection with FSC versus viral mixture. Viral recombinants which were present in this inoculum mixture, however, could not be detected in the plasma or infected tissues of the cats at the end stage of the disease, although their presence in the plasma at the early stages could be detected. Clearly, parental FSC outgrew the recombinants in the infected animals, since its detection was prominent at all stages of the progression of the disease. Therefore, we hypothesize that recombinants initially present in the infected animals, while only poorly replicated compared to FSC in the host, might have had the opportunity to infect certain target cells (potentially erythroid progenitor cells) and then disappeared with the associated cytopathic effect.
authors.affiliation: Center for Retrovirus Research, Ohio State University, Columbus 43210.
authors.forename: L E
authors.initials: LE
authors.lastname: Mathes
authors.forename: R
authors.initials: R
authors.lastname: Pandey
authors.forename: R
authors.initials: R
authors.lastname: Chakrabarti
authors.forename: F M
authors.initials: FM
authors.lastname: Hofman
authors.forename: K A
authors.initials: KA
authors.lastname: Hayes
authors.forename: P
authors.initials: P
authors.lastname: Stromberg
authors.forename: P
authors.initials: P
authors.lastname: Roy-Burman
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000956:Antigens, Viral / Q000032:analysis; D001483:Base Sequence; D002415:Cats; D014644:Genetic Variation; D007150:Immunohistochemistry; D005256:Leukemia Virus, Feline / Q000235:genetics / Q000472:pathogenicity*; D008969:Molecular Sequence Data; D011995:Recombination, Genetic; D012192:Retroviridae Infections / Q000235:genetics* / Q000382:microbiology / Q000473:pathology; D014412:Tumor Virus Infections / Q000235:genetics* / Q000382:microbiology / Q000473:pathology; D014763:Viral Matrix Proteins / Q000032:analysis / Q000097:blood; D014774:Virulence
chemical_list: D000956:Antigens, Viral; D014763:Viral Matrix Proteins