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Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats

Yamamoto, Janet K., Sparger, Elizabeth, Ho, Esther W., Andersen, Philip R., O'Connor, Thomas P., Mandell, Carol P., Lowenstine, Linda, Munn, Robert, Pedersen, Niels C.·1988·American Journal of Veterinary Research

Abstract

SUMMARY: Feline immunodeficiency virus (fiv; formerly, feline T-lymphotropic lentivirus) is a typical lentivirus resembling human and simian immunodeficiency viruses in morphologic features, protein structure, and reverse transcriptase enzyme. It is antigenically dissimilar, however. The virus is tropic for primary and permanent feline T-lymphoblastoid cells and Crandell feline kidney cells. The virus did not grow in other permanent feline non-lymphoblastoid cells that were tested, or in lymphoid and non-lymphoid cells from man, dogs, mice, and sheep. During short-term inoculation studies in cats, the feline immunodeficiency-like syndrome found in nature was not experimentally induced, but a distinct primary phase of infection was observed. Fever and neutropenia were observed 4 to 5 weeks after inoculation; fever lasted several days, and neutropenia persisted from 1 to 9 weeks. Generalized lymphadenopathy that persisted for 2 to 9 months appeared at the same time. Antibodies to fiv appeared 2 weeks after inoculation and then plateaued. Virus was reisolated from the blood of all infected cats within 4 to 5 weeks after inoculation and persisted indefinitely in the face of humoral antibody response. Virus was recovered from blood, plasma, csf and saliva, but not from colostrum or milk. Contact transmission was achieved slowly in one colony of naturally infected cats, but not between experimentally infected and susceptible specific-pathogen-free cats kept together for periods as long as 4 to 14 months. The infection was transmitted readily, however, by parenteral inoculation with blood, plasma, or infective cell culture fluids. In utero and lactogenic transmission were not observed in kittens born to naturally or experimentally infected queens. Lymphadenopathy observed during the initial stage of fiv infection was ascribed to lymphoid hyperplasia and follicular dysplasia. A myeloproliferative disorder was observed in 1 cat with experimentally induced infection.

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Metadata

Authors
Yamamoto, J. K., Sparger, E., Ho, E. W., Andersen, P. R., O'Connor, T. P., Mandell, C. P., Lowenstine, L., Munn, R., & Pedersen, N. C.
Venue
American Journal of Veterinary Research
Published
1988-08-01
Volume
49
Issue
8
Pages
1246-1258
ISSN
0002-9645 (ISSN-L)
OpenAlex
W116619909
Cited by
442
References
0
FWCI
5.57
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats. https://app.cochat.ai/papers/10.2460/ajvr.1988.49.08.1246
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Yamamoto, J. K., Sparger, E., Ho, E. W., Andersen, P. R., O'Connor, T. P., Mandell, C. P., Lowenstine, L., Munn, R., & Pedersen, N. C. (1988). Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats. American Journal of Veterinary Research. https://doi.org/10.2460/ajvr.1988.49.08.1246

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