Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
PATHOGENESIS OF FELINE RETROVIRUS-INDUCED CYTOPATHIC DISEASES: ACQUIRED IMMUNE DEFICIENCY SYNDROME AND APLASTIC ANEMIA
Animal Models of Retrovirus Infection and Their Relationship to AIDS. Salzman LA, ed. Orlando, Florida, Academic Press, p. 59-74, 1986.. Unique Identifier : AIDSLINE ICDB/87629266 Hoover EA; Mullins JI; Quackensush SL; Gasper PW; Dept. of Pathology, Colorado State Univ., Fort Collins, CO
Abstract:
Prototype pathogenic feline leukemia virus (FeLV) strains that induce either feline acquired immune deficiency syndrome (AIDS) or aplastic anemia (AA) have been identified by serial in vivo passage in specific pathogen-free (SPF) cats and have recently been molecularly cloned and shown to possess disease-specific pathogenicity in inoculated SPF cats. The early pathogenesis of progressive feline retrovirus infection in cats involves sequential virus replication in (1) macrophages in local lymphoid tissues, (2) small numbers of circulating mononuclear leukocytes, (3) B and T lymphocytes in systemic lymphoid tissues, (4) bone marrow myeloid, megakaryocytic, and erythroid progenitor cells, (5) circulating leukocytes and platelets, and finally, (6) mucosal and glandular epithelial cells with subsequent viral excretion and horizontal transmission. Experimentally induced feline AIDS, like the naturally occurring disease, is characterized by persistent viremia, progressive wt loss leading to emaciation, intractable diarrhea, lymphocytosis, and elevated blastogenic responses to mitogens, followed by lymphopenia and suppressed lymphocyte mitogenic responses, systemic lymphoid hyperplasia followed by severe lymphoid depletion, chronic enteritis, and opportunistic infections including oral mycotic infections (thrush). FeLV-feline AIDS, like other feline retrovirus strains, replicates extensively in salivary glands, pharyngeal epithelium, and esophageal epithelium and is shed in saliva. The pathogenesis of the experimental feline AIDS model is summarized in a figure. AA has been recognized for over a decade as a major fatal cytosuppressive disease caused by FeLV; FeLV-induced AA was transmitted initially by serial passage of FeLV-KT and other field isolates in newborn cats and subsequently in corticosteroid-treated weanling and adults cats. The incubation period for induction of viremia and progressive marrow aplasia is 4 wk or less, and survival is 9 wk or less, in weanling cats infected with biologically passaged anemogenic isolates such as the FeLV-KT. Experimental FeLV-induced AA and AIDS in cats represent rapid and consistent models of irreversibly fatal cytopathic retroviral diseases in which the causative viral genotypes and the principal cytopathic target cells can be identified and the molecular pathogenetic mechanisms of selective cytopathicity and disease can be studied. (33 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*ETIOLOGY/PATHOLOGY Aging Anemia, Aplastic/ETIOLOGY Animal Bone Marrow/MICROBIOLOGY Cat Diseases/MICROBIOLOGY Cats DNA, Viral Leukemia/*ETIOLOGY/TRANSMISSION Leukemia Virus, Feline/CLASSIFICATION/GENETICS/*PATHOGENICITY Lymph Nodes/MICROBIOLOGY/PATHOLOGY Virus Replication MONOGRAPH
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Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
