Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the identification, experimental transmission, and pathogenesis of a naturally occurring powerfully immunosuppressive isolate of feline leukemia virus (designated here as FeLV-FAIDS) which induces fatal acquired immunodeficiency syndrome (AIDS) in 100% (25 of 25) of persistently viremic experimentally infected specific pathogen-free (SPF) cats after predictable survival periods ranging from less than 3 months (acute immunodeficiency syndrome) to greater than one year (chronic immunodeficiency syndrome), depending on the age of the cat at time of virus exposure. The pathogenesis of FeLV-FAIDS-induced feline immunodeficiency disease is characterized by: a prodromal period of largely asymptomatic viremia; progressive weight loss, lymphoid hyperplasia associated with viral replication in lymphoid follicles, lymphoid depletion associated with extinction of viral replication in lymphoid follicles, intractable diarrhea associated with necrosis of intestinal crypt epithelium, lymphopenia, suppressed lymphocyte blastogenesis, impaired cutaneous allograft rejection, hypogammaglobulinemia, and opportunistic infections such as bacterial respiratory disease and necrotizing stomatitis. The clinical onset of immunodeficiency syndrome correlates with the replication of a specific FeLV-FAIDS viral variant, detected principally as unintegrated viral DNA, in bone marrow, lymphoid tissues, and intestine. Two of seven cats with chronic immunodeficiency disease that survived greater than 1 year after inoculation developed lymphoma affecting the marrow, intestine, spleen, and mesenteric nodes. Experimentally induced feline immunodeficiency syndrome, therefore, is a rapid and consistent in vivo model for prospective studies of the viral genetic determinants, pathogenesis, prevention, and therapy of retrovirus-induced immunodeficiency disease.
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PMID:Experimental transmission and pathogenesis of immunodeficiency syndrome in cats. 282 40

The functions of the surface glycoproteins (SU) of feline leukemia viruses (FeLVs) are of interest since these proteins mediate virus infection and interference and are critical determinants of disease specificity. In this study, we examined the biochemical and genetic determinants of SU important to virus entry and cell killing. In particular, we developed and used vesicular stomatitis virus (VSV)/FeLV pseudotype virus interference assays to determine interference subgroupings and assess mechanisms of host cell restriction. We also assessed roles of SU in virus growth kinetics and in the inhibition of cell killing caused by superinfection with cytopathic virus. Subgroup classification by VSV/FeLV pseudotype assay was in agreement with that defined previously by focus interference assay and was found to be determined by changes near the N terminus of SU for FeLV subgroups A (FeLV-A) and C. Virus host range restriction was found to be mediated at the level of virus entry in most cases, although postentry events mediated restriction in the failure of a subgroup A-like, T-cell cytopathic and immunodeficiency-inducing clone (FeLV-FAIDS-EECC) to replicate in feline fibroblasts. FeLV-FAIDS-EECC-induced cell killing was also inhibited by prior infection with one of two FeLV-A isolates. This inhibition could be conveyed by as few as four amino acid changes near the N terminus of the FeLV-A SU and also appeared to be mediated at a postentry level. Lastly, the SU-coding sequence was also found to determine differences in growth kinetics of viruses within the same subgroup. These studies demonstrate that subtle alterations in the FeLV SU, particularly in the N-terminal region, impart multiple significant functional differences which distinguish virus variants.
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PMID:Interference with superinfection and with cell killing and determination of host range and growth kinetics mediated by feline leukemia virus surface glycoproteins. 838 21