Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used a panel of in vitro assays to investigate the nature of immune dysfunction in cats infected with FeLV-FAIDS, a naturally occurring, molecularly cloned feline leukemia virus (FeLV) isolate which induces a fatal immunodeficiency syndrome in infected cats. During the asymptomatic period preceding immunodeficiency disease, we were unable to detect any deficits in concanavalin A-induced blastogenesis, xenogeneic mixed-lymphocyte reaction assays, stimulation of lymphocytes by soluble protein antigen, and cytotoxic T lymphocyte assays. However, during this period humoral immune responses in the FeLV-FAIDS-infected cats were dramatically impaired. As early as 9 weeks after virus inoculation, the ability to mount either an IgM or IgG response to soluble protein antigens was lost. Neither B cell function, as assessed by lipopolysaccharide-induced blastogenesis or circulating B cell numbers, as assessed by immunofluorescence, differed between infected and control cats. These results suggest that FeLV-FAIDS infection may impair a subpopulation of T helper cells, that provides help for the production of antibody. Consistent with earlier observations of cats naturally infected with FeLV, our results indicate that early impairment of humoral immunity is an important component of the immunodeficiency syndrome induced by FeLV in cats.
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PMID:Selective impairment of humoral immunity in feline leukemia virus-induced immunodeficiency. 165 28

During type 1 human immunodeficiency virus infection, not only can dendritic cells (DCs) prime T cells against the virus, but they can also infect them in trans. Feline AIDS is caused by feline immunodeficiency virus (FIV) and is considered a model for the human illness because the two diseases have many features in common. Little is known about the interaction of feline DCs with FIV; therefore, this study attempts to tackle such an issue. Infection of feline monocyte-derived DCs (MDDCs) was attempted by spinoculation with FIV strains Petaluma (FIV-Pet) and M2. FIV-Pet was released rapidly in the supernatants of both infected MDDCs and activated T cells after spinoculation. It is shown that FIV-Pet was produced by MDDCs by monitoring viral content in the supernatants of infected MDDCs, by intracellular staining for p25 and by showing its cytopathic effect. Although activated T cells were better substrates for FIV replication, leading to prolonged viral shedding, both immature MDDCs and MDDCs matured with lipopolysaccharide supported virus production, mostly during the first 2 days after infection. At later times, FIV induced syncytium formation by MDDCs. Concerning the FIV receptors, MDDCs were shown to be CD134-negative and CXCR4-positive, a phenotype compatible with permissiveness to FIV-Pet. These results also suggest that maturation is not hampered by FIV infection and that virus exposure itself does not induce MDDC maturation. It is also shown that infected MDDCs can infect activated PBMCs efficiently in trans. It is concluded that MDDCs can be infected by FIV, although infection does not appear to influence their functionality.
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PMID:Effects of feline immunodeficiency virus on feline monocyte-derived dendritic cells infected by spinoculation. 1769 69