Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The release of enveloped viruses from infected cells often requires a virally encoded activity, termed a late-budding domain (L domain), encoded by essential PTAP, PPXY, or YPDL sequence motifs. PTAP-type L domains recruit one of three endosomal sorting complexes required for transport (ESCRT-I). However, subsequent events in viral budding are poorly defined, and neither YPDL nor PPXY-type L domains require ESCRT-I. Here, we show that ESCRT-I and other class E vacuolar protein sorting (VPS) factors are linked by a complex series of protein-protein interactions. In particular, interactions between ESCRT-I and ESCRT-III are bridged by AIP-1/ALIX, a mammalian orthologue of the yeast class E VPS factor, Bro1. Expression of certain ESCRT-III components as fusion proteins induces a late budding defect that afflicts all three L-domain types, suggesting that ESCRT-III integrity is required in a general manner. Notably, the prototype YPDL-type L domain encoded by equine infectious anemia virus (EIAV) acts by recruiting AIP-1/ALIX and expression of a truncated form of AIP-1/ALIX or small interfering RNA-induced AIP-1/ALIX depletion specifically inhibits EIAV YPDL-type L-domain function. Overall, these findings indicate that L domains subvert a subset of class E VPS factors to mediate viral budding, some of which are required for each of the L-domain types, whereas others apparently act as adaptors to physically link specific L-domain types to the class E VPS machinery.
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PMID:Divergent retroviral late-budding domains recruit vacuolar protein sorting factors by using alternative adaptor proteins. 1451 44

Three chicken infectious anaemia virus (CIAV) isolates were obtained from broiler flocks with anaemia and poor performance, and were designated AIP-1, 2 and 3. All isolates were resistant to treatment with chloroform and were able to pass through 50-nm pore-size filters. The CIAV isolates induced signs and lesions of chicken infectious anaemia (CIA): thymus atrophy, bone marrow aplasia, low haematocrit values, and body weight reduction when inoculated into 1-day-old susceptible chicks. Microscopic lesions were a reflection of macroscopic observations. CIAV-specific antigens have been demonstrated in tissues of experimentally-infected chicks using monoclonal antibodies specific for CIAV. The presence of antibodies against CIAV in breeders was determined by indirect immunofluorescence tests. Although the chicks derived from breeder flocks that possessed antibodies against CIAV, they were not refractory to infection. These findings, the characteristics of the virus and the virus-induced lesions, demonstrate that CIAV is present in Argentina.
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PMID:Identification of chicken infectious anaemia, isolation of the virus and reproduction of the disease in Argentina. 1867 Oct 94