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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the entire glycoprotein (G) gene nucleotide sequences of 26 vesicular stomatitis virus Indiana serotype (VSV IND) type 1 isolates from North and Central America. These sequences are also compared with partial G gene sequences of VSV IND type 2 (Cocal) and type 3 (Alagoas) viruses and the complete G gene sequences of the more distantly related VSV New Jersey (NJ) and Chandipura viruses. Phylogenetic analysis of the G gene sequences by maximum parsimony revealed four major lineages or subtypes within the classical VSV IND (type 1) viruses, each with a distinct geographic distribution. A high degree of VSV genetic diversity was found in Central America, with several virus subtypes of both VSV IND and NJ serotypes existing in this mainly enzootic disease region. Nineteen percent sequence variation but no deletions or insertions were evident within the 5' noncoding and the coding regions of the VSV IND type 1 G genes. In addition to numerous base substitutions, the 3' noncoding regions of these viruses also contained numerous base insertions and deletions. This resulted in striking variation in G gene sizes, with gene lengths ranging from 1,652 to 1,868 nucleotides. As the VSV IND type 1 subtypes have diverged from the common ancestor with the NJ subtypes, their G mRNAs have accumulated more 3' noncoding sequence inserts, ranging up to 303 nucleotides in length. These primarily consist of an imprecise reiteration of the sequence UUUUUAA, apparently generated by a unique polymerase stuttering error. Analysis of the deduced amino acid sequence differences among VSV IND type 1 viruses revealed numerous substitutions within defined antigenic epitopes, suggesting that immune selection may play a role in the evolution of these viruses.
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PMID:Polymerase errors accumulating during natural evolution of the glycoprotein gene of vesicular stomatitis virus Indiana serotype isolates. 216 74

In this study, we used a dicistronic vesicular stomatitis virus (VSV) minigenome to investigate the effects of either single or multiple nucleotide insertions placed immediately after the nontranscribed intergenic dinucleotide of the M gene on VSV transcription. Both Northern blot and primer extension analysis showed that the polymerase responded to the inserted nucleotides in a sequence-specific manner such that some insertions had no effect on mRNA synthesis from the downstream G gene, nor on the site of transcript initiation, whereas other insertions resulted in dramatic reductions in transcript accumulation. Some of these transcripts were initiated at the wild-type site, while others initiated within the inserted sequence. We also examined the transcriptional events that occurred when a natural, 21-nucleotide intergenic region located between the G and L genes from the New Jersey (NJ) serotype of VSV was inserted into the minigenome gene junction. In contrast to the normal 25 to 30% attenuation observed for downstream transcription at gene junctions containing the typical dinucleotide (3'-GA-5') intergenic region, the NJ variant showed greater than 75% attenuation at the gene junction. In addition, the polymerase initiated transcription at two major start sites, one of which was located within the intergenic sequence. Collectively, these data suggest that the polymerase "samples" the intergenic sequences following polyadenylation and termination of the upstream transcript by scanning until an appropriate start site is found. One implication of a scanning polymerase is that the polymerase presumably switches states from a processive elongation mode to a stuttering mode for polyadenylation to one in which no transcription occurs, before it reinitiates at the downstream gene. Our data support the hypothesis that sequences surrounding the intergenic region modulate these events such that appropriate amounts of each mRNA are synthesized.
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PMID:The length and sequence composition of vesicular stomatitis virus intergenic regions affect mRNA levels and the site of transcript initiation. 962 Oct 14

Gene order is often highly conserved within taxonomic groups, such that organisms with rearranged genomes tend to be less fit than wild type gene orders, and suggesting natural selection favors genome architectures that maximize fitness. But it is unclear whether rearranged genomes hinder adaptability: capacity to evolutionarily improve in a new environment. Negative-sense non-segmented RNA viruses (order Mononegavirales) have specific genome architecture: 3' UTR - core protein genes - envelope protein genes - RNA-dependent RNA-polymerase gene - 5' UTR. To test how genome architecture affects RNA virus evolution, we examined vesicular stomatitis virus (VSV) variants with the nucleocapsid (N) gene moved sequentially downstream in the genome. Because RNA polymerase stuttering in VSV replication causes greater mRNA production in upstream genes, N gene translocation toward the 5' end leads to stepwise decreases in N transcription, viral replication and progeny production, and also impacts the activation of type 1 interferon mediated antiviral responses. We evolved VSV gene-order variants in two prostate cancer cell lines: LNCap cells deficient in innate immune response to viral infection, and PC-3 cells that mount an IFN stimulated anti-viral response to infection. We observed that gene order affects phenotypic adaptability (reproductive growth; viral suppression of immune function), especially on PC-3 cells that strongly select against virus infection. Overall, populations derived from the least-fit ancestor (most-altered N position architecture) adapted fastest, consistent with theory predicting populations with low initial fitness should improve faster in evolutionary time. Also, we observed correlated responses to selection, where viruses improved across both hosts, rather than suffer fitness trade-offs on unselected hosts. Whole genomics revealed multiple mutations in evolved variants, some of which were conserved across selective environments for a given gene order.
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PMID:Genome rearrangement affects RNA virus adaptability on prostate cancer cells. 2588 1