Vesicular stomatitis virus (VSV) causes sporadic outbreaks of vesicular disease in the southwestern United States. The intrinsic characteristics of epidemic strains associated with these outbreaks are poorly understood. In this study, we report the distinctive genomic and biological characteristics of an epidemic (NJ0612NME6) strain of VSV compared with an endemic (NJ0806VCB) strain. Genomic comparisons between the two strains revealed a total of 111 nucleotide differences (23 non-synonymous) with potentially relevant replacements located in the P, G, and L proteins. When tested in experimentally infected pigs, a natural host of VSV, the epidemic strain caused higher fever and an increased number of vesicular lesions compared to pigs infected with the endemic strain. Pigs infected with the epidemic strain showed decreased systemic antiviral activity (type I – IFN), lower antibody levels, higher levels of interleukin 6, and lower levels of tumor necrosis factor during the acute phase of disease compared to pigs infected with the endemic strain. Furthermore, we document the existence of an RNAemia phase in pigs experimentally infected with VSV and explored the cause for the lack of recovery of infectious virus from blood. Finally, the epidemic strain was shown to be more efficient in down-regulating transcription of IRF-7 in primary porcine macrophages. Collectively, the data shows that the epidemic strain of VSV we tested has an enhanced ability to modulate the innate immune response of the vertebrate host. Further studies are needed to examine other epidemic strains and what contributions a phenotype of increased virulence might have on the transmission of VSV during epizootics.
OmpC, a major outer-membrane protein, is highly expressed when Salmonella typhi is grown in nutrient broth (NB) of either low (NB + 0% sucrose) or high (NB + 20% sucrose) osmolarity. This contrasts with the expression of Escherichia coli OmpC, which is inhibited in low osmolarity and enhanced in high osmolarity, as has been described previously (van Alphen and Lugtenberg, 1977; Verhoef et al., 1979; Kawaji et al., 1979). Nevertheless, expression of S. typhi OmpC is dependent on the E. coli OmpR transcriptional activator. These findings suggest differences between the mechanisms of osmoregulation of gene expression in both bacteria, although common effectors appear to be shared.
We analyzed the phylogenetic and time-space relationships (phylodynamics) of 181 isolates of vesicular stomatitis New Jersey virus (VSNJV) causing disease in Mexico and the United States (US) from 2005 through 2012. We detail the emergence of a genetic lineage in southern Mexico causing outbreaks in central Mexico spreading into northern Mexico and eventually into the US. That emerging lineage showed higher nucleotide sequence identity (99.5%) than that observed for multiple lineages circulating concurrently in southern Mexico (96.8%). Additionally, we identified 58 isolates from Mexico that, unlike previous isolates from Mexico, grouped with northern Central America clade II viruses. This study provides the first direct evidence for the emergence and northward migration of a specific VSNJV genetic lineage from endemic areas in Mexico causing VS outbreaks in the US. In addition we document the emergence of a Central American VSNJV genetic lineage moving northward and causing outbreaks in central Mexico.
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