The emergence of West Nile virus (WNV) in the WesternWest Nile virus (WNV) is a positive-sense single-stranded RNA virus in the family Flaviviridae. Isolates of WNV are subdivided into two lineages: lineage I viruses are represented by emergent strains distributed throughout the world and have been associated with outbreaks of encephalitis and meningitis in Europe, the Middle East, and, most recently, in North America, whereas lineage II isolates are largely nonemergent/ endemic strains that are confined to the African subcontinent and the island countries of Madagascar and Cyprus (5,7,25,26). In most cases, WNV infection of humans can be characterized as asymptomatic or as a mild, febrile illness termed West Nile fever. However, a significant increase in the global incidence of severe neurological disease associated with WNV lineage I infections arose in the mid-1990s, culminating in the U.S. outbreak in 2003, which included 9,862 reported cases and 264 deaths (CDC website, http://www.cdc.gov/ncidod/dvbid /westnile/index.htm). After its introduction in New York City in 1999, WNV rapidly spread across the continent and now appears to have firmly established itself in the ecology of North America. The rapid emergence of WNV and its virulence within a naïve population suggest that epidemic forms of the virus may encode mechanisms to evade host immunity.Infection with WNV triggers a delayed host response that includes the activation of interferon regulatory factor-3 (IRF-3) and the subsequent production of alpha/beta interferon (IFN-␣/␤) (14,15,38). IFNs are a family of immunomodulatory cytokines that are produced in response to virus infection and serve as integral signal initiators of host intracellular defenses (40,46). Binding of IFN to the cognate IFN-␣/␤ receptor (IFNAR) on target cells results in the activation of the JAK-STAT pathway, which includes the receptor-associated kinases JAK1 and Tyk2 that in turn phosphorylate and activate their downstream effectors, STAT1 and STAT2. Activated phospho-STAT1/STAT2 heterodimers translocate to the nucleus to form a heterotrimeric complex with IRF-9 and induce the transcription of hundreds of interferon-stimulated genes (ISGs), whose products can direct antiviral and antiproliferative actions that limit virus replication and spread. Many viruses encode proteins that direct mechanisms to disrupt innate antiviral defenses and IFN-induced JAK-STAT signaling, and these processes have been linked to viral emergence in new host populations and species (16,23,44) and to pathogenic outcomes of infection (reviewed in references 11, 40, and 46). Importantly, virulent isolates of WNV have been shown to be capable of attenuating IFN actions by preventing STAT1 and STAT2 activation, although the mechanisms of this regulation and its influence in vivo were not defined (17, 29). Here we describe in vitro and in vivo studies comparing the genetic and phenotypic properties of a lineage I/emergent strain and a lineage II/nonemergent strain of WNV. Our data show that viral control of I...

In 2007, a novel coronavirus associated with an acute respiratory disease in alpacas (Alpaca Coronavirus, ACoV) was isolated. Full-length genomic sequencing of the ACoV demonstrated the genome to be consistent with other Alphacoronaviruses. A putative additional open-reading frame was identified between the nucleocapsid gene and 3'UTR. The ACoV was genetically most similar to the common human coronavirus (HCoV) 229E with 92.2% nucleotide identity over the entire genome. A comparison of spike gene sequences from ACoV and from HCoV-229E isolates recovered over a span of five decades showed the ACoV to be most similar to viruses isolated in the 1960’s to early 1980’s. The true origin of the ACoV is unknown, however a common ancestor between the ACoV and HCoV-229E appears to have existed prior to the 1960’s, suggesting virus transmission, either as a zoonosis or anthroponosis, has occurred between alpacas and humans.

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Large numbers of a reovirus-like agent were visualized with electron microscopy in bacteria-free gut homogenates obtained from piglets with a fatal diarrhea resembling transmissible gastroenteritis. The syndrome, of vomiting, diarrhea, dehydration, and death, was reproduced in piglets artificially infected with these bacteria-free gut homogenates. Reovirus-like particles persisted in serial piglet passage and none was seen in uninfected, asymptomatic controls. Hyperimmune sera (made in recovered piglets) aggregated the reovirus-like particles, as judged by immunoelectron microscopy, and neutralized the infectious agent. The cytoplasm in enterocytes on infected intestinal epithelium fluoresced when this hyperimmune sera was used in an indirect fluorescent antibody test. Feeding cow colostrum or diets containing porcine gamma globulin protected infected piglets. No cytopathogenic effect was noted in infected tissue cultures, nor did this agent affect neonatal guinea pigs, hamsters, mice, and rats. The agent did not agglutinate human 0 or A erythrocytes. In 1972 we reported on an infectious abacterial enteritis resembling transmissible gastroenteritis (TGE) of swine (

Abstract. Although the causative agent of bovine viral diarrhea was initially categorized as 1 species, phylogenetic analysis revealed that these viruses belong to 2 different species, Bovine viral diarrhea virus 1 (BVDV-1) and BVDV-2, with 2-11 subgenotypes within each species. Distribution of species and subgenotypes has been shown to vary with geographic region. Whether distribution shifts over time is not known. Surveys conducted between 1994 and 2008 reported 3 subgenotypes circulating among cattle in the United States: BVDV-1a, BVDV-1b, and BVDV-2a. The average percent prevalence of BVDV-1a, BVDV-1b, and BVDV-2a strains reported in surveys before 2001 were 21%, 43%, and 36%, respectively. Surveys conducted on viruses isolated after 2001 reported decreasing percentages of BVDV-1a and BVDV-2a strains, with BVDV-1b strains accounting for 75-100% of samples. Comparison of these surveys is confounded by differences in geographic location, collection methods, and sample type used in the survey. The purpose of the present study was to determine whether the prevalence of BVDV subgenotypes shifted in samples collected from the same geographic region and by the same laboratory over time. BVDV strains isolated in years 1988BVDV strains isolated in years , 1998BVDV strains isolated in years , and 2008, at the Texas Veterinary Medical Diagnostic Laboratory, Amarillo, Texas, were genotyped, and the prevalence of BVDV-1a, BVDV-1b, and BVDV-2a strains were determined. Typing, on the basis of phylogenetic analysis, was done on 148 samples. The strongest trend detected among these samples was a pronounced decrease in the number of BVDV-1a strains over time.