Peripheral human red blood cell development in human immune system mouse model with heme oxygenase-1 deficiency.

A challenge for human immune system (HIS) mouse models has been the lack of human red blood cell (hRBC) survival after engraftment of these immune-deficient mice with human CD34+ hematopoietic stem cells (HSCs). This limits the use of HIS models for preclinical testing of targets directed at hRBC-related diseases. Although human white blood cells can develop in the peripheral blood of mice engrafted with human HSCs, peripheral hRBCs are quickly phagocytosed by murine macrophages upon egress from the bone marrow.

Experimental Seneca Valley virus infection in sows and their offspring.

Neonatal mortality has been increasingly reported on swine breeding farms experiencing swine idiopathic vesicular disease (SIVD) outbreaks, which can be accompanied by lethargy, diarrhea, and neurologic signs in neonates. Seneca Valley Virus (SVV), or Senecavirus A, has been detected in clinical samples taken from pigs with SIVD. Experimental SVV inoculation has caused vesicular disease in pigs, particularly during the stages from weaning to finishing.

Experimental Seneca Valley virus infection in market-weight gilts.

Seneca Valley virus (SVV) is a picornavirus that causes vesicular disease in swine. Since it is clinically indistinguishable from vesicular disease caused by food-and-mouth disease virus (FMDV), investigations must be performed to rule out this high consequence pathogen. A large portion of these investigations have involved market-weight swine at slaughter plants.

Dexamethasone treatment did not exacerbate Seneca Valley virus infection in nursery-age pigs.

Background: Senecavirus A, commonly known as Seneca Valley virus (SVV), is a picornavirus that has been infrequently associated with porcine idiopathic vesicular disease (PIVD). In late 2014 there were multiple PIVD outbreaks in several states in Brazil and samples from those cases tested positive for SVV. Beginning in July of 2015, multiple cases of PIVD were reported in the United States in which a genetically similar SVV was also detected.

Porcine reproductive and respiratory disease virus: Evolution and recombination yields distinct ORF5 RFLP 1-7-4 viruses with individual pathogenicity.

Recent cases of porcine reproductive and respiratory syndrome virus (PRRSV) infection in United States swine-herds have been associated with high mortality in piglets and severe morbidity in sows. Analysis of the ORF5 gene from such clinical cases revealed a unique restriction fragment polymorphism (RFLP) of 1-7-4. The genome diversity of seventeen of these viruses (81.

Increased frequency of porcine epidemic diarrhea virus shedding and lesions in suckling pigs compared to nursery pigs and protective immunity in nursery pigs after homologous re-challenge.

Porcine epidemic diarrhea virus (PEDV) causes enteric disease in pigs and spreads rapidly after entering naïve pig populations. The objectives were to (1) compare the disease course following inoculation with PEDV isolate US/Colorado/2013 in naïve 10 day and 8 week-old pigs, and (2) contrast the naïve response to homologous challenge in 8 week-old pigs. Pigs were randomly assigned into group 1 (n = 40, no PEDV exposure), group 2 (n = 43, PEDV inoculation at 10 days of age) and group 3 (n = 48, PEDV inoculation at 8 weeks of age).

Status of vaccines for porcine epidemic diarrhea virus in the United States and Canada.

In 2013, porcine epidemic diarrhea virus (PEDV) emerged in the United States as a rapidly spreading epidemic causing dramatic death losses in suckling piglets. Neonatal piglets are most vulnerable to clinical disease and their only protection is passive immunity from their dam. At the end of the third year of the PEDV outbreak, most US sow herds have been infected and many are entering into an endemic disease with much less, but still chronic losses.

Vesicular Disease in 9-Week-Old Pigs Experimentally Infected with Senecavirus A.

Senecavirus A has been infrequently associated with vesicular disease in swine since 1988. However, clinical disease has not been reproduced after experimental infection with this virus. We report vesicular disease in 9-week-old pigs after Sencavirus A infection by the intranasal route under experimental conditions.

Leucine residues in conserved region of 33K protein of bovine adenovirus - 3 are important for binding to major late promoter and activation of late gene expression.

The L6 region of bovine adenovirus 3 (BAdV-3) encode 33K (spliced) and 22K (unspliced) proteins. Earlier, anti-33K serum detected five major and three minor proteins in BAdV-3 infected cells. Here, we demonstrate that anti-sera raised against L6-22K protein detected two proteins of 42 and 37 kDa in BAdV-3 infected cells and one protein of 42 kDa in transfected cells expressing splice-site variant 22K protein (pC.

Conserved arginines of bovine adenovirus-3 33K protein are important for transportin-3 mediated transport and virus replication.

The L6 region of bovine adenovirus (BAdV)-3 encodes a spliced protein designated 33K. The 33K specific sera detected five major proteins and three minor proteins in transfected or virus infected cells, which could arise by internal initiation of translation and alternative splicing. The 33K protein is predominantly localized to the nucleus of BAdV-3 infected cells.

Identification of the 3' and 5' terminal sequences of the 8 rna genome segments of European and North American genotypes of infectious salmon anemia virus (an orthomyxovirus) and evidence for quasispecies based on the non-coding sequences of transcripts.

Background: Infectious salmon anemia (ISA) virus (ISAV) is a pathogen of marine-farmed Atlantic salmon (Salmo salar); a disease first diagnosed in Norway in 1984. This virus, which was first characterized following its isolation in cell culture in 1995, belongs to the family Orthomyxoviridae, genus, Isavirus. The Isavirus genome consists of eight single-stranded RNA segments of negative sense, each with one to three open reading frames flanked by 3' and 5' non-coding regions (NCRs).

Interaction of bovine adenovirus-3 33K protein with other viral proteins.

The adenovirus 33K protein appears to be a multifunctional protein performing different roles in viral infection. The involvement of 33K protein in different steps of adenovirus replication may require protein-protein interaction. Using 33K protein as a bait in the yeast two-hybrid system, we screened open reading frames (ORFs) of bovine adenovirus (BAdV)-3 for potential interactions with 33K protein.

Role of bovine adenovirus-3 33K protein in viral replication.

The L6 region of bovine adenovirus type (BAdV)-3 encodes a nonstructural protein named 33K. To identify and characterize the 33K protein, rabbit polyclonal antiserum was raised against a 33K-GST fusion protein expressed in bacteria. Anti-33K serum immunoprecipitated a protein of 42 kDa in in vitro translated and transcribed mRNA of 33K.