Comparison of historical and contemporary isolates of Senecavirus A.

Senecavirus A (SVA) was discovered as a cell culture contaminant in 2002, and multiple attempts to experimentally reproduce disease were unsuccessful. Field reports of porcine idiopathic vesicular disease (PIVD) cases testing PCR positive for SVA in addition to outbreaks of PIVD in Brazil and the United States in 2015 suggested SVA was a causative agent, which has now been consistently demonstrated experimentally. Ease of experimental reproduction of disease with contemporary strains of SVA raised questions concerning the difficulty of reproducing vesicular disease with historical isolates. The following study was conducted to compare the pathogenicity of SVA between historical and contemporary isolates in growing pigs. Six groups of pigs (n = 8) were intranasally inoculated with the following SVA isolates: SVV001/2002, CAN/2011, HI/2012, IA/2015, NC/2015, SD/2015. All isolates induced vesicular disease in at least half of the inoculated pigs from each group. All pigs replicated virus as demonstrated by serum and/or swab samples positive for SVA by quantitative PCR. Pig sera tested by virus neutralization assay demonstrated cross-neutralizing antibodies against all viruses utilized in the study. Cross-neutralizing antibodies from pigs inoculated with historical isolates were lower than those pigs that were inoculated with contemporary isolates. Phylogenetic analysis revealed two clades with SVV001/2002 being in a separate clade compared to the other five isolates. Although differences in the infection kinetics and sequences of these six isolates were found, clinical presentation of vesicular disease was similar between both historical and contemporary isolates.

Diversity of human parechovirus in infants and children with acute gastroenteritis in Japan during 2014-2016.

A total of 972 stool samples were collected from infants and children with acute gastroenteritis (AGE) in pediatric clinics encompassing six localities (Hokkaido, Tokyo, Shizuoka, Kyoto, Osaka, and Saga) in Japan during the 2-year period from July 2014 to June 2016. Sixty six of the samples (6.8%) were found to be positive for human parechovirus (HPeV) by multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) and subjected to genotyping based on viral protein 1 (VP1) sequences. Four different HPeV genotypes consisting of HPeV1, -3, -4 and -6 were detected, with HPeV1 clade B being predominant and followed by HPeV3 and -6. The first-time presence of HPeV1 clade A in Japan and rare HPeV4 were noted. This study provides up-to-date information on the genetic diversity of HPeV circulating in Japanese infants and children with AGE.

Epidemiology of Human Parechovirus Type 3 Upsurge in 2 Hospitals, Freiburg, Germany, 2018.

In 2018, a cluster of pediatric human parechovirus (HPeV) infections in 2 neighboring German hospitals was detected. Viral protein 1 sequence analysis demonstrated co-circulation of different HPeV-3 sublineages and of HPeV-1 and -5 strains, thereby excluding a nosocomial outbreak. Our findings underline the need for HPeV diagnostics and sequence analysis for outbreak investigations.

Clinico-epidemiology and genetic diversity of Salivirus in acute gastroenteritis cases from Pune, Western India: 2007-2011.

Acute gastroenteritis is a leading cause of mortality in children from developing countries. Recently, Salivirus has been frequently detected in acute gastroenteritis patients, suggesting its possible aetiological role. Conflicting reports available on disease association of Salivirus have made it difficult to ascertain their causative role. The overall epidemiology and clinical features of Salivirus infections are poorly understood. The present five year study was undertaken to investigate the presence and genetic diversity of Salivirus in acute gastroenteritis cases from Pune, Western India and to determine the clinico-epidemiological features of Salivirus infections. A total of 985 faecal samples (778 acute gastroenteritis and 207 asymptomatic controls), collected from three local hospitals (Jan2007-Dec2011) were examined for the presence of Salivirus by RT-PCR. Molecular characterization was performed by PCR amplification of the 3D and VP regions. Frequency of Salivirus detection in cases (2.6%) and controls (1.93%) was not significantly different (p = 0.57). Co-infection with other enteric viruses was seen in 50% of the cases. Comparison of clinical features between Salivirus mono and mixed infections revealed that Salivirus alone did not exacerbate gastroenteritis. The frequency of diarrhoea and overall clinical severity of mixed infections was significantly greater than mono infections (p = 0.02). Based on clinical findings, our study suggests that Salivirus does not cause severe gastroenteritis. Phylogenetic analysis indicated that study strains belonged to Salivirus A1 and formed 2 distinct clusters which shared nucleotide identities of 94.1-96.2% and 88.9-93.8% between themselves in 3D and VP regions, respectively. Interestingly, the more divergent Cluster2 strains shared a low nucleotide identity with the closest reference strain in both regions (~95% in 3D and ~92% in VP) suggesting that they could represent a variant type of Salivirus A1. The genetic diversity in strains detected from study region, emphasizes the need for Salivirus surveillance from other regions of India.