Hepatitis E virus (HEV) causes infections in humans and a wide range of animal hosts. Wild boar is an important natural reservoir of HEV genotypes 3–6 (HEV-3–HEV-6), but comparative analysis of HEV infections in both feral and farmed wild boars remains limited. In this study, samples from 599 wild boars were collected during 2017–2020, including 121 feral wild boars (collected 121 fecal, 121 serum, and 89 liver samples) and 478 farmed wild boars (collected 478 fecal and 478 serum samples). The presence of anti-HEV IgG antibodies were detected by the HEV-IgG enzyme-linked immunosorbent assay (ELISA) kit. HEV RNA was detected by reverse transcription polymerase chain reaction (RT-PCR), targeting the partial ORF1 genes from fecal and liver samples, and the obtained genes were further genotyped by phylogenetic analysis. The results showed that 76.2% (95% CI 72.1–79.9) of farmed wild boars tested anti-HEV IgG seropositive, higher than that in feral wild boars (42.1%, 95% CI 33.2–51.5, p < 0.001). HEV seropositivity increased with age. Wild boar HEV infection presented a significant geographical difference (p < 0.001), but not between sex (p = 0.656) and age (p = 0.347). HEV RNA in fecal samples was detected in 13 (2.2%, 95% CI 1.2–3.7) out of 599 wild boars: 0.8% (95% CI 0.0–4.5, 1/121) of feral wild boars and 2.5% (95% CI 1.3–4.3, 12/478) of farmed wild boars. Phylogenetic analysis showed that all these viruses belonged to genotype HEV-4, and further grouped into sub-genotypes HEV-4a, HEV-4d, and HEV-4h, of which HEV-4a was first discovered in the wild boar populations in China. Our results suggested that farms could be a setting for amplification of HEV. The risk of HEV zoonotic transmission via rearing and consumption of farmed wild boars should be further assessed.
Visna/Maedi virus (VMV) is a neglected pathogen that damages sheep and goats' nervous and respiratory systems. The virus was discovered 80 years ago and has been endemic in China for nearly four decades; nevertheless, there is little information regarding Chinese isolates' genotypes and genomic characteristics. In this study, the proviral DNA of strains isolated in 1985 and 1994 were extracted, and the proviral DNA was subjected to Illumina sequencing combined with Sanger sequencing of poor coverage regions. The results showed that the two isolates were clustered with genotype A2 and shared 78.3%−89.1% similarity to reference VMV genome sequences, with the highest similarity (88.7%−89.1%) to the USA strain USMARC-200212120-r (accession no. MT993908.1) and lowest similarity (78.3%−78.5%) to the Italian strain SRLV009 (accession no. MG554409.1). A maximum-likelihood tree showed that the Chinese VMV strains and the USA strain 1150 (accession no. MH916859.1) comprise a monophyletic group with a short tree branch. Our data filled the gap in genomic analysis and viral evolution in Chinese VMV strains, and would be benefit China's source-tracing and eradication program development in China.
Avian influenza viruses crossing the host barrier to infect humans have caused great panic in human society and seriously threatened public health. Herein, we revealed that knockdown of SRSF7 significantly down-regulated influenza virus titers and viral protein expression. We further observed for the first time that human SRSF7, but not avian SRSF7, significantly inhibited polymerase activity (PB2627E). Molecular mapping demonstrated that amino acids 206 to 228 of human SRSF7 play a decisive role in regulating the polymerase activity, which contains the amino acid motif absent in avian SRSF7. Importantly, our results illustrated that the PB2627K-encoding influenza virus induces SRSF7 protein degradation more strongly via the lysosome pathway and not via the proteasome pathway. Functional enrichment analysis of SRSF7-related KEGG pathways indicated that SRSF7 is closely related to cell growth and death. Lastly, our results showed that knocking down SRSF7 interferes with normal polymerase activity. Taken together, our results advance our understanding of interspecies transmission and our findings point out new targets for the development of drugs preventing or treating influenza virus infection.