RESUMEN
Porcine astroviruses (PAstVs), are widely distributed viruses that are highly prevalent in swine herds. In this study, a novel type 4 porcine astrovirus strain (designated as PAstV4/Tianjin/2018) was identified in a fecal sample from a diarrheal piglet in Tianjin, China and its complete genomic sequence was determined by RT-PCR. Sequence analysis showed that this strain had a capsid protein with a highly variable C-terminal domain, a typical ribosomal frameshifting signal, and a conserved subgenomic promoter sequence. Recombination analysis indicated that PAstV4/Tianjin/2018 was a novel recombinant strain, and a recombination breakpoint was identified at nt position 4220 of the genome. The novel recombinant porcine astrovirus identified in China will be useful for understanding the origin, genetic diversity, and evolution of enteric viruses.
Asunto(s)
Infecciones por Astroviridae/veterinaria , Variación Genética/genética , Genoma Viral/genética , Mamastrovirus/genética , Animales , Infecciones por Astroviridae/virología , China , Heces/virología , Regiones Promotoras Genéticas/genética , Análisis de Secuencia de ARN , Porcinos , Enfermedades de los Porcinos/virologíaRESUMEN
Type-I IFNs (IFN-I) provide a key mediator of innate antiviral response during virus proliferation. Porcine epidemic diarrhea virus (PEDV), which causes diarrhea in swine of all ages, is a worldwide-distributed alphacoronavirus with economic importance. Here, we screened PEDV RNA modification enzymes involved in regulating antiviral response. Whereas the PEDV nsp13 barely regulates type I IFN, inflammatory cytokines (IL-6, TNF-a) and MHCII, nsp16 and nsp14 (to a lesser extent) down-regulate these antiviral effectors. Importantly, we found nsp16 KDKE tetrad appears to play a key role in interferon inhibition by mutating the D129 catalytic residue. Mechanistically, nsp16 down-regulates the activities of RIG-I and MDA5 mediated IFN-ß and ISRE. In turn, the mRNA levels of IFIT family members (IFIT1, IFIT2, IFIT3) was inhibited in cells overexpressing nsp16. In addition, nsp10 enhanced the inhibitory effect of nsp16 on IFN-ß. Altogether these results indicate PEDV nsp16 negatively regulates innate immunity to promote viral proliferation. Findings from this study provides novel perspective to advance the understanding in the pathogenesis of PEDV.