Publications by authors named "Baopeng Zhao"

Porcine parvovirus 8 (PPV8), the most recently discovered PPV genotype, was first reported in pigs in Guangdong, China, in 2021. In this study, we assessed 69 lung tissue samples collected from animals with high fever or respiratory syndrome on pig farms in Guangxi in 2018. Five nearly full-length genome sequences were characterized and analyzed.

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Porcine deltacoronavirus (PDCoV) has caused enormous economic losses to the global pig industry. However, the immune escape mechanism of PDCoV remains to be fully clarified. Transcriptomic analysis revealed a high abundance of interferon (IFN)-induced protein with tetratricopeptide repeats 3 (IFIT3) transcripts after PDCoV infection, which initially implied a correlation between IFIT3 and PDCoV.

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Porcine teschovirus (PTV) can cause reproductive dysfunction and respiratory diseases, with high mortality rates for sick pigs. Among Picornaviridae family virus-encoded proteins, the VP1 structural protein is critical for viral immune evasion. However, whether PTV VP1 inhibits the type I interferon (IFN) response remains unknown.

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Article Synopsis
  • - Seneca Valley virus (SVV) can lead to serious diseases in pregnant sows and high mortality rates in newborn piglets, causing economic losses in pig farming.
  • - The 3C protease is essential for SVV's development, affecting both the virus's replication process and the host's immune response by targeting key factors that regulate these processes.
  • - Recent studies focus on the 3C protease's roles in boosting viral replication, influencing cell death, and bypassing host immunity, which could guide future strategies for preventing SVV infections.
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Swine acute diarrhoea syndrome coronavirus (SADS-CoV), which is a recently discovered enteric coronavirus, is the major aetiological agent that causes severe clinical diarrhoea and intestinal pathological damage in pigs, and it has caused significant economic losses to the swine industry. Nonstructural protein 5, also called 3C-like protease, cleaves viral polypeptides and host immune-related molecules to facilitate viral replication and immune evasion. Here, we demonstrated that SADS-CoV nsp5 significantly inhibits the Sendai virus (SEV)-induced production of IFN-β and inflammatory cytokines.

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