Zhiqiang Huang

Learn More
The H9N2 avian influenza virus is a pandemic threat which has repeatedly caused infection in humans and shows enhanced replication and transmission in mice. Previous reports showed that host factors, the interferon-inducible transmembrane (IFITM) protein, can block the replication of pathogens and affect their pathogenesis. BALB/c mice are routine(More)
Activation of the innate immune system requires recognition of pathogen-associated molecular patterns, such as NOD-like receptors. The NOD-like receptor protein 3 (NLRP3) inflammasome is involved in induction of the pro- inflammatory cytokine, IL-1β, and subsequent inflammatory responses. NLRP3 inflammasome plays important roles in the inflammatory and(More)
In chicken, ST3 beta-galactoside alpha-2, 3-sialyltransferase III (ST3GAL III) is one of the key enzymes participating in the biosynthesis of avian influenza virus receptors. Knowledge about ST3Gal III could increase our understanding of its function in the occurrence and development of avian influenza. To date, no detailed data have been published about(More)
H9N2 avian influenza virus (AIV) becomes the focus for its ability of transmission to mammals and as a donor to provide internal genes to form the new epidemic lethal influenza viruses. Residue 627 in PB2 has been proven the virulence factor of H9N2 avian influenza virus in mice, but the detailed data for inflammation difference between H9N2 virus strains(More)
The pathological damage inflicted by virulent AIV strains is often caused by inducing a positive feedback loop of cytokines in immune cells that cause excessive inflammation. Previous research has shown that a G protein-coupled receptor, sphingosine-1-phosphate receptor 1 (S1PR1), plays a crucial role in the development of excessive inflammation in(More)
  • 1