Autophagy is involved in the replication of H9N2 influenza virus via the regulation of oxidative stress in alveolar epithelial cells.

Background: Oxidative stress is an important pathogenic factor in influenza A virus infection. It has been found that reactive oxygen species induced by the H9N2 influenza virus is associated with viral replication. However, the mechanisms involved remain to be elucidated.

Molecular characterization and pathogenesis of H9N2 avian influenza virus isolated from a racing pigeon.

H9N2 avian influenza viruses (AIVs) can cross species barriers and expand from birds tomammals and humans. It usually leads to economic loss for breeding farms and poses a serious threat to human health.This study investigated the molecular characteristics of H9N2 AIV isolated from a racing pigeon and its pathogenesis in BALB/c mice and pigeons.

Autophagy is involved in the acute lung injury induced by H9N2 influenza virus.

Influenza A virus usually leads to economic loss to breeding farms and pose a serious threat to human health. Virus infecting tissues directly and influenza virus-induced excessive production of inflammatory factors play the key role in pathogenesis of the disease, but the mechanism is not well clarified. Here, the role of autophagy was investigated in H9N2 influenza virus-triggered inflammation.

Epigallocatechin-3-gallate inhibits TLR4 signaling through the 67-kDa laminin receptor and effectively alleviates acute lung injury induced by H9N2 swine influenza virus.

Epigallocatechin-3-gallate (EGCG) was found to inhibit the Toll-like receptor 4 (TLR4) pathway involved in influenza virus pathogenesis. Here, the effect of EGCG on TLR4 in an H9N2 virus-induced acute lung injury mouse model was investigated. BALB/c mice were inoculated intranasally with A/Swine/Hebei/108/2002 (H9N2) virus or noninfectious allantoic fluid, and treated with EGCG and E5564 or normal saline orally for 5 consecutive days.

The complete mitochondrial genome of the Fancy Pigeon, Columba livia (Columbiformes: Columbidae).

The fancy pigeons are domesticated varieties of the rock pigeon developed over many years of selective breeding. In the present work, we report the complete mitochondrial genome sequence of fancy pigeon for the first time. The total length of the mitogenome was 17,233 bp with the base composition of 30.

N-acetyl-l-cystine (NAC) protects against H9N2 swine influenza virus-induced acute lung injury.

The antioxidant N-acetyl-l-cysteine (NAC) had been shown to inhibit replication of seasonal human influenza A viruses. Here, the effects of NAC on H9N2 swine influenza virus-induced acute lung injury (ALI) were investigated in mice. BALB/c mice were inoculated intranasally with 10(7) 50% tissue culture infective doses (TCID(50)) of A/swine/HeBei/012/2008/(H9N2) viruses with or without NAC treatments to induce ALI model.

Development of latex agglutination test with nucleoprotein as antigen for detection of antibodies to swine influenza virus.

As pigs are susceptible to infection with both avian and human influenza A viruses, they have been proposed to be an intermediate host for the generation of pandemic virus through reassortment. The broad susceptibility of pigs to influenza viruses emphasizes the importance of surveillance of swine influenza virus. Thus, A latex agglutination test (LAT) was developed for rapid detection of antibodies to swine influenza virus.

A mouse model of swine influenza virus H9N2 infection with acute lung injury.

Unlabelled: BALB/c mice inoculated intranasally with A/swine/HeBei/012/2008/ (H9N2) virus (SIV), showing acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), were observed for morbidity (lung histopathology, lung coefficient, lung wet/dry weight (W/D) ratio, arterial blood gas characteristics and inflammatory cells in bronchial alveolar lavage fluid (BALF)) and mortality. The results showed that, (1) on days 1-4 post infection (p.i.

Molecular characterization and pathogenicity of swine influenza H9N2 subtype virus A/swine/HeBei/012/2008/(H9N2).

The H9N2 subtype influenza virus (IV) is a remarkable member of the influenza A viruses because it can infect not only chickens, ducks and pigs, but also humans. Pigs are susceptible to both human and avian influenza viruses and have been proposed to be intermediate hosts for the generation of pandemic influenza viruses through reassortment or adaptation to the mammalian host. To further understand the genetic characteristics and evolution, we investigated the source and molecular characteristics of the H9N2 subtype swine influenza virus (SIV), and observed its pathogenicity in BALB/c mice.