How a Bird Flu Virus Promotes Bacterial Infection in Reproductive Tracts

Jenn Hoskins
22nd March, 2024

How a Bird Flu Virus Promotes Bacterial Infection in Reproductive Tracts

Image Source: Natural Science News, 2024

Key Findings

  • Study at Northwest A&F University found H9N2 flu virus increases chicken cell vulnerability to bacterial infection
  • The virus boosts a protein, fibronectin, which helps bacteria stick to chicken cells, worsening infection
  • H9N2 does this by activating a cell pathway, TGF-β, which could be a new target for preventing such infections
Influenza in birds is not just a concern for the health of the avian population but also poses significant risks to the poultry industry and food safety. A recent study conducted by researchers at Northwest A&F University[1] has shed light on how the H9N2 avian influenza virus, a low-pathogenic strain circulating in poultry, contributes to secondary bacterial infections, specifically exacerbating conditions like salpingitis caused by avian pathogenic Escherichia coli (APEC). Salpingitis, inflammation of the oviduct in chickens, can lead to decreased egg production and quality, resulting in substantial economic losses. While it was known that H9N2 could predispose chickens to additional bacterial infections, the mechanisms behind this viral-bacterial interplay remained unclear until now. The study employed both in vitro and in vivo methods to explore the interaction between the H9N2 virus and APEC. Using a chicken oviduct epithelial cell (COEC) model, researchers observed that H9N2 infection increased the susceptibility of cells to subsequent APEC infection. This was also confirmed in live chicken models, where co-infection with H9N2 and APEC led to more severe symptoms. One of the pivotal discoveries of the research was the identification of a protein called fibronectin, which plays a crucial role in APEC's ability to adhere to COECs. The H9N2 virus was found to upregulate the expression of fibronectin on the surface of COECs. This upregulation is significant because it essentially provides a 'sticky' surface for APEC to latch onto, facilitating infection. Digging deeper into the "how," the team discovered that the NS1 protein of the H9N2 virus activates the transforming growth factor beta (TGF-β) signaling pathway. This pathway is responsible for various cellular processes, including the regulation of fibronectin expression. The activation of TGF-β by the viral protein NS1 is a key step in the increased expression of adhesive molecules that promote APEC adhesion and infection. This study's findings are consistent with earlier research[2], which highlighted the extrapulmonary effects of viral infections on secondary bacterial infections. Specifically, it was found that influenza A virus can promote bacterial translocation and damage to extrapulmonary organs, such as the heart, by exacerbating the effects of secondary bacterial infections. Furthermore, another related study[3] demonstrated that the pneumococcal surface protein A (PspA) acts as an adhesin to dying host cells during co-infection with influenza A virus, which increases pneumococcal localization in the lower airway. This aligns with the current study's findings, as both suggest that influenza virus infection can enhance bacterial adhesion and infection severity. The results of the study not only provide a clearer understanding of the molecular mechanisms behind the H9N2 virus's role in facilitating secondary APEC infections but also open the door to potential preventative strategies. Targeting the TGF-β signaling pathway or fibronectin expression could be a viable approach to mitigating the severity of APEC infections following H9N2 influenza infection. In conclusion, the study from Northwest A&F University adds a significant piece to the puzzle of how viral infections can pave the way for secondary bacterial infections. By uncovering the role of the TGF-β signaling pathway and fibronectin in this process, the research offers new avenues for intervention, with the potential to improve the health of poultry and safeguard the poultry industry from the dual threat of viral and bacterial infections.

HealthBiotechAnimal Science


Main Study

1) The H9N2 avian influenza virus increases APEC adhesion to oviduct epithelia by viral NS1 protein-mediated activation of the TGF-β pathway.

Published 19th March, 2024

Related Studies

2) Pandemic Influenza Infection Promotes Streptococcus pneumoniae Infiltration, Necrotic Damage, and Proteomic Remodeling in the Heart.

3) Streptococcus pneumoniae binds to host GAPDH on dying lung epithelial cells worsening secondary infection following influenza.

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