Abstract
Influenza A virus (IAV) is a major concern to human health due to the ongoing global threat of a pandemic. Inflammatory and cell death signalling pathways play important roles in host defence against IAV infection. However, severe IAV infections in humans are characterised by excessive inflammation and tissue damage, often leading to fatal disease. While the molecular mechanisms involved in the induction of inflammation during IAV infection have been well studied, the pathways involved in IAV-induced cell death and their impact on immunopathology have not been fully elucidated. There is increasing evidence of significant crosstalk between cell death and inflammatory pathways and a greater understanding of their role in host defence and disease may facilitate the design of new treatments for IAV infection.
Highlights
Influenza A virus (IAV) infects approximately 3 to 5 million people each year, and the World HealthOrganisation estimates that 290–650 thousand deaths occur annually worldwide, with the young, old, immunocompromised and individuals with underlying lung and heart conditions at the highest risk.One of the most significant pandemics was the H1N1 Spanish Influenza, with deaths estimated at50–100 million people between 1918 and 1920 [1]
TLR3-deficient mice have been shown to be more susceptible to highly pathogenic avian influenza (HPAI) H5N1 infection [34], but are surprisingly protected from A/Scotland/20/74 (H3N2) and 2009 pandemic H1N1 infection [34,35], suggesting that the contribution of TLR3 responses to IAV infection may vary amongst strains
The results suggest that a Z-DNA binding protein-1 (ZBP1)-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)-mediated cell death axis exists to limit viral replication in mice [23,85]
Summary
Influenza A virus (IAV) infects approximately 3 to 5 million people each year, and the World Health. Vaccines are likely to protect poorly against an emerging strain of IAV, such as in the event of a pandemic. Antivirals, such as oseltamivir, target the virus and show limited efficacy due to IAV resistance and the need to administer within the first 48 h of infection [3]. IAV infects respiratory epithelial cells of the upper-respiratory tract, where it is generally confined in cases of mild infections involving seasonal strains. In the case of severe IAV infections, the virus can reach the lower respiratory tract, in which it infects pulmonary epithelial cells [6]. This review will discuss the induction and interplay between inflammation and cell death during IAV infection
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