Abstract
Highly pathogenic avian influenza virus (HPAIV) H5N1 is a highly contagious virus that can cause acute respiratory infections and high human fatality ratio due to excessive inflammatory response. Short-term heat shock, as a stressful condition, could induce the expression of heat shock proteins that function as molecular chaperones to protect cells against multiple stresses. However, the protective effect of short-term heat shock in influenza infection is far from being understood. In this study, mice were treated at 39°C for 4 h before being infected with HPAIV H5N1. Interestingly, short-term heat shock significantly increased the levels of HSP70 and pro-inflammatory cytokines IL-6, TNF-α, IFN-β, and IFN-γ in the lung tissues of mice. Following HPAIV H5N1 infection, short-term heat shock alleviated immunopathology and viral replication in lung tissue and repressed the weight loss and increased the survival rate of H5N1-infected mice. Our data reported that short-term heat shock provided beneficial anti-HPAIV H5N1 properties in mice model, which offers an alternative strategy for non-drug prevention for influenza infection.
Highlights
The global prevalence of highly pathogenic avian influenza virus (HPAIV), with startling rates of avian morbidity and mortality, has a major socioeconomic impact in recent decades
We reported that chronic heat shock significantly suppressed innate immunity, resulting in the growing rate of mortality and viral loads in the lungs of mice infected with HPAIV H5N1 (Jin et al, 2011)
In the present study, the exposition of mice to short-term heat shock resulted in the increment of IL-6, TNF-α, IFNβ, and IFN-γ, and their resistant ability to HPAIV H5N1 infection
Summary
The global prevalence of highly pathogenic avian influenza virus (HPAIV), with startling rates of avian morbidity and mortality, has a major socioeconomic impact in recent decades. The H5N1 subtype of HPAIV causes pneumonia leading to acute respiratory distress syndrome and even death in humans (Peiris et al, 2007). Recent evidence showed that the host immune response to influenza virus infection involved the production of inflammatory cytokines, which play a critical role in both innate and adaptive immunity (Sladkova and Kostolansky, 2006; McGill et al, 2009; Kreijtz et al, 2011; Iwasaki and Pillai, 2014; Killip et al, 2015). Patients infected by HPAIV H5N1 have higher serum levels of pro-inflammatory cytokines (e.g., IL-6, TNF-α) compared to those with seasonal influenza
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
