Novel paradigms of innate immune sensing of viral infections.
According to the existing paradigm, cellular recognition of viral infection is mediated by molecular patterns within the virus particle or produced during virus replication. However, there are various physical cellular changes indicative of infection that could also trigger innate antiviral responses. The type-I interferon response is rapidly engaged to limit viral infection and a number of studies have shown that the interferon response, or components of it, are induced by general perturbations to cellular processes. Virus entry requires membrane and cytoskeletal perturbation, and both membrane fusion or actin depolymerising agents alone are able to activate antiviral genes. Viruses cause cellular stress and change the cellular environment, and oxidative stress or endoplasmic reticulum stress will amplify antiviral signaling. Many of these responses converge on interferon regulatory factor 3, suggesting that it plays a crucial role in determining the degree to which the cell responds. This review highlights novel paradigms of viral recognition and speculates that viral infection is sensed as a danger signal.
['Hare|David|D|', 'Mossman|Karen L|KL|']
D000818:Animals D059865:Endoplasmic Reticulum Stress D006801:Humans D007113:Immunity, Innate D050838:Interferon Regulatory Factor-3 D007370:Interferon Type I D018384:Oxidative Stress D017382:Reactive Oxygen Species D015398:Signal Transduction D014777:Virus Diseases D014779:Virus Replication D014780:Viruses
Innate immunity Recognition Virus Interferon Interferon regulatory factor 3