Exposure to cold impairs interferon-induced antiviral defense

• Published in: Archives of virology Vol. 162; no. 8; pp. 2231 - 2237
• Main Authors: Boonarkart, Chompunuch, Suptawiwat, Ornpreya, Sakorn, Kittima, Puthavathana, Pilaipan, Auewarakul, Prasert
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01.08.2017; Springer Nature B.V
• Subjects: 2',5'-Oligoadenylate Synthetase - metabolism; Antiviral Agents - pharmacology; Antiviral drugs; Biomedical and Life Sciences; Biomedicine; Cell lines; cold; Cold Temperature - adverse effects; HEK293 Cells; Humans; Infections; Infectious Diseases; Influenza; Influenza A virus - drug effects; Influenza A virus - pathogenicity; Influenza A virus - physiology; Influenza, Human - virology; Interferon; interferon-beta; Interferon-beta - pharmacology; Medical Microbiology; messenger RNA; Myxovirus resistance proteins; Myxovirus Resistance Proteins - metabolism; Original Article; Orthomyxoviridae; Replication; respiratory system; Respiratory tract; temperature; Temperature effects; Viral infections; Virology; virus replication; Virus Replication - drug effects; viruses; Influenza Virus; Avian Influenza Virus; Antiviral Defense; MDCK Cell; Rhinovirus Infection
• ISSN: 0304-8608; 1432-8798; 1432-8798
• DOI: 10.1007/s00705-017-3334-0

It is commonly believed that exposure to low temperature increases susceptibility to viral infection in the human respiratory tract, but a molecular mechanism supporting this belief has yet to be discovered. In this study, we investigated the effect of low temperature on viral infection and innate defense in cell lines from the human respiratory tract and found that interferon-induced antiviral responses were impaired at low temperatures. Cells maintained at 25°C and 33°C expressed lower levels of myxovirus resistance protein 1 (MxA) and 2′5′-oligoadenylate synthetase 1 (OAS1) mRNAs when compared to cells maintained at 37°C after infection by seasonal influenza viruses. Exogenous β-interferon treatment reduced the viral replication at 37°C, but not at 25°C. Our results suggest that the impairment of interferon-induced antiviral responses by low temperature is one of several mechanisms that could explain an increase in host susceptibility to respiratory viruses after exposure to cold temperature.