Effect of infection temperature on infectivity and host response of human coronavirus OC43.

This study aimed to investigate the changes in human coronavirus (HCoV)-OC43-infected cells upon the viral infection temperature and the associated intracellular mechanisms. To examine the influence of temperature during viral propagation, viral infectivity and host defense responses were tested under different infection temperature conditions. The results showed that the efficient viral adsorption temperature was 33 °C, where nasal epithelial or oropharyngeal tissue cells were firstly faced to respiratory viruses, compared to normal tissue temperature 37 °C. Viral adsorption at 33 °C significantly decreased the expression of IFNA1 and IFNB1, whereas increased angiotensin-converting enzyme-2 (ACE2) expression, inflammatory cytokine interleukin-6 level, NOD-like receptor protein 3 (NLRP3), and cleaved caspase-7 expression compared to the one at 37 °C. Additionally, physiological changes in intercellular communication via tight junctions were observed after HCoV-OC43 infection. The levels of ZO-1 and occludin expression were downregulated at 33 °C infection temperature, while ER stress expression level were upregulated. Immunofluorescence analysis further revealed that ZO-1 and occludin exhibited a diffuse and discontinuous staining pattern with reduced localization at cell-cell junctions, indicating structurally underdeveloped tight junctions. These findings suggest that lower temperatures facilitate respiratory viral infection by attenuating host antiviral responses, which may contribute to the pathogenesis and transmissibility of seasonal coronaviruses.