IFNA1 and viral infectious disease: Plausible mechanisms of positive virus–virus interactions include enhanced viral growth through syncytia formation of a coinfecting virus (22), the virus-mediated down-regulation of IFN, which may promote invasion by opportunistic viruses (41), and the virus-induced release of cytokines such as interleukin 10, which prevents the detrimental effects of dysregulated immune responses and might lead to immunosuppression and enhanced susceptibility to secondary viral infections (53, 54).