G3BP1 and viral infectious disease: SGs are reported to be scant or absent in SARS-CoV-2-infected cells despite the presence of double-stranded RNA, which is capable of inducing SG formation through activation of EIF2AK2 (also known as PKR, protein kinase R).39–42 Both SARS-CoV-2 infection and ectopic N expression inhibit SG formation in response to exogenous stimuli.17,39–45 However, the relationship between the N protein and G3BP1-dependent SG formation during viral infection in vivo is less clear.