In the pre-SARS era, it was generally accepted that HCoVs cause mild respiratory disease only. This concept was changed after the emergence of SARS-CoV. The first reported case of SARS-CoV infection was retrospectively dated back to November 2002 in Guangdong Province of China. In the subsequent seven months, the SARS epidemic resulted in over 8000 reported cases in 37 countries with a case fatality of 9.6% [7]. The superspreading events in SARS-CoV transmission caused fears in the society. Although the exact cause of superspreading remains to be understood, the host but not the virus only is thought to play a key role in the release of large amounts of virions in superspreading. In this regard, the use of immunosuppressive agents such as high-dose steroid in an early phase of viral infection as a treatment modality might boost viral replication leading to the shedding of large amounts of virus. Likewise, the immunocompromised status of the superspreader could have the same effect. In addition, mutation of virus susceptibility genes encoding restriction factors implicated in host antiviral defence would also result in the shedding of extraordinarily large quantities of the virus [8]. In other words, compromising host antiviral defence or decoupling host antiviral immune response from viral replication might allow or facilitate superspreading.