Molecular advances in the cell biology of SARS-CoV and current disease prevention strategies

Stark, Caren J; Atreya, CD

As mentioned above, IL-8 induction was shown to be dependent upon AP-1 activation by SARS-CoV S protein and in this process NF-κB was not involved [34] . This may partially explain the clinical observation of dramatic cytokine storm (high serum levels of IL-6 and IL-8) and inflammation responses observed in SARS patients in the acute stage associated with lung lesions; it has been also suggested that the elevations of IL-6 and IL-8 due to SARS-CoV infection of the respiratory tract can induce the hyper-innate inflammatory response [39] . It is established that cellular MAPKs regulate AP-1 activation-dependent IL-8 induction in viral infections [40] [41] [42] . In SARS-CoV infection, the IL-8 induction signaling pathway is perhaps related to angiotensin-converting enzyme 2 (ACE2), as anti-ACE2 antibodies inhibit IL-8 induction/release [34] . ACE2 is the cellular receptor for the SARS-CoV and the receptor-binding sites on the virion are located in the 12-672 amino acid region of the S protein [43] .