The Leader protein of Saffold virus is a multifunctional protein that suppresses type I interferon induction and has anti-apoptotic effects, which may contribute to its pathogenicity.
Hypothesis-generating for Saffold virus pathogenesis in neuroimmunology; leaves open human translational relevance.
Objective Saffold virus (SAFV) classified in the species Theilovirus of the genus Cardiovirus is a novel human cardiovirus. The pathogenicity of SAFV in humans still remains unclear. Viruses in the genus Cardiovirus produce Leader protein, which is a small non‐structural protein. Evidence that Leader protein of murine cardioviruses is a key factor in their biological activities has been provided. Therefore, the studies on the function of SAFV‐L are likely to be important in order to clarify the pathogenicity of SAFV. Methods We investigated the interferon (IFN) response in the early stage of SAFV infection by reverse transcription polymerase chain reaction and the growth kinetics of the chimera virus, SAFL/DA. Results The study showed that SAFV‐L suppresses the type I IFN response, and that the responsible region of anti‐IFN activity of SAFV‐L is a zinc‐binding motif. Furthermore, the anti‐apoptotic activity of SAFV‐L was suggested from the growth kinetics analysis of SAFL/DA. Conclusions The present study suggested that SAFV‐L might be a multifunctional protein; for example, the suppression of IFN induction, anti‐apoptotic effect and/or productive virus growth.
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Shimizu et al. (2014) studied this question.
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