摘要
Dear Editor, Enteroviruses, including poliovirus, enterovirus 71 (EV71), enterovirus 68, coxsackievirus A16, cause millions of infections every year. The infection can lead to serious human diseases and is a significant public health problem. Among them, EV71 is an emerging pathogen that causes severe hand, foot and mouth disease (HFMD) and neurological disease, especially in young children. Currently, there is no effective treatment to EV71-caused diseases, partially blaming to a lack of understanding EV71 replication mechanism (Solomon et al., 2010). As a member of Picornaviri-dae, EV71 infection induces a rapid induction of host shutoff, which is marked by the inhibition of cellular protein synthesis (Holland, 1963). In the meantime, viral protein synthesis takes over the cellular translational machinery. It is believed that the cellular protein synthesis shutoff benefits viral replication by relocating cellular resources and facilitating viral escape from host cell immune responses (Cao et al., 2017). Both transcription and translation inhibition have been suggested to contribute to the host protein synthesis shutoff during picornavirus infection (Holland, 1963;Belsham, 2009). However, the relative role of transcription and translation inhibition in virus-induced host shutoff is yet elusive.
