PDF(Pubmed)
Abstract：
Enterovirus D68 (EV-D68) is a member of the species Enterovirus D in the genus Enterovirus of the family Picornaviridae. As an emerging non-polio enterovirus, EV-D68 is widely spread all over the world and causes severe neurological and respiratory illnesses. Although the intrinsic restriction factors in the cell provide a frontline defense, the molecular nature of virus-host interactions remains elusive. Here, we provide evidence that the major histocompatibility complex class II chaperone, CD74, inhibits EV-D68 replication in infected cells by interacting with the second hydrophobic region of 2B protein, while EV-D68 attenuates the antiviral role of CD74 through 3Cpro cleavage. 3Cpro cleaves CD74 at Gln-125. The equilibrium between CD74 and EV-D68 3Cpro determines the outcome of viral infection. IMPORTANCE As an emerging non-polio enterovirus, EV-D68 is widely spread all over the world and causes severe neurological and respiratory illnesses. Here, we report that CD74 inhibits viral replication in infected cells by targeting 2B protein of EV-D68, while EV-D68 attenuates the antiviral role of CD74 through 3Cpro cleavage. The equilibrium between CD74 and EV-D68 3Cpro determines the outcome of viral infection.
摘要：
肠道病毒D68（EV-D68）是小病毒科肠道病毒属中肠道病毒D种的成员。作为一种新兴的非脊髓灰质炎肠道病毒，EV-D68在世界各地广泛传播，会导致严重的神经系统和呼吸系统疾病。尽管细胞中的内在限制因素提供了前线防御，病毒-宿主相互作用的分子性质仍然难以捉摸。这里,我们提供的证据表明，主要的组织相容性复合体II类伴侣，CD74，通过与2B蛋白的第二个疏水区相互作用抑制EV-D68在感染细胞中的复制，而EV-D68通过3Cpro裂解减弱CD74的抗病毒作用。3Cpro在Gln-125处切割CD74。CD74和EV-D683Cpro之间的平衡决定了病毒感染的结果。重要性作为一种新兴的非脊髓灰质炎肠道病毒，EV-D68在世界各地广泛传播，会导致严重的神经系统和呼吸系统疾病。这里,我们报道,CD74通过靶向EV-D68的2B蛋白抑制感染细胞中的病毒复制,而EV-D68通过3Cpro裂解减弱CD74的抗病毒作用.CD74和EV-D683Cpro之间的平衡决定了病毒感染的结果。
