Seneca Valley Virus 3C ^pro Mediates Cleavage and Redistribution of Nucleolin To Facilitate Viral Replication

Abstract

The nucleolus is a subnuclear cellular compartment, and nucleolin (NCL) resides predominantly in the nucleolus. NCL participates in viral replication, translation, internalization, and also serves as a receptor for virus entry.

Seneca Valley Virus 3Cpro Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication

“…The hnRNP K gene was cloned and inserted into the pCMV-HA vector (Clontech, 631604) with ClonExpress One Step Cloning Kit (Vazyme, C112, China). GFP-infused SVV proteins were reported in our previous study (Song et al, 2021a , b , 2022 ). Mutagenesis of HA-hnRNP K to generate HA-hnRNP K (Q364A) using KOD DNA polymerase (TOYOBO, KFX-201), GFP-3C-H48A, GFP-3C-C160A, and GFP-3C-DM (H48A and C160A double mutants) were reported in our previous study (Song et al, 2021b ).…”

“…Mutagenesis of HA-hnRNP K to generate HA-hnRNP K (Q364A) using KOD DNA polymerase (TOYOBO, KFX-201), GFP-3C-H48A, GFP-3C-C160A, and GFP-3C-DM (H48A and C160A double mutants) were reported in our previous study (Song et al, 2021b ). The 3C sequence of EMCV, FMDV, rhinovirus, CVB3, and EV71 were synthesized from Tsingke Biotechnology (Beijing, China) and recombined into the vector pEGFP-C1 that was used in our previous study (Song et al, 2022 ). The primers used for this study are listed in Table 1 .…”

Advances and Breakthroughs in IRES-Directed Translation and Replication of Picornaviruses

“…Viruses often cleave host proteins to promote their replication or benefit from them. SVA 3C pro cleaved host nuclear protein NCL during infection, which caused its translocation to the cytoplasm and promoted viral replication ( 176 ). However, in the case of FMDV infection, NCL does not show any cleavage.…”

Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA

“…When an organism is infected with a picornavirus, 3C triggers the host innate immune system to employ host pattern recognition receptors (PRRs) to identify the presence of pathogen-associated molecular patterns [87]. These include retinoic-acid-induced gene-I (RIG-I), cytosolic RIG-like RNA helicases such as melanoma differentiation-associated gene (MDA-5), and transmembrane PRRs such as Toll-like receptors (TLRs) [135,136]. PRRs enlist various particular adaptor proteins to initiate a signaling cascade downstream and stimulate three primary pathways for the production of IFNs: the IFN regulatory factor (IRF) pathway, the mitogen-activated protein kinase (MAPK) pathway, and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway [137].…”