Host factors in the replication of positive-strand RNA viruses

Abstract

Viruses are obligate, intracellular parasites that depend on host cells for successful propagation. Upon infection of host cells, positivestrand RNA viruses exploit and hijack cellular machinery and reprogram these cells into viral "factories" through various protein-protein, protein-RNA, and protein-lipid interactions. The molecular interplay between host factors and invading viruses is a continuous process throughout the entire viral life cycle and determines virus host range and viral pathogenesis, as well as driving viral evolution. Studies of host factors have contributed insights into their normal cellular functions and helped identify attractive targets for antiviral drug development. With the development of high throughput screening, functional genomics, and proteomics technologies, host factors participating in viral life cycles have been identified rapidly in recent years. In this review, we summarize the recent advances in virus-host cell interactions in positive-strand RNA virus infections and focus on host factors that facilitate viral replication.

Forkhead Box Transcription Factor Regulation and Lipid Accumulation by Hepatitis C Virus

“…Replication of another flavivirus, West Nile virus (WNV), is associated with intracellular membrane rearrangements and requires fatty acid synthesis (40). Positive-strand RNA viruses have evolved mechanisms to reprogram the host cells for their propagation by exploiting and hijacking host proteins, membranes, lipids, and even microRNAs during infection (41). Since positive-strand RNA viruses depend on intracellular membranes for their replication, perturbations in membrane lipid composition and/or protein lipidation are likely to impact viral replication.…”

Proteome Demonstration of Alpha-1-Acid Glycoprotein and Alpha-1-Antichymotrypsin Candidate Biomarkers for Diagnosis of Enterovirus 71 Infection

“…12,19 Protein spots were excised from stained 2-DE gel, followed by incubation with sequencing-grade modified trypsin (Promega, Madison, WI ) prior to the MS analysis.…”

“…3 Endothelial nitric oxide synthase G894T gene polymorphism was associated with EV71 infection, and it could be a susceptibility factor in the development of EV71 infection. 11,12 In addition, host factors are important for determining EV71 cell tropism. It has been demonstrated that the neurotropic EV71 strain, derived from an encephalitis clinical sample, was able to replicate efficiently in the neuroblastoma (SF268) and rhabdomyosarcoma (RD) cell lines, indicating that EV71 can replicate in a wide range of different cells.…”

Human coronavirus NL63 replication is cyclophilin A-dependent and inhibited by non-immunosuppressive cyclosporine A-derivatives including Alisporivir

“…Although coronaviruses encode a proofreading exoribonuclease (nsp14 ExoN) increasing replicative robustness of its large genomes, mutations within this domain increase mutation rates significantly (Smith and Denison, 2013). Virus replication depends on a variety of host factors (de Haan and Rottier, 2006;Vogels et al, 2011;Wang and Li, 2012) which represent potential antiviral targets. These might be more preferable targets than viral proteins as development of resistance is much less likely.…”