The multifarious roles of heterogeneous ribonucleoprotein A1 in viral infections

Abstract

Summary Viruses are obligate parasites known to interact with a wide variety of host proteins at different stages of infection. Current antiviral treatments target viral proteins and may be compromised due to the emergence of drug resistant viral strains. Targeting viral‐host interactions is now gaining recognition as an alternative approach against viral infections. Recent research has revealed that heterogeneous ribonucleoprotein A1, an RNA‐binding protein, plays an essential functional and regulatory role in the life cycle of many viruses. In this review, we summarize the interactions between heterogeneous ribonucleoprotein A1 (hnRNPA1) and multiple viral proteins during the life cycle of RNA and DNA viruses. hnRNPA1 protein levels are modulated differently, in different viruses, which further dictates its stability, function, and intracellular localization. Multiple reports have emphasized that in Sindbis virus, enteroviruses, porcine endemic diarrhea virus, and rhinovirus infection, hnRNPA1 enhances viral replication and survival. However, in others like hepatitis C virus and human T‐cell lymphotropic virus, it exerts a protective response. The involvement of hnRNPA1 in viral infections highlights its importance as a central regulator of host and viral gene expression. Understanding the nature of these interactions will increase our understanding of specific viral infections and pathogenesis and eventually aid in the development of novel and robust antiviral intervention strategies.

Cellular Proteo-Transcriptomic Changes in the Immediate Early-Phase of Lentiviral Transduction

“…RNA transport (GO:0050658), regulation of mRNA stability (GO:0043488), regulation of DNA metabolic process (GO:0051052), protein folding (GO:0006457), mRNA splicing via spliceosome (GO:0000398), and cellular response to stress (GO:0033554), were visualized with the corresponding proteins in Figure 7. Our analyses show that the seven downregulated proteins associate with wide networks of proteins, key members of which are mostly involved in the cellular defence against invading pathogens [34][35][36][37].…”

“…Our matching terms, including ribonucleoprotein complex assembly (GO:0022618), RNA transport (GO:0050658), regulation of mRNA stability (GO:0043488), regulation of DNA metabolic process (GO:0051052), protein folding (GO:0006457), mRNA splicing via spliceosome (GO:0000398), and cellular response to stress (GO:0033554), were visualized with the corresponding proteins in Figure 7. Our analyses show that the seven downregulated proteins associate with wide networks of proteins, key members of which are mostly involved in the cellular defence against invading pathogens [34][35][36][37]. RNA transport (GO:0050658), regulation of mRNA stability (GO:0043488), regulation of DNA metabolic process (GO:0051052), protein folding (GO:0006457), mRNA splicing via spliceosome (GO:0000398), and cellular response to stress (GO:0033554), were visualized with the corresponding proteins in Figure 7.…”

Proteomic Profiling of the Human Fetal Multipotent Mesenchymal Stromal Cells Secretome

“…Moreover, the higher HLA-C surface expression is associated with slower HIV disease progression [47]. Both hnRNPA1 and HSPA8 have an ambiguous influence on viral infection: they can enhance replication of some viruses, but they decrease it for some others [48,49]. Lactadherin has been reported to bind specifically to rotavirus and inhibits its replication [50].…”

hnRNP A/B Proteins: An Encyclopedic Assessment of Their Roles in Homeostasis and Disease

“…In both instances, post-translational modifications are the means by which the cell rapidly induces changes in A1 facilitation of translation [51]. Many viruses also contain IRES structures in order to bypass cellular restrictions, and will hijack A1 for their own benefit; this was recently reviewed by Kaur and Lal [172], although it is important to note that they use a non-standard naming convention for A1 isoforms. A1-mediated altered translation has been implicated in cellular proliferation and cancer, where growth factor receptors and oncogenes like FGF-2 (fibroblast growth factor 2), MYC (c-Myc), IQGAP1 (IQ motif containing GTPase activating protein 1), and CYLD (cyclin D1) are aberrantly translated [119,166,[173][174][175].…”