Abstract
Viruses are obligate parasites and can only reproduce within host cells because they lack metabolic pathways to complete their replication cycles. Host factors required in viral replication are mainly those involved in lipid metabolism, cell cycle control and apoptosis, cell-to-cell interactions, immune system regulation, etc. Several inhibitors targeting viral polymerases have been designed. However, the rapid appearance of resistant mutants, as a direct consequence of the viral population structure, diminishes the efficacy of this kind of molecules. To elude the rapid loss of treatment efficiency due to the appearance of resistance mutations, cellular factors have been proposed as a promising therapeutic target to inhibit RNA(+) virus replication. In this review, we focus on those interactions between host factors and HCV replicase, to modulate either cellular metabolism or HCV polymerase activity.
Highlights
Viruses are obligate parasites and can only reproduce within host cells because they lack metabolic pathways to complete their replication cycles
Host factors required in viral replication are mainly those involved in lipid metabolism, cell cycle control and apoptosis, cellto-cell interactions, immune system regulation, etc
RNA(+) viruses replicate their RNA genomes through a negative strand intermediate and this reaction is catalyzed by a viral RNA dependent RNA Polymerase (RdRP) (Ferrer-Orta et al, 2015)
Summary
Viruses are obligate parasites and can only reproduce within host cells because they lack metabolic pathways to complete their replication cycles. The cytoplasmic double-stranded RNA binding protein Staufen 1 (Stau1) coimmunoprecipitates HCV NS5B and the host factor Protein Kinase R (PKR), which is critical for interferon-induced cellular antiviral and antiproliferative responses (Dixit et al, 2016). HCV polymerase interacts with several host factors that are important for viral replication process and to control cell cycle, cell metabolism, etc (Lee et al, 2006). By these interactions, NS5B replicates HCV genome and controls several cellular functions important for virus-cell relationship. Several cellular pathways are shared by different RNA(+) viruses and targeting host factors could be useful for inhibiting viral infections from different viruses
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