Antiviral Activities of Zn2+ Ions for Viral Prevention, Replication, Capsid Protein in Intracellular Proliferation of Viruses
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In zinc homeostasis, zinc transporters ZIP and ZnT show tissue specificity and developmental and stimulus responsive expression patterns. The course of the life cycles of viral infections is governed by complex interactions between the virus and the host cellular system. Viruses depend on a host cell for their protein synthesis that the virus must first bind to the host cell, and then the virus enters in the cytoplasm which the genome is liberated from the protective capsid and, either in the nucleus or in the cytoplasm. The use of cellular zinc metalloproteases is effective for virus entry and coronavirus fusion. Molecular aspects of dengue virus genome uncoating and the fate of the capsid protein and RNA genome early during infection were investigated and found that capsid is degraded after viral internalization by the host ubiquitin-proteasome system. These results provide the first insights for antiviral intervention into dengue virus uncoating by Zn-binding degradation and enzyme inhibition of nucleocapsid, capsid protein, viral genome. AZPs inhibit virus DNA replication. Increasing the intracellular Zn2+ concentration with zinc-ionophores like pyrithione can efficiently impair the replication of a variety of RNA viruses, including poliovirus and influenza virus. ZAP is a host antiviral factor that specifically inhibit the replication of certain viruses, including HIV-1, Sindbis virus, and Ebola virus. ZAP specifically binds to the viral mRNA and recruits the cellular RNA degradation machinery to degrade the target RNA, while molecular mechanism by which ZAP inhibits target RNA expression and regulation of antiviral activity have been remained unclear. ROS as byproducts play an important role in cell signaling and regulate hormone action, growth factors, cytokines, transcription, apoptosis, iron transport, immunomodulation, and neuromodulation which many retroviruses, DNA and RNA viruses can cause cell death by generating oxidative stress in infected cells.
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