Biomedical Science and Research Journals | Review on The Role of Zn2+ Ions in Viral Pathogenesis and the Effect of Zn2+ Ions for Host Cell-Virus Growth Inhibition

Antiviral activities of Zn²⁺ ions for viral pathogenesis process and inhibition by Zn²⁺ ions for host cell-virus growth have been investigated. Zn²⁺ ions inhibit viral entry, local replication, and spread to organ during viral pathogenesis process. ZFNs may become a potential antiviral agent for restricting HIV-1 integration. The ZAP inhibits viral entry and HIV-1 infection. ZMPSTE24 cooperates with IFITM to inhibit viral entry. ZNF502 was confirmed with siRNA knockdown of the host protein levels resulting in reduced RSV virus production in infected cells. Zinc finger-attacking compound can inhibit HIV-1 and MuLV zinc fingers viral replication in vivo, in which anti-retroviral drugs which target the nucleocapsid zinc finger may be clinically useful against HIV-1. Zn²⁺ ions also inhibit Nidovirus replication that increasing the intracellular Zn²⁺ concentration can efficiently impair the replication of a variety of RNA viruses. A viral infection spread in the infected cell is involved in direct cell-to-cell transmission and cellfree transmission to spread within a host that the effects of zinc ions (using 15 mM - ZnSO₄ solution) against HSV infection. Zinc oxide tetrapods also inhibit viral entry and spread of HSV infection.

Zinc binding motifs such as catalyst, structural, and regulatory ion are found in many proteins encoded by the human genome physiologically and free zinc is many regulated at the single-cell level. Zinc interferes with IFN-λ₃ binding to IFNL-receptor 1 (Lambda interferons), resulting in decreased antiviral activity and increased viral replication (HCV, influenza) in vitro. Zn-treated viral capsids are still able to interact with receptor binding sites and Zn-treated HRVs exhibit an increased susceptibility to genomic RNA degradation, a phenomena that may be facilitated by a Zn-mediated cleavage of viral RNA within the viral capsid, in which the mechanism of Zn-mediated inhibition could occur in a cell-independent, extracellular manner to degrade viral RNA and thereby abrogate viral infectivity. Measles virus V protein of an RNA-binding modulatory factor represses genome replication that MV may modulate the immune response, in which these results provide a modular view of common and unique dendritic cells (DC) responses after infection.

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American Journal of Biomedical Science