Abstract

Zinc homeostatic status is a key factor in maintaining a healthy immune system that zinc(Ⅱ) ions has antiviral effects; it improves immune responses and suppresses viral replication. The zinc-homeostatic immune concentration may provide a protective role against the COVID-19 pandemic, likely by improving the host’s resistance against viral infection. 2019-nCoV RNA virus structure at least contains four viral proteins, the spike (S) protein, the membrane (M) protein, the envelope (E) protein, and nucleocapsid (N) protein. When S1 protein recognizes its receptor on human cells, the heptad repeat 1 (HR1) and heptad repeat 2 (HR2) domains are exposed to interact with each other, forming six-helical bundle (6-HB) to mediate membrane fusion between virus and target cell. Factor of present outbreak of disease 19 COVID-19 may be considered to be due to RNA virus mutation that the RNA viruses have high mutation rate and these high rates are correlated with enhanced virulence and evolvability, traits considered beneficial for viruses. Zinc ions could inhibit virus entry and membrane fusion of S1 and S2 domains of spike protein with zinc ion-binding interaction.

Zn2+ ions can prevent in the early stage of 2019-nCoV infected patient with antiviral zinc homeostatic immunity and have important roles for respirarory and pulmonary process of COVID-19 disease. Zn2+ inhibits coronavirus and anterivirus RNA polymelase activity, and zinc ionophores block the virus replication that the combination of Zn2+ and pyrithione at low concentrations inhibits the replication of SARS-CoV and arterivirus RNA. The transmembrane protease, serine 2 (TMPRSS2) inhibitors block the cellular entry of the SARS-CoV-II virus through the downregulated priming of the SARS-CoV-II spike protein. In order to prevent that an outbreak of respiratory sickness caused by a novel coronavirus (Covid-19) has become a serious public threat and disrupted many lives, assessing the efficacy of Zn-ejector drugs such as disulfiram combined with interferon to treat Covid-19 infected patients has been proposed. Zinc supplementation plus CQ/HCQ should be recommended for high risk or also younger patients outside of clinical trials as prevention or treatment approach during SARS-CoV-2 pandemic should be considered only on a case-by-case basis. SARS coronavirus envelope protein ion channel activity promotes virus fitness and pathogenesis, in which E protein ion channel activity represents a new determinant for SARS-CoV virulence. Transient zinc chelation (TPEN) induces ER stress and antiviral response by activating NF-κB leading to induction of interferon signaling and zinc plays divergent roles in rotavirus and dengue virus infections in epithelial cells. The antiviral compounds including zinc N-ethyl-N-phenyldithio-carbamate (EPDTC) inhibit the viral protease, thus preventing humancoxsackie-virus strain B3 (CVB3) 2 https://chembiopublishers.com/ANPCIJ/ https://chembiopublishers.com/submit-manuscript.php Advanced Nursing & Patient Care International Journal genome replication. The interactions had been found on the binding specificity by Zn2+ ions-centered tetrahedral geometric coordination of the inhibitors against 3C and 3C-like proteases.

Zinc-finger antiviral protein (ZAP) controls virus entry, DNA/RNA replication, and spreading against viral infection. ZAP specifically inhibits the replication of certain viruses and promotes viral RNA degradation that ZAP inhibits Retroviral RNA production and HIV-1 infection by promoting the degradation of specific viral mRNAs. The mutations of both protein and RNA at the RNA-ZAP interacting surface reduce the in vitro binding affinity and antiviral activity, in which ZAP coordination promotes downstream RNA degradation. ZAP specifically inhibits the replication of Moloney murine leukemia virus (MLV) and Sindbis virus (SIN) by preventing accumulation of the viral mRNA. The mRNA decay is largely determined by the cis-acting elements. However, this ZAP’s efficiency for COVID-19 remains yet unclear. Zinc-ions complexes as 2019-nCoV 3C-like protease inhibitors may play important role for this Zn2+-centered coordination pattern that the zinc-coordinating inhibitor is tetrahedrally coordinated to such as the catalytic dyad of CVB3 3Cpro.