Virucidal Activities of Zinc-Finger Antiviral Proteins and Zinc-Binding Domains for Virus Entry, DNA/RNA Replication and Spread

Abstract

The novel EBV (Epstein-Barr virus)-induced ZNFEB including its intronless locus and human protein variants, controls virus entry and exit from cell cycling in activated lymphocytes. ZNF ZCCHC3 binds RNA and facilitates viral RNA that is critical for RLR-mediated innate immune response to RNA virus. ZAP (Zinc-Finger Antiviral Protein) inhibits entry, replication and spread of certain viruses and promotes viral RNA degradation. ZAP may regulate DNA and RNA virus replication that ZAP inhibits Retroviral RNA production and HIV-1(Human Immuno-Deficiency Virus Type 1) infection by promoting the degradation of specific viral mRNAs. Futhermore, ZAP could regulate RNA virus degradation of SARS-CoV's (SARS Corona Virus) and MERS-CoV's (MERS Corona Virus) RNA virus. Replication of SARS-CoV requires proteolytic processing of the replicase polyprotein by a PLpro (Papain-Like Protease) that zinc conjugate inhibits SARSCoV PLpro protease activity. Zinc conjugated complexes as SARS-CoV 3C-like protease inhibitors play important role for this Zn2+-centered coordination pattern that the zinc-coordinating inhibitor is tetrahedrally coordinated. ZBD (Zinc-Binding Domain) is essential for formation of the functional Junin virus envelope glycoprotein complex. Complex ZBD regulates replicative arterivirus helicase and controls mRNA decay helicase. Viral inhibitor p53 down-regulates SARS-CoV replications that p53 inhibits replication of infectious SARS-CoV as well as of replicons and HCoV-NL63 (Human Coronavirus NL63). ZAP-70 kinase regulates HIV cell-to-cell spread that HIV usurps components of the immunological synapse machinery to ensure its own spread through cell-to-cell contacts. Enveloped viruses enter cells and initiate disease-causing cycles of replication that in all cases virus-cell fusion is executed by one or more viral surface glycoproteins denoted as the fusion protein. Virucidal activities of ZNF, ZAP and ZBD are recognised by which Zn2+ ions bind RNA and facilitates viral RNA that is critical for RLR (RIG-1 Like Receptor)-mediated innate immune response to RNA virus and highly diverse fusion proteins have converged on the same overall strategy to mediate a common pathway of membrane fusion, causing to lead enhancement of the anti-viral activity. Zinc ions become used as Zn-coordinated inhibitors for viral regulation of virucidal activities.

Association of genetic variants of Forebrain Embryonic Zinc Finger-like (FEZL) gene exon 3 with clinical mastitis in Murrah buffaloes (Bubalus bubalis)

“…It has been established that there exists crosstalk between neuronal development and immunity via downstream cytokine expression. Zinc fingers act as regulators of T helper cell differentiation, cytokines, cytokine receptors, and other components of cytokine signaling pathways (Powell et al 2019), inhibit the replication and expression of certain viruses, promote viral degradation (Ishida, 2020) and exhibit immunomodulatory function through activation of T lymphocyte differentiation, which provide defense against invading pathogens (Zhu et al 2020).…”

Antiviral and Antibacterial Efficacy of Nanocomposite Amorphous Carbon Films with Copper Nanoparticles

“…Similarly like for herpes virus, the study for IBV suggests that proteins and nucleic acids are targeted by Cu nanoparticles or/and ions but might be damaged at different speeds. IBV protein capsid protects nucleic acid for replication, spike protein, membrane glycoprotein, envelope protein, and nucleocapsid proteins are located on the surface and are the first target while RNA genome sequences are affected later at significantly lower rates [79][80][81][82][83] .…”