Biology:Antiviral protein

From HandWiki
Mechanism of zinc-finger antiviral protein (ZAP) recognition of specific target RNA, and the process by which ZAP coordinates downstream RNA degradation (left). ZAP-RNA complex protein ribbon diagram (right).

Antiviral proteins are proteins that are induced by human or animal cells to interfere with viral replication. These proteins are isolated to inhibit the virus from replicating in a host's cells and stop it from spreading to other cells.[citation needed] The Pokeweed antiviral protein and the Zinc-Finger antiviral protein are two major antiviral proteins that have undergone several tests for viruses, including HIV and influenza.[citation needed]

Pokeweed antiviral protein

Pokeweed antiviral protein (PAP) is a ribosome inactivating protein that provides pokeweed plants protection against both viral and fungal infections.[1] It also protects other types of plants that have genetically engineered to express RAP that do not normally do so.[1] Recombinant PAP has also been proposed as a treatment of human diseases such as AIDS and cancer.[2][3]

ZC3HAV1

ZAP (Zinc finger Antiviral Protein) is encoded by the ZC3HAV1 gene[4] whose expression is induced by interferon and helps fight a number of viral infections including influenza.[5]

IFITM3

Interferon-induced transmembrane protein 3 (IFITM3) inhibits the replication of number of enveloped RNA viruses including influenza A, HIV and the Ebola and Dengue viruses.[6] Consequently pharmacological induction of IFITM3 potentially could be used to treat a number of viral infections.[5]

Protein kinase R

Protein kinase R is interferon stimulated and activated either by double-stranded RNA (occurring as an intermediate in RNA viruses replication) or by other proteins. It is able to phosphorylate the eukaryotic translation initiation factor eIF2α thus inhibiting further cellular mRNA translation.[7]

References

  1. 1.0 1.1 "Pokeweed antiviral protein: its cytotoxicity mechanism and applications in plant disease resistance". Toxins 7 (3): 755–72. March 2015. doi:10.3390/toxins7030755. PMID 25756953. 
  2. "High-level expression and purification of biologically active recombinant pokeweed antiviral protein". Protein Expression and Purification 16 (2): 359–68. July 1999. doi:10.1006/prep.1999.1084. PMID 10419833. 
  3. "Structure-based design and engineering of a nontoxic recombinant pokeweed antiviral protein with potent anti-human immunodeficiency virus activity". Antimicrobial Agents and Chemotherapy 47 (3): 1052–61. March 2003. doi:10.1128/aac.47.3.1052-1061.2003. PMID 12604541. 
  4. "PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes". Genes & Development 31 (2): 101–126. January 2017. doi:10.1101/gad.291518.116. PMID 28202539. 
  5. 5.0 5.1 "Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection". PLOS ONE 14 (1): e0210132. 2019. doi:10.1371/journal.pone.0210132. PMID 30650117. Bibcode2019PLoSO..1410132B. 
  6. "IFITM3: How genetics influence influenza infection demographically". Biomedical Journal 42 (1): 19–26. February 2019. doi:10.1016/j.bj.2019.01.004. PMID 30987701. 
  7. Fensterl, V.; Sen, G. C. (2009), "Interferons and viral infections", BioFactors 35 (1): 14–20, doi:10.1002/biof.6, PMID 19319841, https://www.ncbi.nlm.nih.gov/pubmed/19319841