Virology

Biography

Biography: Mohammad Intakhab Alam

Abstract

RNA viruses have evolved very fast due to high degree of mutation rate in their genome. Due to this high mutation rate and subsequently antiviral resistance developed by viruses, many FDA (Food and Drug Administration) approved antiviral drugs are being restricted in clinical settings. Antiviral resistance means that a virus is changed in such a way that the antiviral drug becomes less effective in treating infections caused by that virus. The therapeutic efficacy of current interferon (IFN) against RNA viruses is constantly becoming less effective, even tolerant with great side effects. Many notorious RNA viruses have been shown to escape the host immune defence by blocking the function of retinoic acid-inducible gene-1 (RIG-I) and also IFN-signaling. We have investigated immunostimulatory and antiviral effect of a RIG-I agonist 3p-RNA molecule that potentially produces IFN in Hepatitis C and Yellow Fever virus replicating cells and also enhances IFN-signaling to provide an antiviral state. The antiviral effect of 3p-RNA seems to be superior to recombinant IFN-alpha. Also influenza targeted FDA approved antiviral drugs rimantadine and amantadine have been shown to be ineffective because influenza has developed resistance against it. New antiviral drug strategies are based on understating the molecular mechanism involved in influenza viral infections and viral host factors that supports the virus replication. We have studied that influenza activates and utilize calcium dependent PKC-alpha mediated MAPK signaling-cascade for their efficient replication and using calcium antagonist impairs this virus host essential function leading to strong reduction in influenza replication. Calcium antagonist does not allow influenza to develop resistance against it however Oseltamivir does. This suggests that host essential factors of influenza targeted by calcium antagonist could be an interesting new antiviral strategy.