Infectious Diseases

Biography

Biography: Suresh Kumar Kali

Abstract

COVID-19 exhibits a global health threat among the elderly and the population with underlying health conditions. During infection, the host’s innate immune response acts as a frontline of defense by releasing cytokines such as type I interferon (IFN α and β) thereby initiating antiviral activity. However, this particular interferon response is interrupted by factors such as SARS-CoV-2 non-structural proteins, aging, diabetes and germ-line errors eventually making the host more susceptible to illness. Thus, the deficiency of type I IFN leads to poor innate immune responses in the host against SARS-CoV-2 infection, eventually leading to severe illness. Therefore, enhancing the host’s innate immune response by administering type I IFN could be a key to prevent the host from COVID- 19 severity. Several viral diseases primarily target the innate immune response to replicate and progress in the host. Intriguingly, COVID-19 severity was associated with a significantly low innate immune response. IFN β monotherapy would be an effective early-stage treatment option to prevent COVID-19 severity. For instance, SNG001, an IFN β product, is in phase 3 clinical trial against COVID-19 and its final data will reveal the efficiency of IFN β monotherapy. We evaluated here the importance of the innate immune response during SARS-CoV-2 infection and the molecular mechanism of IFN β-mediated antiviral activity against SARS- CoV[1]2 infection and concluded that the IFN β monotherapy as an attractive potent treatment option against SARS[1]CoV-2. Therefore, IFN β monotherapy-mediated enhancement of innate immune response could be a key component in future strategies to prevent large-scale viral disease outbreaks.