A Review of Strategic Immune Evasion by Influenza Virus and Antiviral Response of Interferon

Abstract

Influenza virus is -ss RNA virus of family orthomyxovirida. The viral genome codes for 11 different types of proteins however Hemagglutinin (HA) and Neuraminidase (NA) proteins are important in virus classification. The insertion of a basic amino acid residue to the cleavage site of HA converts the low pathogenic avian influenza to highly pathogenic avian influenza. The infection of same cell by different influenza virus of human and animal origin may lead to viral re-assortment. Pigs may act as mixing vessels for the re-assortment that is responsible for viral establishment and spread of infections to human. Virus evade the immune system probably due to the immune stress, viral non-structural proteins are involved in innate immune evasion. The selective pressure of antibodies and positive genetic selection also helps in genetic drift and evasion of humoral immune evasion. Several mechanisms are adopted to evade cellular immune evasion however mutation in virus specific T cell receptors is important. Mutations are used as weapons to evade immune responses. Upon detection of viral components interferons are produced and secreted in antiviral response. Sinus and lungs are common and predominantly induces the expression of IFN-λ instead of IFN-α. IFN-λ may be a potential vaccine candidate for the influenza virus infections. The antigenic instability of influenza virus is probably the root cause of outbreaks. Despite the well-built immune system, influenza virus adopts various competent strategies to evade immune response. The present review is to highlight the important evasion mechanisms of influenza virus, furthermore, IFN-λ are discussed as vaccine candidates.

Dual Host and Pathogen RNA-Seq Analysis Unravels Chicken Genes Potentially Involved in Resistance to Highly Pathogenic Avian Influenza Virus Infection

“…After viral recognition by the PRRs, some pathways are activated to induce the expression of type I interferon (IFN-I), which in turn enhance the expression of interferon stimulated genes (ISGs) and pro-inflammatory cytokines ( 15 , 16 ). Several viral proteins are involved in the viral evasion of the innate immune response: the nucleoprotein (NP) and the matrix (M)-2 protein (M2) protein inhibit the activity of the IFN-I-dependent double-stranded RNA-activated protein kinase (PKR), which inhibits viral replication; while the non-structural (NS1) protein interferes with several innate immune signaling pathways ( 17 ).…”