Role of RIGI, MDA5 and interferon alpha of duck in Duck Plague infection – a novel report

Author:

Pal Subhomoy,Banerjee Samiddha,Pal AbantikaORCID,Kalita Dhruba Jyoti,Batabyal Subhasis,Debnath Manti,Chakraborty Argha,Mondal Gourhari,Roy Barun,Chatterjee Paresh Nath,Chatterjee Jayanta Kumar,Pal ArunaORCID

Abstract

AbstractDuck Plague (DP) or Duck viral enteritis is an acute contagious and highly fatal disease in water fowl commonly caused by Anatidalphavirus-1 belonging from Herpesviridae family and contains double stranded DNA as genetic material. Pathogen associated molecular pattern (PAMP)s when identified by Pathogen Recognition Receptor (PRR)s acts as effective immunity system action against the pathogen. Melanoma Differentiation-Associated protein 5 (MDA5) and Retionic Acid Inducible Gene I (RIG1) are protein sensor commonly sense for viral double stranded RNA and helps for pro-inflammatory cytokine expression. Gut Associated Lymphoid Tissue (GALT)s have important role in immune response. The current study depicts the important role of three important immune response genes as RIGI, MDA5 and INFalpha in duck plague infestation for the first time. In silico studies followed by differential mRNA expression of RIG1, MDA5 and INFalpha was employed to detect effectiveness of gut associated immune responsiveness in liver, where kupfer cells are the major immune response cells. This was further confirmed through histological section of liver, kupfer cell and immunohistochemistry. This will be helpful to identify molecular mechanism of host innate immunity through duck plague virus infection in indigenous duck. This information may be helful for production of duck with the inherent resistance against duck plague virus infection through suitable biotechnological approaches as gene editing.Due to this inherent nature of better immunity in terms of resistance to other common avian diseases, duck will evolve as one of the major sustainable poultry species.The current study explores the scope to study host immunity against herpes virus in animal model.

Publisher

Cold Spring Harbor Laboratory

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