Hari Mohan Saxena* and Pushpinder Kaur
Department of Veterinary Microbiology, College of Veterinary Science, GADVASU, Ludhiana, India
*Corresponding Author: Hari Mohan Saxena, Department of Veterinary Microbiology, College of Veterinary Science, GADVASU, Ludhiana, India.
Received: September 29, 2020; Published: October 29, 2020
Infectious Bursal Disease (IBD), caused by IBD virus (IBDV) is an acute, highly contagious immunosuppressive disease of chickens of 3 - 6 weeks of age which causes significant economic losses globally. Lymphoid cells in the bursa of Fabricius are the target cells of IBDV infection. However, the exact identity of the target molecule to which the IBDV binds on the lymphoid cells is still elusive. Immature B lymphocytes, dendritic cells and monocytes, the cells to which the IBDV binds, all express MHC II. Activation of lymphocytes enhances MHC II expression. We have found enhanced binding of IBDV to lymphocytes after activation which could possibly be due to increased expression of the putative target molecule on activation. LPS activation of B cells resulted in enhanced binding of IBDV as compared to the untreated cells. TGF β treatment which downregulates MHC II expression, decreased IBDV binding on B cells. IFN γ treatment, which upregulates MHC II expression, increased IBDV binding on B cells. Activation of T cells with Con A, which induces MHC II expression, led to IBDV binding on T cells. Thus, as suggested by the above findings, MHC II molecule may be the putative target for IBDV on chicken B cells.
Keywords: Infectious Bursal Disease; IBD Virus; Molecular Target; Bursa; Chicken B Cells; Lymphocytes
Citation: Hari Mohan Saxena and Pushpinder Kaur. “Insights into the Identity of the Putative Molecular Target of Infectious Bursal Disease Virus on Chicken Bursal Cells". Acta Scientific Microbiology 3.11 (2020): 61-73.
Copyright: © 2020 Hari Mohan Saxena and Pushpinder Kaur. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.