IFN-Lambda: The Key to Norovirus’s Secret Hideaway Sonja M. Best, Shelly J. Robertson  Cell Host & Microbe  Volume 22, Issue 4, Pages 427-429 (October 2017) DOI: 10.1016/j.chom.2017.09.010 Copyright © 2017 Terms and Conditions

Figure 1 The Role of IFN-λ Antagonism in Norovirus Persistence Left panel: acute NoV infection does not result in infection of intestinal epithelial cells (IECs) due to induction of host IFN-λ signaling that cannot be antagonized by the virus. In this case, infection of alternative cell types such as macrophages, dendritic cells, and B cells results in efficient antigen presentation, proliferation of virus-specific tissue-resident memory CD8 T (Trm) cells, and virus clearance. Right panel: persistent NoV infection is associated with efficient antagonism of IFN-λ signaling specifically in IECs. Infection of IECs creates an immunologically privileged site and may result in failure of antigen availability for proliferation of Trm cells, thus facilitating prolonged virus shedding. Cell Host & Microbe 2017 22, 427-429DOI: (10.1016/j.chom.2017.09.010) Copyright © 2017 Terms and Conditions