Editorial: Unconventional Animal Models in Infectious Disease Research

Abstract

Beyond an in vitro setting, the use of a biological system is considered imperious to unravel the enigma of host-pathogen interactions, particularly those eventuating in an infectious disease scenery. In the past two-decades, the use of animal models, especially the unconventional ones, in studying infectious disease occurrence and progression has stemmed out. This rise in the use of animal models in research was greatly reinforced by the furtherance advancements in the field of genetics that has opened up for feasible genetic manipulation of both the host and the pathogen as needed throughout the course of conducted studies. Within this frame of reference, our launched topic envisioned to bring in research work that have used a broad spectrum of unconventional animal models to introduce pioneering findings in host-pathogen interaction studies. These findings will not only shed more light on our understanding of host-pathogen interfaces, but also set the foundation for innovative therapeutic regimens to control infectious diseases. In the first contributed article to our Research Topic (Li et al.), the authors described the characteristics of the duck enteritis virus (DEV) ICP22 protein and explored its role in DEV replication. Their findings present ICP22 as a non-essential immediate early protein chiefly located in the nucleus of infected duck embryo fibroblasts cells and reveal that ICP22 encloses a classical nuclear localization signal at 305-314 AA, with a need of residue 309 for ICP22 nuclear localization. Moreover, their verdicts evidently highlight the role of the US1 gene encoding ICP22 in DEV replication. One potential benefit of this finding could be implicated in combating Duck plague infectious disease caused by DEV. Within the poultry viral infectious disease contexture as well, and as part of the ongoing search for novel anti-viral control strategies, the second contributed article to our Research Topic (Hu et al.) present autophagy as a potential therapeutic target for Duck tembusu virus (DTMUV) infection. In this study conducted on ducks as the animal model of choice, and as a follow up on their previous in vitro work divulging that autophagy promotes DTMUV replication (Hu et al., 2020), the authors show that autophagy is triggered in a DTMUV infection setting and that autophagy inhibitors impedes DTMUV replication and attenuates DTMUV-caused pathological manifestations possibly through a host innate immune response-dependent manner.