DHAV-1 Inhibits Type I Interferon Signaling to Assist Viral Adaption by Increasing the Expression of SOCS3

In conclusion, the DHAV-1 CH60 strain may inhibit the expression of IFNα by increasing the SOCS3 protein and SOCS3 can in turn decrease STAT1 and STAT3 mRNA levels, thereby inhibiting the antiviral protein MX1 and ultimately promoting viral proliferation, indirectly assisting in viral adaptation in chicken embryos. Introduction Duck hepatitis A virus type 1 (DHAV-1) is one of the most lethal pathogens for ducks, especially ducklings <1 week old, as it can cause 100% morbidity and 95% mortality (1). DHAV-1 is responsible for acute hepatitis characterized by petechial and ecchymotic hemorrhages of liver surfaces (2–5). To prevent and control the disease, we have established a variety of methods for virological detection of DHAV-1 and have characterized the functions of several viral proteins (6–11). At present, the prevention and control of the disease mainly depends on live attenuated vaccines (12, 13), such as the DHAV-1 CH60 strain (14). However, the focus and research on attenuated vaccines remain insufficient. The CH60 strain attenuated vaccine is cultivated through serial passage in chicken embryos and is widely used for the prevention and control of the disease. Intensive research has found that incompatible host translational selection pressure is one of the main mechanisms of viral attenuation and adaptation in chicken embryos (15). In addition, transcriptome sequencing has revealed that infection of chicken embryo livers with the ...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research