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Avian Coronavirus Infectious Bronchitis Virus Activates Mitochondria-Mediated Apoptosis Pathway and Affects Viral Replication by Inducing Reactive Oxygen Species Production in Chicken HD11 Cells
School of Bioscience and Technology, Chengdu Medical College, Chengdu 610500, China
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Biology 2024, 13(7), 491; https://doi.org/10.3390/biology13070491
Submission received: 29 April 2024
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Revised: 20 June 2024
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Accepted: 30 June 2024
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Published: 1 July 2024
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
Simple Summary
Avian infectious bronchitis is an important infectious disease that causes heavy losses in the poultry industry. Vaccination is an effective preventive measure, but the ability of infectious bronchitis virus (IBV) to mutate reduces the vaccine’s protective effect. Therefore, it is quite important to study the pathogenic mechanism of IBV. In this study, we found that IBV infection leads to ROS accumulation in chicken macrophage HD11 cells. The oxidative stress further induced cell apoptosis mediated by mitochondria-mediated apoptotic signaling. In addition, IBV replication was essential to ROS accumulation, and IBV proliferation decreased when ROS activation was blocked. IBV nucleocapsid (N) protein can cause ROS accumulation and cell apoptosis. Our findings may provide insights into the interaction between IBV and its host and uncover the pathogenesis of IBV infection.
Abstract
Infectious bronchitis virus (IBV), a coronavirus that causes severe respiratory and gastrointestinal illness in poultry, leads to substantial economic losses. According to earlier research, IBV infection causes chicken macrophage HD11 cells to undergo cell apoptosis. Reactive oxygen species (ROS) and the IBV-activated intrinsic apoptotic signaling pathway were examined in this work. The findings demonstrate that IBV infection causes ROS to accumulate. Moreover, IBV infection decreased the mitochondrial transmembrane potential in HD11 cells, which could be blocked by ROS antioxidants (PDTC and NAC). The two antioxidants significantly affected the expression of Bcl-2 and Bax and further inhibited the activation of caspase-3 and apoptosis in HD11 cells. Additionally, IBV replication was decreased by blocking ROS accumulation. Pretreating HD11 cells with ammonium chloride (NH4Cl) prevented IBV from entering the cells and reduced the oxidative stress which IBV causes. The ability to accumulate ROS was also lost in UV-inactivated IBV. The IBV N protein induces cell apoptosis through the activation of ROS. These findings provide an explanation for the processes of IBV infection in immune cells by indicating that IBV-induced ROS generation triggers cell apoptosis in HD11 cells.
