Infectious bronchitis virus like QX strain transmission, pathogenesis, replication and host miRNA biogenesis pathway hijacking mechanism

Asad Khan^1*Iftikhar Ali Khan²Chao Huang¹Qihui Luo¹Abdul Qadeer³Lanlan Jia¹Mourad A. M. Aboul-Soud⁴Noorah A. Alkubaisi^4*Zhengli Chen^1*

• ¹Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Sichuan Agricultural University, College of Vterinary Medicine, China, Chengdu, China
• ²Shenzhen Key Laboratory of Marine Microbiome Engineering, Institute for Advanced Study, Shenzhen University, Shenzhen University Institute for Advanced Study, Shenzhen, China
• ³Department of Cell Biology, School of Life Science, Central South University, Central South University of Forestry and Technology School of Life Science and Technology, Changsha, China
• ⁴King Saud University College of Applied Medical Sciences, Riyadh, Saudi Arabia

The infectious bronchitis virus (IBV) is an acute, highly contagious, single-stranded RNA (ssRNA) gammacoronavirus, mainly transmitted to chickens through the intranasal route.Positive-sense ssRNA viruses primarily act on mRNA and enhance the replication of viral copies. We identified the nasal entry site of the IBV-QX strain and provided insights into the minimal viral replication in systemic organs. Here's an overview of its entry mechanisms and tropism in systemic organ tissues. It enters the host cells via spike proteins, which bind to highly expressed receptors in respiratory, renal, and gastric epithelial cells. Viral RNA primarily replicates in the host cell environment, where it is directly translated into viral proteins. The precise replication of the IBV-QX strain in gastric epithelial cells was previously unknown.The IBV-QX strain precise replication in gastric epithelial cells was unknown previously. Different IBV strains have varying tropism. For the first time, we revealed the key players involved in the microRNA (miRNA) biogenesis pathway by transfecting gastric cells with the IBV-QX strain. Our findings suggest that the QX strain may bind with to angiotensinconverting enzyme-2 (ACE2) receptors by circulating throughout the lymphatic system at the very least and influence the translation of argonaute2 (AGO2), dicer, exportin5 (XPO5), and drosha proteins. Taken together, QX viral proteins disrupt host miRNA biogenesis, leading to dysregulated immune and cellular responses that enhance viral replication and systemic spread, thereby enabling cross-organ tropism and multi-system pathogenesis.Consequently, QX inhibits the synthesis and translation of miRNA biogenesis components, resulting in highly replication.