Orchestrated efforts on host network hijacking: Processes governing virus replication

Abstract

With the high pervasiveness of viral diseases, the battle against viruses has never ceased. Here we discuss five cellular processes, namely "autophagy", "programmed cell death", "immune response", "cell cycle alteration", and "lipid metabolic reprogramming", that considerably guide viral replication after host infection in an orchestrated manner. On viral infection, "autophagy" and "programmed cell death" are two dynamically synchronized cell survival programs; "immune response" is a cell defense program typically suppressed by viruses; "cell cycle alteration" and "lipid metabolic reprogramming" are two altered cell housekeeping programs tunable in both directions. We emphasize on their functionalities in modulating viral replication, strategies viruses have evolved to tune these processes for their benefit, and how these processes orchestrate and govern cell fate upon viral infection. Understanding how viruses hijack host networks has both academic and industrial values in providing insights toward therapeutic strategy design for viral disease control, offering useful information in applications that aim to use viral vectors to improve human health such as gene therapy, and providing guidelines to maximize viral particle yield for improved vaccine production at a reduced cost. ARTICLE HISTORY

Host receptors: the key to establishing cells with broad viral tropism for vaccine production

“…Lastly, we would like to mention that establishing a cell line that can be infected by a broad range of viruses not only requires sufficient knowledge and good design of surface receptors, but also needs to ensure rapid virus replication so that they could effectively complete their life cycles in cells. The latter is not the topic of this review, but is addressed in another paper of us (Dai et al 2019).…”

Effective Immune Functions of Micronutrients against SARS-CoV-2

“…The host’s natural immune system recognizes viral components through pattern recognition receptors (PRRs) such as toll-like receptors (TLRs). Binding to TLRs induces the expression of inflammatory factors that can mediate lung inflammation and fibrosis [ 12 , 13 ].…”

Cold atmospheric plasma increases IBRV titer in MDBK cells by orchestrating the host cell network

“…Using infectious bovine rhinotrachieitis virus (IBRV) and Madin-Darby Bovine Kidney (MDBK) cells as the models of virus and host cell, respectively, we investigated how CAP modulates the host cell machinery toward orchestrated networking favorable for virus production. Following modulated events on viral infection as previously identified [ 6 ], we examined how CAP modulated calcium (Ca 2+ ) influx, autophagy, and immune response in addition to cell cycle to gain a full picture of CAP-triggered cell network alteration*. Our study makes CAP a potential tool for rapid viral vaccine production and opens a novel research field for physical plasma application in medicine.…”

“…Low to medium doses of CAP could subject cells to programmed events such as cell cycle arrest, senescence, autophagy, apoptosis, and immunogenic cell death [ 3 ]. Of particular interest here is the possible trigger of cell cycle arrest by CAP that has been reported almost 10 years ago [ 5 ], as virus infection could alter cell cycle toward arrest at G 2 /M, G 1 /S and G 0 /G 1 phases to favor virus multiplication [ 6 ]. This makes CAP a possible tool to boost viral particle yield by setting cells at the basal metabolic level that maximizes cell resources for virus production.…”