Enhancing virus multiplication could assist in the rapid production of vaccines against viral diseases. Cold atmospheric plasma (CAP), a physical approach relying on reactive oxygen species to achieve the desirable cellular outcome, was shown to be effective in enhancing virus propagation, where bovine rhinotrachieitis virus and Madin-Darby Bovine Kidney cells were used as the modeling virus and cell line, respectively. CAP was shown to create synergies with virus infection in arresting host cells at the G2/M stage, decreasing cell membrane potential, increasing intracellular calcium level, and inducing selective autophagy. In addition, CAP was demonstrated to suppress virus-triggered immunogenic signaling as evaluated by IRF7 expression. We presented evidences on CAP-triggered maximization of host resources toward virus multiplication that is advantageous for viral vaccine production, and opened a novel regime for applying CAP in the sector of medical care and health.

Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axes, and EGFR inhibitor could not reverse this process. Our results contribute to our understandings on the mechanism of CPV-induced host cellular response and can be used in the onco-therapeutic design utilizing CPV by preventing host cancer cells from entering cell cycle arrest.

Cell-based vaccine manufacturing is an important strategy for viral disease prevention. Cultivating cells in suspension could maximize the utility of large bioreactors for cost-effective and scaled up vaccine production, where adapting adherent cells to suspension culture is the bottleneck and key. Through whole transcriptome sequencing of suspension and adherent strains of BHK-21 and CHO-K1 cells followed by the identification of differentially expressed genes, mutational analysis, gene ontology, and pathway enrichment analysis, we identified four candidate genes, PABPC1, LARS, GLUL, PFN1, feasible for genetically modulating anchorage-dependent cells toward cell suspension culture, and experimentally validated the functionality of PABPC1 in both BHK-21 and CHO-K1 cells. Our study unveiled a novel role of PABPC1 that could potentially aid in the establishment of a cost-effective vaccine manufacturing platform relying on cell cultivation in suspension.