Responses of Neural Cells (U87) to HCoV-229E and HCoV-OC43 Infections

Abstract

Respiratory viruses, such as Coronaviruses (CoVs), can be neuroinvasive and exacerbate neurological pathologies via their capacity for direct viral replication and/or by inducing excessive host immune responses in the Central Nervous System (CNS). HCoV-229E is a primary COVID-19 and HCoV-OC43 is a beta COVID-19 belonging to the same genus as SARS-CoV-2 and both can cause acute infections in glioblastoma, neuroblastoma, and germline cells. These viruses tend to exhibit different infectivity mechanisms and HCoV-OC43 tends to be more toxic than HCoV-229E for CNS cells. To gain an in-depth understanding of how respiratory viruses, such as SARS-CoV, infect nerve cells (U87) and promote inflammation and determine the different mechanisms underlying HCoV-229E and HCoV-OC43 infection, we evaluated Lactic Acid Dehydrogenase (LDH) activity, cell viability, and IL-8 absorptions. HCoV-OC43 tended to show greater cytotoxicity against U87 nerve cells than HCoV-229E. Further study into the connection between the HCoV-229E and HCoV-OC43 viruses and brain cell reactions will be supported by our results.