To identify druggable targets for host-directed antiviral therapies, we mapped human proteins and signaling pathways hijacked and rewired by SARS-CoV-2. Inhibitors of mRNA translation, e.g. anti-cancer drugs, regulators of the Sigma1 and Sigma2 receptors, antipsychotics, as well as protein kinase inhibitors (p38, CK2, CDKs, AXL, and PIKFYVE), demonstrated antiviral activity, providing the opportunity of drug repurposing for the treatment of COVID-19.

Eliciting a potent long-lasting immune response (e.g. Ab, CD4, and CD8 T cells) against the SARS-CoV-2 virus with a vaccine will most likely be essential to reduce morbidity and mortality during future waves of viral propagation. To this end our lab has been working on a way to increase the potency of vaccines for 20 years through engagement of the TNF-receptor family member, OX40. This talk will cover the data generated over the last 20 years in vaccinated hosts boosted with OX40 agonists and present preliminary data in mice injected with a COVID-19 vaccine w/wo OX40 agonists.

Covid-19 has been declared a global pandemic by WHO. There are hundreds of active clinical programs focused on developing and repurposing therapeutic drugs for treatment of Covid-19. In this talk, we highlight how our cell-based assays are supporting these programs, particularly in managing proinflammatory cytokines associated with high mortality rate in Covid-19 patients.

Cytokine release syndrome (CRS) has been observed with infectious diseases like COVID-19.  JAX has developed a rapid, sensitive and reliable PBMC humanized mouse model for CRS that allows for the evaluation of therapeutics for screening of new drugs for CRS susceptibility and evaluation of new therapies capable of suppressing CRS.