Abstract

Late stage detection of COVID-19 disease pathogenesis induced by SARS-CoV-2 infection may prove to be fatal to the infected patients with the severity increasing, if inhibition of differentiation of hematopoietic endothelial progenitor cells, or their sustained deficiency, is not reversed. Antiviral drug treatments of such individuals need not necessarily resuscitate from a severe impairment of normal angiogenesis of the vascular endothelium. The virus targets the endothelial progenitor cells which co-express the hematopoietic stem cell marker CD34 and the angiotensin converting enzyme 2 (ACE2), latter being the host receptor for this pathogen. There is not an apparent segregation of CD34 and ACE2 antigens, strongly implicating inhibition of differentiation of virus infected progenitor cells. The embattled clinical condition of SARSCoV- 2 infected patients may well require a dual-mode endothelial progenitor cellular infusion and antiviral drug molecular therapies to stage a rapid clinical recovery. Umbilical cord blood derived CD34+ progenitor cells are the most optimal for rapid availability, harvesting and infusion into the severely ill infected patients, who are most likely to be non-responsive to solely antiviral drug treatments. This is about rapidly prepared allogeneic cell infusion therapy and not autologous cell transplantation which is impractical for these relatively acute and short-term conditions and treatments of SARS-CoV-2 infections. A combination progenitor cell and antiviral drug treatment is suggested for recovery and maintenance of normal angiogenesis of infected patients who may otherwise not survive. Hence the concept and its basis discussed needs to be urgently advanced to translation stage.

Keywords: SARS-CoV-2, CD34, CD133, endothelial progenitor cells, angiogenesis inhibition, transient treatment, progenitor cell therapy, neovascularization, thrombocytopenia, microRNA, iPSC, organoids