The Improbability of the Rapid Development of a Vaccine for SARS-CoV-2 (Editorial)

Abstract

The coronavirus SARS-CoV-2 (Cov-2) has emerged on the world stage as a pandemic. It is a highly infectious agent that can spread rapidly and has a mortality rate of ∼2%–5%. Similar to its cousin, SARS-CoV-1 (Cov-1), CoV-2 employs the angiotensin converting enzyme 2 (ACE2) receptor and the serine protease TMPRSS2 to infect lung epithelial cells. CoV-2 also infects lung endothelial cells and macrophages and monocytes.1 Intriguingly, macrophages do not express appreciable levels of ACE2 or TMPRSS2,1 suggesting that this virus might use an entirely different receptor and a serine protease other than TMPRSS2 to infect these immune cells. An alternative, and possibly more likely explanation, based on a plethora of past studies with other coronaviruses, is that Cov-2 employs antibody-dependent enhancement (ADE) to infect immune cells.2