With the recent global pandemic of COVID-19, also known as the coronavirus, many researches have been done in an attempt to understand its underlying structure in hopes of leading to prevention. Right now, researchers are hoping its genetic similarity to the previously identified SARS and MERS viruses could provide a breakthrough.
The viral strain that caused the outbreak has been named SARS-CoV-2 (Severe Acute Respiratory Syndrome coronavirus - 2), named so because of the spiked peplomers that surround the capsid of the virion which resemble a solar corona. The virus is positive-sense and single-strand, and has been associated with a variety of respiratory illnesses since the discovery of its predecessors in the 1960s.
Right now there are several potential treatments proposed to counter COVID-19: the virus's entry point seems to rely on the presence of angiotensin-converting enzyme - 2 (ACE2) and its receptors. Past research has established the connection between ACE2 and SARS infections, and given the genetic similarity this could also apply to COVID-19. The research established the two retroviruses - Simian Immunodeficiency Virus (SIV) and murine leukemia virus - both pseudotyped with SARS-CoV spike (S) proteins, were able to infect cells stably expressing ACE2. (1) Considering ACE2's crucial role in the Renin-Angiotensin system, its importance in regulating vasoconstriction/vasodilation and blood pressure, it is very likely ACE2 is the future pathway to countering COVID-19, or at least minimizing the virus's damage to the lungs.
However, merely decreasing the level of ACE2 or creating more inhibitors may not effectively combat the disease. In fact, ACE2's role in upregulating production of angiotensin 1-7 and vasodilation has proven protective against COVID-19. And it's because of this that a drop in ACE2 production is observed as spike protein comes in contact.
Other treatment proposals involve an injection of soluble ACE2 into the bloodstream, making them competitive inhibitors to the virus and replenish damaged ACE2 inside infected cells. (2)
This raises future concern for treatment of diabetes and hypertension, since a co-morbidity link has been established between cardiovascular diseases and COVID-19. Treatments typically involve ACE inhibitors and Angiotensin-Receptor Blockers (ARBs), which would lead to a decrease in ACE2 level and potentially magnify lung damage. (3)
More research are being done at the moment, and more than 30 vaccines are in development. In the meantime, focusing on the genetic similarity of COVID-19 to SARS, MERS, and other viral strains causing acute respiratory failure could help identify an antigen.