by Denise Karounos
Late in 2019 a new disease emerged out of Wuhan, China, the novel coronavirus disease of 2019, or COVID-19. On March 11, 2020, it was declared a global pandemic by the World Health Organization (WHO)1, with case numbers growing exponentially. COVID-19 is also called 2019-nCoV and is a result of the severe acute respiratory syndrome-related coronavirus, SARS-CoV-2. SARS-CoV-2 is a beta coronavirus and coronaviruses are named for the crown-like spikes on the cell surface. These “spikes” are called spike proteins (S proteins) and enable them to gain entry into host cells. There several known coronaviruses, including some common colds, influenza, MERS, and SARS.
When a coronavirus like SARS-CoV-2 wants to gain entrance into a cell, it uses its S proteins like a key to fit into the angiotensin converting enzyme 2 (ACE2) receptor’s “lock”. Viruses do not need a perfect key, in fact, they only need a partial match to the lock to gain entrance. SARS-CoV-2 is dangerous because its “key” or spike proteins fit the receptor quite well, and are estimated at 10-20 times better fit, or affinity, than the previous SARS. This results in increased infections, transmissions, and symptoms, and it is imperative to prevent spread with social distancing. ACE2, an important player in the renin-angiotensin-aldosterone system, is a regulator of blood pressure and whose expression also limits lung injury. This site of viral entry it can potentially be more of an issue for individuals faced with ACE2 related illnesses. Some avenues of treatment include: vaccine generation, cell entry, targeting, antivirals, and more.2,3 References and sources are included below for additional reading. This is a time where we see how interconnected our lives are as we try to work, with appropriate social distancing, as a global community to eradicate this virus.
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- C. Liu, et al., ACS Central Science, Article ASAP (2020).
- M Hoffmann, et al., Cell, 181, 1 (2020).