A profile of SARS-CoV-2, and other Coronaviruses.

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It was a family of dynamic killers: dog coronaviruses could harm cats, the cat coronavirus could ravage pig intestines. Researchers thought that coronaviruses caused only mild symptoms in humans, until the outbreak of severe acute respiratory syndrome (SARS) in 2003 revealed how easily these versatile viruses could kill people.
Coronaviruses are also one of the few RNA viruses with a genomic proofreading mechanism — which keeps the virus from accumulating mutations that could weaken it. That ability might be why common antivirals such as ribavirin, which can thwart viruses such as hepatitis C, have failed to subdue SARS-CoV-2. The drugs weaken viruses by inducing mutations.
SARS-CoV-2 is uniquely equipped for forcing entry into cells. Both SARS-CoV and SARS-CoV-2 bind with ACE2, but the receptor-binding domain of SARS-CoV-2 is a particularly snug fit. It is 10–20 times more likely to bind ACE2 than is SARS-CoV9. Wendtner says that SARS-CoV-2 is so good at infecting the upper respiratory tract that there might even be a second receptor that the virus could use to launch its attack.