Researchers used sequencing data and phenotypic traits to predict which of 5,400 species were most likely to be susceptible to contracting and spreading the virus back to humans.

Genetically engineered cells that overproduce ACE2, the receptor the novel coronavirus uses to enter cells, neutralize infection in vitro and mop up inflammatory cytokines in mice.

While sick with COVID-19, President Trump is taking an antacid. Doctors have been exploring whether these medicines can treat SARS-CoV-2 infections, and the results are mixed.

Some critically endangered animals are on the list.

Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. Clinical trials of inhibitors are putting this hypothesis to the test.

The leaky blood vessels and lung fluid build-up in some COVID-19 patients might be explained by the virus’s corruption of an inflammation safeguard.

The results are a proof-of-concept that the novel coronavirus can replicate in neurons, but it’s too soon to say whether this occurs in people with COVID-19.

Eight amino acids are identical to part of the human epithelial sodium channel, leading researchers to suspect the virus might interfere with the channel’s function.

Analyses from single-cell sequencing datasets support the idea that COVID-19 is not just a respiratory disease but an illness that can affect multiple organs.

The virus’s tool for prying open host cells is coated in a protective armor of sugar—but gaps may offer vulnerability to disruption by antibodies.

Infected children may harbor SARS-CoV-2 while showing less-severe symptoms than adults. Their young immune systems, ACE2 receptor levels, and even exposure to other coronaviruses might play a role in their resilience.