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.