There is little evidence that antihypertensive drugs worsen COVID-19, and scientists are instead exploring the idea that such medications—or their downstream effects—may actually alleviate symptoms.

The host transcriptional signature elicited by the coronavirus appears to be less robust and lacks the induction of key antiviral genes.

The symptoms suggest SARS-CoV-2 might infect neurons, raising questions about whether there could be effects on the brain that play a role in patients’ deaths, but the data are preliminary.

President Donald Trump has touted the drug as a treatment but scientists still don’t know for sure that it is effective in patients. A number of clinical trials aim to find out.

Rhesus macaques can be infected with SARS-CoV-2, leading primate center scientists to try to prevent outbreaks in their colonies, especially as experiments on coronavirus start.

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.

Preliminary modeling studies provide a shortlist of potential coronavirus intermediate host species.

A preprint indicates that coronavirus transmission from surfaces is possible, but does not provide evidence that this has occurred in the COVID-19 pandemic.

Emerging data as well as knowledge from the SARS and MERS coronavirus outbreaks yield some clues as to why SARS-CoV-2 affects some people worse than others.