LONDON – Six weeks on from the initial alert, “the window of opportunity” to control the COVID-19 epidemic is “narrowing,” according to the latest assessment from WHO Director General Tedros Adhanom Ghebreyesus.
SEATTLE – Tracing the family tree of COVID-19 through its evolving DNA sequence makes it possible to disprove many false claims circulating on social media about the novel coronavirus, and, in particular, that it was generated in a covert biological weapons program. “From everything I’ve looked at, there is zero evidence for genetic engineering; it looks like normal evolution,” said Trevor Bedford, a computational biologist at Fred Hutchinson Cancer Research Center, who has been using genomes sequences taken from patient samples to track the spread of the virus since Jan. 11.
The drug screens prompted by the SARS and MERS outbreaks have been useful for quickly identifying drug candidates. But in terms of their epidemiology, “SARS and MERS were different from this coronavirus,” Allison McGeer explained at a Feb. 3 webinar by Evercore ISI.
An international collaborative study led by geneticists at the Queensland Institute of Medical Research Berghofer Medical Research Institute (QIMR) in Brisbane, Australia, has used a multivariate approach to develop a polygenic risk score (PRS) for glaucoma.
A mitochondrial glutamine transporter variant is a key regulator of glutamine metabolism and metabolic reprogramming in cancer cells, and targeting such transporters could be a new strategy for controlling tumor growth.
A reference genome from the Indian cobra compiled in an international collaborative study should lead to the development of new safer and more effective antivenoms, while the elucidated genome and predicted associated proteome may be a powerful platform for studies of venomous snakes.
A Chinese study has established a previously unknown direct mechanistic link between elevated mechanical tension caused by impaired alveolar regeneration and progressive idiopathic pulmonary fibrosis (IPF), highlighting a pathogenic mechanism that may underlie fibrosis.
Targeting prostate cancer (PCa) neuroendocrine (NE) cells via inhibition of the C-X-C motif chemokine receptor 2 (CXCR2) is an androgen receptor (AR)-independent therapeutic strategy that can improve the efficacy of treatment for PCa, a leading cause of male cancer mortality.