SARS-CoV-2 mutations similar to those in the B1.1.7 UK variant could arise in cases of chronic infection, where treatment over an extended period can provide the virus multiple opportunities to evolve, say scientists.

Writing in Nature, a team led by Cambridge researchers report how they were able to observe SARS-CoV-2 mutating in the case of an immunocompromised patient treated with convalescent plasma. In particular, they saw the emergence of a key mutation also seen in the new variant that led to the UK being forced once again into strict lockdown, though there is no suggestion that the variant originated from this patient.

Using a synthetic version of the virus Spike protein created in the lab, the team showed that specific changes to its genetic code — the mutation seen in the B1.1.7 variant — made the virus twice as infectious on cells as the more common strain.

Analysis reveals genetic control elements that are linked to hundreds of human traits.

Twenty years ago this month, the first draft of the human genome was publicly released. One of the major surprises that came from that project was the revelation that only 1.5 percent of the human genome consists of protein-coding genes.

Over the past two decades, it has become apparent that those noncoding stretches of DNA, originally thought to be “junk DNA,” play critical roles in development and gene regulation. In a new study published on February 32021, a team of researchers from MIT has published the most comprehensive map yet of this noncoding DNA.