Yes, many characteristics of a child may be written into his or her DNA and specifically into protein-coding genes-the sequences of DNA code that dictate the shapes and functions of proteins, the work-horses of the cell. Of course, I understood that DNA is not destiny. At the time, the transfer of DNA from sperm or egg to an embryo was thought to be the only way that heritable information could flow from parents to children, at least in humans and other mammals. But every once in a while, as the theory goes, a variant gets lucky, infects a large number of people and launches a new whole stage of the pandemic.When my kids were born, about 30 years ago, I knew they had inherited about half their DNA from me. Most of these viral versions probably don't spread beyond the chronically infected patient. While inside one person, the virus can try out all these different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious. In other words, perhaps the coronavirus uses long-term infections as a mutational testing ground. "I think that's the leading theory," Luban says. That perhaps the new variants arose inside people similar to the man in Boston - that is, people who are immunocompromised and have long-term coronavirus infections. So scientists are starting to think the two phenomena could be related. And other cases have likely gone undetected, he says. "So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. Shots - Health News Is It Ever OK To Jump Ahead In The Vaccine Line? Scientists had never seen SARS-CoV-2, the coronavirus that causes the disease COVID-19, mutate so quickly during the whole pandemic. But rather, it acquired a whole cluster of more than 20 mutations. The virus wasn't picking up just one or two mutations at a time. The sequences showed Li and his team that the virus was changing very quickly inside the man's body. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important." Every few weeks, the team extracted coronavirus from the man's body and sequenced the virus's genome. Throughout the man's infection, Li and his colleagues ran an illuminating experiment. He passed away five months after the initial diagnosis. Eventually, he ended up in the intensive care unit. He would get better for a while, and then the virus would counterattack. So his body couldn't fight off the coronavirus infection as well as a healthy person could. This man had a severe autoimmune disease that required him to take drugs to suppress his immune system. "In fact, he was highly infectious even five months after the initial diagnosis." "That is one of the remarkable aspects of this case," Li says. The same infection lasted for five months. This man had living, growing virus in his body for five months, Li says. To be clear here, the man wasn't what doctors call a "long hauler," or a person who clears a coronavirus infection and then continues to have health problems for months. So extraordinary in fact that this man's case is offering scientists surprising clues about where the new coronavirus variants emerged and why they're causing explosive outbreaks on three continents. "So this is an extraordinary individual," Li says. "He was readmitted to the hospital several times over the subsequent five months for recurrence of his COVID-19 infection and severe pneumonia," says infectious disease doctor Jonathan Li at Harvard Medical School, who helped treat the man. Doctors treated him with steroids and discharged him five days later.īut the infection never went away - for 154 days. Mutations help the virus bind more tightly.īack in the spring of last year, a 45-year-old man went to the Brigham and Women's Hospital in Boston because of a coronavirus infection. To infect a cell, the virus's spike protein (red) has to bind to a receptor on the cell's surface (blue). An illustration of the variant found in the United Kingdom.
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