Mannick has studied the effect of rapamycin-like drugs on Covid-19. Her trial took place in nursing homes where the disease had broken out. Half of the participants received the drug and the other half a placebo for four weeks. Among those given a placebo, “25% of them developed severe Covid-19 infection, and half of them died,” says Mannick, who has yet to publish the work. None of those taking the drug developed any Covid-19 symptoms.

“There are several strategies to help the aging immune system fight better against Covid,” she says. “Aging is the greatest risk factor for severe Covid and a modifiable risk factor.”

She hopes to expand use of her drug beyond Covid-19; A rejuvenated immune system could theoretically fight off many other viral and bacterial infections. Her colleague Stanley Perlman, a coronavirusologist at the University of Iowa who co-authored research on BioAge’s Covid drug in mice, has future pandemics in mind. “Next time there’s another coronavirus in 2030, maybe all this information will be very useful,” he says.

Out with the old man

The immune system isn’t the only target of anti-aging drugs. Others aim to eliminate aged cells. Most cells in our body divide up to a point. Once they reach that limit, they should die and be eliminated by the immune system. But this is not always the case – some cells remain. These cells stop dividing and some instead produce a toxic concoction of chemicals that trigger harmful inflammation in the environment and beyond.

Cells that do this are called “senescent” and accumulate in our organs as we age. They have been linked to an ever-increasing number of age-related diseases, including diabetes, heart disease, osteoporosis, cataracts, Alzheimer’s—the list goes on. They also seem to play an important role in coronavirus infections.

In yet-to-be-published research, James Kirkland, who studies aging and cellular senescence at the Mayo Clinic in Rochester, Minnesota, says he has evidence that the coronavirus infects senescent cells faster than non-senescent cells. His research also suggests that senescent cells release chemicals that cause neighboring non-senescent cells to pick up the virus as well, he says.

Not only do these cells take on more coronaviruses, but they appear to provide a breeding ground for new virus variants. “There is evidence that senescent cells infected with the coronavirus can mutate this virus,” says Kirkland. “So they can even be a cause of viral mutations.”

As an added concern, the coronavirus can age healthy cells. Given all of this, senescence has become an obvious target of both anti-aging and Covid-19 therapies. Studies in mice and hamsters suggest compounds that kill senescent cells may improve symptoms of Covid-19 and increase chances of survival.

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