Photo/Illutration The novel coronavirus (Provided by the U.S. National Institute of Allergy and Infectious Diseases)

SUITA, Osaka Prefecture--The novel coronavirus at its onset triggers aging of cells in the human body, which would explain the lingering aftereffects of COVID-19, researchers here discovered.

A team headed by Eiji Hara, a professor of biology at Osaka University’s Research Institute for Microbial Diseases, confirmed through animal experiments that cells affected by COVID-19 help to spread inflammation.

As patients often complain of lethargy, headaches, loss of hair and other symptoms after the virus is gone, the team concluded that the inflammatory mechanism might be the reason.

The researchers have studied a process known as cellular senescence under which damaged cells stop proliferating simply as a survival mechanism, which in turn causes them to scatter around inflammatory substances.

The phenomenon is known to lead to cancer, arterial sclerosis and other disorders associated with advanced age.

Team members decided to examine the correlation between those aftereffects and cellular senescence following studies on the effects of inflammation on COVID-19 patients.

When the researchers infected cultured human cells with the novel coronavirus, they found that many of the infected cells died within a few days and the virus vanished.

At the same time, they discovered that infected cells release substances to accelerate cellular senescence before they die out. Surrounding cells that aged due to the substances survived and secreted inflammatory materials.

The team, using hamsters deliberately infected with the virus, also found that inflammation-triggering substances continued emanating from senescent cells in the lungs even after the virus had disappeared.

While the team confirmed that senescent cells in the lungs of severe COVID-19 patients continued to release inflammatory materials, the members also discovered that administering a drug to remove senescent cells in mice with the novel coronavirus succeeded in decreasing pulmonary inflammation.

Based on the results, the team concluded that infection entails aged cells and lasting inflammation, likely bringing about COVID-19 aftereffects among other causes.

Hara, however, noted it is too early to decide whether the mechanism should be targeted for treatment of new coronavirus patients.

“Senescent cells may have not only a negative impact but also some benefits, such as preventing infection,” he said. “It is not simply a matter that aged cells should be eradicated.”

The findings were published in the online edition of the British specialized journal Nature Aging at (https://www.nature.com/articles/s43587-022-00170-7).

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