Long COVID and chronic fatigue may share features in common

Embargoed until: Publicly released: 2025-07-09 16:46

International

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US scientists looked at the characteristics of peripheral blood lymphocytes - immune cells circulating in the blood - of 27 people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), 20 with long COVID, and 25 with neither condition. They found higher levels of oxidative stress (which damages cells) in the people with ME/CFS and long COVID than in healthy people’s cells. They also found that women with ME/CFS were less able than healthy women to clear damaging substances called reactive oxygen species from their cells. Although this was not the case among men, those with ME/CFS had other signs of cell damage which were not seen in their healthy counterparts. The findings suggest there are similarities between ME/CFS and long COVID, the authors say.

Media release

From: AAAS

Shared underpinnings of ME/CFS and Long COVID

Researchers analyzed peripheral blood lymphocytes in 27 individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), 20 individuals with Long COVID, and 25 healthy individuals to compare the cells’ bioenergetic characteristics. The analysis revealed similarly elevated signs of oxidative stress in the lymphocytes—particularly in the memory cell subset—from people with ME/CFS and Long COVID, compared with healthy individuals. The authors also found sex-specific changes in pathways involved in clearing reactive oxygen species (ROS). Women with ME/CFS exhibited higher total ROS and mitochondrial calcium levels, but men with ME/CFS had normal ROS levels but other signs of oxidative stress. Further, high ROS levels were tied to increased proliferation of T cells in women. The findings suggest common mechanistic underpinnings of ME/CFS and Long COVID as well as the potential for the development of diagnostic tests and tailored treatments, according to the authors.

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Research PNAS, Web page

Journal/
conference: PNAS

Research:Paper

Organisation/s: Stanford University, USA

Funder: We are grateful for funding by the National Institute of Allergy and Infectious Diseases (U19-AI057229, 5R01AI139550) and the Howard Hughes Medical Institute to M.M.D., along with funding from the NIH to M.S. (5RM1HG00773510). We also acknowledge funding from the Khosla family gift fund.

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