How ME/CFS and Long COVID (PASC) Mimic Accelerated Aging
When you live with a postviral condition like myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or long COVID, it often feels like your body has aged overnight. Symptoms such as fatigue, muscle weakness, cognitive decline, and poor immune resilience are strikingly similar to what we see in advanced aging.
This isn’t just a metaphor. A growing body of research shows that certain viruses—including Epstein-Barr virus (EBV), cytomegalovirus (CMV), and SARS-CoV-2—can trigger biological changes that mirror the aging process (Proal & VanElzakker, 2025). This is why many researchers now refer to these illnesses as aging phenotypes: conditions in which the body behaves as though it is much older than it really is.
Understanding this link between viral infections and aging helps explain why symptoms persist for years and why treatments often need to target core aging mechanisms rather than just acute infection. It also lays the foundation for why nutrition strategies for these illnesses often borrow from the field of anti-aging science—a topic I’ll cover in an upcoming post.
💡 Looking for quick answers? Jump to the FAQ
An aging phenotype describes a condition in which the body expresses hallmark features of accelerated aging, even when the person is relatively young.
For people with ME/CFS and long COVID, this can include:
Persistent low-grade inflammation (inflammaging)
Immune system dysfunction (immunosenescence)
Declining mitochondrial energy production
Loss of muscle strength and endurance
Premature cellular aging, seen in telomere shortening
Research supports this connection. For instance, one study found that individuals with ME/CFS have premature telomere attrition, a marker of cellular aging, compared to healthy controls (Rajeevan et al., 2018). Another paper described the condition as having "old muscle in a young body," based on muscle biopsies showing similar patterns to those seen in elderly adults (Pietrangelo et al., 2018).
In long COVID, similar mechanisms have been observed. A 2024 review highlighted how COVID-19 infection may accelerate brain aging and hasten the decline of immune system function (Müller & Di Benedetto, 2024). Together, these findings suggest that postviral illnesses are not simply chronic infections—they represent a profound shift in how the body operates, much like fast-forwarding the biological clock.
Do Viruses Cause Accelerated Aging in ME/CFS and Long COVID (PASC)?
Viruses don’t just cause short-term illnesses like a cold or flu. Some can stay hidden in the body for years, quietly disrupting vital systems. Over time, this can make the body behave as if it’s aging faster than normal.
Many common pathogens—including herpesviruses like Epstein-Barr virus (EBV), SARS-CoV-2 (the virus that causes COVID-19), and even some bacteria and parasites—can persist long after the initial infection. These pathogens interfere with your body’s immune defenses, energy production, and even the way your genes work (Proal & VanElzakker, 2025).
This helps explain why conditions like ME/CFS and long COVID look and feel like accelerated aging, even in young or middle-aged people.
Cellular Senescence—Zombie Cells in ME/CFS and Long COVID
When a virus infects a cell, it can push that cell into a dysfunctional state known as cellular senescence. These "zombie cells" don’t divide or function normally, but they also refuse to die.
Instead, they release inflammatory signals that damage nearby tissues and keep the immune system on constant alert.
This same process drives natural aging and is a core feature of chronic postviral illness, especially ME/CFS and long COVID.
Over time, the buildup of these senescent cells contributes to fatigue, tissue damage, and slow recovery.
How Does Telomere Shortening Contribute to Premature Aging in ME/CFS?
Telomeres are protective caps at the ends of chromosomes that shorten each time a cell divides.
When telomeres become too short, the cell can no longer repair itself properly—a hallmark of cellular aging.
Viral infections can speed up this process, causing premature cellular aging.
Research shows that people with ME/CFS have significantly shortened telomeres, and this shortening is linked to disease severity (Rajeevan et al., 2018). This suggests their cells are biologically older than their actual age.
How Does Mitochondrial Dysfunction Drive Fatigue and Aging in ME/CFS and PASC?
Mitochondria are the energy factories of your cells, turning nutrients into the fuel your body needs.
Many viruses, including SARS-CoV-2 and herpesviruses, hijack mitochondria to survive and replicate.
This leaves the body with less energy for normal functions, a problem that shows up as chronic fatigue and post-exertional crashes—key symptoms of ME/CFS and long COVID.
Over time, this mitochondrial strain mirrors what happens naturally with aging, but the decline happens faster and more dramatically in postviral illnesses.
Inflammaging and Immunosenescence in Postviral Illness
When an infection never fully resolves, the immune system stays switched on, producing constant low-grade inflammation.
This process, called inflammaging, damages tissues and accelerates aging.
Eventually, the immune system becomes exhausted and less effective, a state known as immunosenescence (Müller & Di Benedetto, 2024).
This helps explain why many people with ME/CFS or long COVID:
Struggle to fight off new infections
Experience frequent viral reactivations (like EBV flare-ups)
Suffer ongoing flu-like symptoms
Muscle Aging in ME/CFS and Long COVID
Postviral illnesses don’t just affect energy production—they also cause structural changes in muscle tissue, making it behave like aged muscle even in younger patients.
In a landmark study, researchers examined muscle biopsies from ME/CFS patients and found features normally seen only in elderly adults (Pietrangelo et al., 2018):
Atrophy of muscle fibers, especially slow-twitch fibers
Loss of mitochondrial density within the muscle
Signs of oxidative stress and tissue damage
The researchers described this as having “old muscle in a young body.”
These changes are similar to sarcopenia, the age-related loss of muscle mass and function.
They help explain why people with ME/CFS or long COVID experience profound physical fatigue and very slow recovery after exertion.
Do ME/CFS and Long COVID Shorten Lifespan or Affect Long-Term Outlook?
When patients hear that ME/CFS and long COVID resemble accelerated aging, a natural question arises: Does this mean my life expectancy will be shorter?
Right now, we don’t have a clear answer. Research on mortality in ME/CFS is very limited, and studies have been small or inconsistent.
One study reported an average age of death of 55.9 years among a sample of ME/CFS patients (McManimen et al., 2016). However, it’s critical to interpret this finding with caution:
The sample size was small and may not represent the broader ME/CFS population.
Causes of death varied and included factors like suicide and cardiovascular disease, which may be influenced by poor medical care, stigma, or lack of support rather than the illness itself.
No study has definitively shown that ME/CFS or long COVID directly shortens lifespan.
Bottom line: At this time, no firm conclusions can be drawn about whether these conditions reduce life expectancy.
Why Does It Matter That ME/CFS and Long COVID Resemble Aging Phenotypes?
Even without clear data on lifespan, viewing ME/CFS and long COVID as aging phenotypes is still incredibly useful. It shifts the focus toward supporting the body systems that are most affected:
Reducing chronic inflammation
Supporting mitochondrial health and energy production
Improving immune system resilience
Preserving muscle strength and mobility
These are the same areas targeted in longevity research, which means strategies developed for healthy aging may also benefit people with postviral conditions.
In the next post, we’ll explore how this understanding guides nutrition and lifestyle strategies—practical tools you can use to support your health and potentially slow some of these aging-like processes.
FAQ: ME/CFS, Long COVID (PASC), and Accelerated Aging
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Yes. Research shows that people with ME/CFS and long COVID (also called Post-Acute Sequelae of COVID, or PASC) display biological changes such as telomere shortening, chronic inflammation, and mitochondrial dysfunction. These changes mirror hallmarks of accelerated aging, even in younger patients.
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An aging phenotype is when the body shows features of advanced aging—like fatigue, immune dysfunction, and muscle loss—despite the person’s chronological age. ME/CFS and PASC are considered aging phenotypes because their symptoms overlap with those seen in older adults.
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Current research is inconclusive. Some small studies suggest a lower average age of death in ME/CFS patients, but these findings are limited and may be influenced by poor medical care, stigma, and lack of treatment rather than the illness itself. No definitive evidence shows reduced lifespan in ME/CFS or PASC.
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Certain viruses—including Epstein–Barr virus (EBV), cytomegalovirus (CMV), and SARS-CoV-2—can stay in the body long after the initial infection. They interfere with immunity, energy production, and DNA stability, which can drive cellular senescence, chronic inflammation, and other aging-like changes.
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Yes. While not a cure, strategies that support mitochondrial health, reduce chronic inflammation, and preserve muscle mass may help. These overlap with many approaches studied in longevity research. Nutrition and lifestyle can play a meaningful role in managing postviral illness.
References
Müller L, Di Benedetto S. The impact of COVID-19 on accelerating of immunosenescence and brain aging. Front Cell Neurosci. 2024;18:1471192. Published 2024 Dec 10. doi:10.3389/fncel.2024.1471192
Proal AD, VanElzakker MB. Pathogens accelerate features of human aging: A review of molecular mechanisms. Ageing Res Rev. Published online August 7, 2025. doi:10.1016/j.arr.2025.102865
Rajeevan MS, Murray J, Oakley L, Lin JS, Unger ER. Association of chronic fatigue syndrome with premature telomere attrition. J Transl Med. 2018;16(1):44. Published 2018 Feb 27. doi:10.1186/s12967-018-1414-x
Pietrangelo T, Fulle S, Coscia F, Gigliotti PV, Fanò-Illic G. Old muscle in young body: an aphorism describing the Chronic Fatigue Syndrome. Eur J Transl Myol. 2018;28(3):7688. Published 2018 Sep 7. doi:10.4081/ejtm.2018.7688
McManimen SL, Devendorf AR, Brown AA, Moore BC, Moore JH, Jason LA. Mortality in Patients with Myalgic Encephalomyelitis and Chronic Fatigue Syndrome. Fatigue. 2016;4(4):195-207. doi:10.1080/21641846.2016.1236588
