For practitioners of Traditional East Asian Medicine (TEAM), the idea that an illness can become dormant without being entirely gone is not particularly foreign.
TEAM has long described patterns in which a pathogenic process appears to retreat from the surface yet remains hidden within the body, capable of resurfacing when circumstances change. One concept used to describe this phenomenon is latent heat—the idea that something can remain relatively quiet beneath the surface and later re-emerge when the body's regulatory capacity is challenged.
Modern virology, of course, uses very different language.
Viruses such as Epstein–Barr virus (EBV), cytomegalovirus (CMV), and herpes simplex virus type 1 (HSV-1) can establish lifelong infections. Following the initial infection, these viruses may enter states of latency or persistence in particular tissues and cell populations. They may remain clinically silent for years, but physiological stress, illness, sleep deprivation, surgery, hormonal changes, or alterations in immune surveillance can create circumstances in which viral activity re-emerges.
For many practitioners working in integrative and TEAM, that general idea will sound very familiar.
What makes a newly published 2026 Nature study particularly interesting is the scale and sophistication with which researchers were able to observe this phenomenon during COVID-19.
COVID May Be More Than a Single-Virus Event
The study examined 1,154 people hospitalized with COVID-19 across 20 U.S. hospitals. Rather than looking only at SARS-CoV-2, researchers asked a much broader question:
What happens to the other viruses already living within us when the body is confronted with a major infection?
Participants were followed during hospitalization and for as long as 12 months afterward. Researchers analyzed peripheral blood mononuclear cells, nasal swabs and, in mechanically ventilated patients, endotracheal aspirates. They combined viral RNA sequencing with immune-cell profiling, cytokines, antibodies, proteomics and metabolomics.
What they found was striking.
Nearly 48% of participants had evidence of reactivation of at least one chronic virus during acute COVID-19. The researchers detected activity from several members of the herpesvirus family—including EBV, CMV and HSV-1—as well as viruses from the Anelloviridae family.
And these viruses did not all wake up at the same time.
Different Viruses Reactivated at Different Stages
One of the most fascinating findings was the temporal pattern.
EBV tended to reactivate early. Approximately 24% of participants had detectable EBV transcripts near the time of hospital admission, during days 1–8.
HSV-1 and CMV tended to emerge later. HSV-1 detection peaked later in the disease course, as did CMV activity in blood cells.
This matters because the researchers weren't simply measuring whether someone had antibodies indicating that they had encountered EBV sometime in their life.
They were detecting viral transcripts—evidence of transcriptionally active virus.
That distinction strengthens this study considerably. Previous studies of viral reactivation during COVID have often relied heavily on antibody responses. Here, RNA sequencing allowed researchers to look for evidence that these normally quiet viruses were actively expressing their genomes.
Additional findings reinforced that interpretation. Participants with EBV transcripts had persistently elevated EBV IgG and IgA antibodies, while HSV-1 proteins were more frequently detected in the plasma of people who also had HSV-1 transcripts.
In other words, SARS-CoV-2 wasn't necessarily acting alone.
The immune system was dealing with a changing virological landscape.
Reactivation Was Associated With Inflammation and More Severe Disease
The researchers also found that reactivation wasn't biologically silent.
EBV, CMV and HSV-1 reactivation were associated with distinct changes in inflammatory signaling. Depending upon the virus and the tissue being examined, these included alterations in IL-6, IL-18, IFN-γ, TNF, CXCL9, CXCL10, CXCL11 and other cytokines and chemokines.
Viral reactivation was also associated with COVID-19 severity and a number of clinical complications.
Importantly, however, this was an observational study. The findings do not establish that viral reactivation caused the worse outcomes. Severe illness could facilitate viral reactivation; viral reactivation could potentially amplify aspects of the inflammatory response; or both processes could occur together.
That distinction is important clinically.
But another finding challenges a common assumption about viral reactivation.
You Don't Have to Be Immunosuppressed for a Dormant Virus to Reactivate
We often associate reactivation of latent viruses with people who are profoundly immunocompromised—transplant recipients, chemotherapy patients or people taking immunosuppressive medications.
That is clearly part of the story, but it isn't the entire story.
The researchers found that chronic viral reactivation occurred frequently in immunocompetent individuals experiencing severe illness and was associated with increased systemic inflammation.
For TEAM practitioners, this may be one of the most interesting findings in the entire paper.
It shifts the conversation away from a simplistic model of:
strong immune system = virus suppressed
weak immune system = virus activated
The actual biology appears considerably more dynamic.
Severe physiological stress can alter immune regulation, inflammatory signaling, cellular metabolism and antiviral surveillance in ways that allow previously controlled viruses to become active again.
A Modern Parallel to the Idea of Latent Heat?
This is where TEAM offers an interesting conceptual lens.
We should be careful not to retrofit a traditional medical theory directly onto modern virology. Latent heat is not another name for EBV, and this study does not validate the traditional TEAM theory of latent pathogens.
But there is a compelling conceptual parallel.
TEAM recognized centuries ago that the clinical story of an illness does not necessarily end simply because the original acute symptoms disappear. Something may remain relatively quiescent and later become clinically relevant when the internal environment changes.
Modern infectious disease now gives us a very concrete example of how something resembling that pattern can occur.
EBV is extraordinarily common. CMV is common. HSV-1 is common. After infection, these viruses do not simply disappear from the human body. They persist, typically under immune control.
Then another physiological stressor arrives.
In this study, that stressor was SARS-CoV-2.
And suddenly the biological terrain changed.
That makes the traditional idea of looking beyond the immediate pathogen particularly interesting. The person in front of us may be experiencing the downstream consequences of an interaction between the new illness, previously acquired infections, immune regulation and the inflammatory response.
That is a much more complex model than “COVID infection → COVID symptoms.”
And Then There Is Long COVID
Perhaps most relevant to clinicians treating patients months after infection, the investigators found evidence that viral activity did not necessarily end when acute COVID ended.
They observed viral reactivation during convalescence and investigated whether it was associated with long-COVID symptom patterns.
Interestingly, acute EBV, CMV or HSV-1 reactivation did not significantly predict the study's later patient-reported outcome groups. That is an important nuance.
The strongest long-COVID signal in this particular dataset instead involved Anelloviridae, a less familiar family of persistent viruses. Anellovirus transcripts during convalescence were significantly more prevalent among participants in the physical-deficit group, even after adjustment for age, sex, immunosuppressive medications and severity of the original COVID infection. The authors suggest this could potentially become a biological signature associated with persistent physical disability, although considerably more research is needed.
That prevents us from making the overly broad claim that “EBV reactivation causes long COVID.”
This paper does not demonstrate that.
What it does demonstrate is arguably more interesting:
COVID can disturb the equilibrium between the human immune system and the collection of chronic viruses already residing within the body.
What This Means for TEAM Practitioners
For practitioners who have spent years thinking about latent pathogens, constitutional vulnerability and why one illness sometimes seems to awaken an entirely different pattern of symptoms, this research may feel validating.
Not because Western medicine has finally “proven latent heat.”
Rather, modern immunology is increasingly demonstrating something that holistic systems of medicine have long encouraged clinicians to consider:
The illness that precipitated a patient's symptoms may not be the only biological process occurring in that patient.
The human body is not sterile between infections. People may carry multiple chronically infecting viruses at any given time, generally without infectious symptoms. Under the right circumstances, some of those viruses can become biologically active again.
This raises fascinating questions for practitioners of acupuncture and Chinese herbal medicine.
When a patient tells us, “I haven't been the same since COVID,” what exactly changed?
Is the immune system still responding to SARS-CoV-2?
Did the infection alter autonomic or inflammatory regulation?
Did it disrupt the body's previous control over another chronic infection?
Could several of these mechanisms be occurring simultaneously?
Those are no longer questions confined to the margins of integrative medicine. They are questions being investigated using transcriptomics, proteomics, metabolomics and immune profiling.
And that is precisely why this new paper deserves our attention.
Clinical Pearl
When taking the history of a patient with persistent symptoms following COVID-19, consider asking not only about the acute infection but also about previous infectious history and symptoms that appeared to “return” after COVID.
That history does not establish viral reactivation, and symptoms alone cannot tell us whether EBV, CMV or HSV-1 has reactivated. But it may reveal a much more informative timeline of how the patient's health changed following the infection.
For TEAM practitioners, it also provides an opportunity to do what our medicine has always encouraged us to do: look at the pattern that preceded the illness, the event that disrupted it, and what emerged afterward.