Viral Reactivation Long COVID: Why EBV, Herpes and Shingles Can Return
Viral reactivation is increasingly recognised as one of the biological processes that may contribute to Long COVID. Researchers are investigating whether dormant viruses such as Epstein-Barr virus (EBV), herpes simplex virus (HSV) and varicella-zoster virus (VZV) can reactivate after COVID-19 and whether this contributes to persistent symptoms such as fatigue, brain fog and post-exertional malaise.Yes. Research increasingly suggests that dormant viruses such as Epstein-Barr virus (EBV), herpes simplex virus (HSV) and varicella-zoster virus (VZV) can reactivate after COVID-19, particularly in people living with Long COVID.
COVID appears to disrupt the immune system in ways that reduce its ability to keep these latent viruses under control. Changes in T cells, natural killer (NK) cells, inflammation and immune signalling may allow viruses that have been dormant for years to become active again.
Not everyone with Long COVID experiences viral reactivation, and scientists are still investigating whether it is a cause of persistent symptoms, a consequence of immune dysfunction, or both. However, viral reactivation is now considered one of the leading biological mechanisms being investigated in Long COVID research.
Before COVID you might have had one cold sore a year, if that. Now they appear whenever you push too hard, whenever you hit a bad week, whenever your body has had enough of something. Or perhaps you developed shingles months after your infection, at 38, when you thought shingles was something that happened to other people’s grandparents. Or you feel an exhaustion so heavy and so specific, like having glandular fever again, that you have started wondering whether that is exactly what is happening.
You might be right. And there is a growing body of research explaining why.
What viral reactivation actually is
Your body is carrying more viruses than you probably want to think about right now. Most of them are doing absolutely nothing. They moved in during childhood or early adulthood, your immune system contained them, and they have been quietly dormant ever since, checked in but not causing trouble.
The Epstein Barr virus (EBV), which causes glandular fever, infects over 90 percent of adults worldwide and then hides inside certain immune cells for the rest of your life. Herpes simplex virus 1, which causes cold sores, takes up residence in nerve cells near your lips and stays there indefinitely. Varicella zoster, the chickenpox virus, retreats into nerve tissue and can re emerge decades later as shingles. None of this is unusual. It is how herpesviruses work.
What keeps them dormant is immune surveillance, particularly T cells and natural killer cells that constantly patrol for viral activity. When that surveillance is disrupted, dormant viruses can reactivate. Not as a new infection. As a flare of something already present.
COVID as a reactivation trigger
COVID is an unusually effective disruptor of this immune balance.
A study published in Pathogens found that 66.7 percent of Long COVID patients showed evidence of EBV reactivation, compared with just 10 percent of people who had recovered from COVID without persistent symptoms, as documented in this study on EBV reactivation in Long COVID. That is not a subtle signal. A December 2025 review described this through the concept of immunity theft, where acute SARS CoV 2 infection undermines the immune control of other latent infections, as covered in this overview of viral suspects fuelling Long COVID.
The mechanism makes biological sense. COVID causes significant T cell exhaustion, disrupts natural killer cell activity, drives systemic inflammation and, in Long COVID, appears to leave the immune system in a state of ongoing imbalance. The viruses that were being quietly managed suddenly have less oversight. Some take the opportunity.
Reactivation of multiple human herpesviruses has been documented in critically ill COVID patients, and herpesvirus dysregulation is now considered a suspected contributor to Long COVID pathogenesis, where this reactivation triggers immune dysregulation that could itself cause or perpetuate symptoms, as discussed in this overview of herpesvirus dysregulation in Long COVID from the Bateman Horne Center.
Which Viruses Can Reactivate After COVID?
Several dormant viruses have been reported to reactivate after COVID-19. While the strongest evidence currently exists for Epstein-Barr virus (EBV), researchers are also investigating other members of the herpesvirus family.
| Virus | Common illness | Possible signs of reactivation |
|---|---|---|
| Epstein-Barr virus (EBV) | Glandular fever (infectious mononucleosis) | Profound fatigue, swollen lymph nodes, sore throat, brain fog |
| Herpes simplex virus type 1 (HSV-1) | Cold sores | More frequent or severe cold sores |
| Herpes simplex virus type 2 (HSV-2) | Genital herpes | Recurrent genital outbreaks |
| Varicella-zoster virus (VZV) | Chickenpox and shingles | Painful shingles rash |
| Human herpesvirus 6 (HHV-6) | Roseola in childhood | Possible fatigue and neurological symptoms (research ongoing) |
| Cytomegalovirus (CMV) | Usually mild or silent infection | Occasionally linked with immune dysfunction in Long COVID research |
Not every virus has the same level of evidence. EBV currently has the strongest association with Long COVID, while research into other herpesviruses continues to evolve.
What this can feel like day to day
EBV reactivation is the one that catches people most off guard, because it often has no visible sign. No rash. No sore. Just a fatigue that is qualitatively different from ordinary tiredness. The glandular fever fatigue you recognise from years ago, or a new version of it you have never experienced before. Swollen lymph nodes, particularly in the neck. A sore throat that comes and goes. A cognitive heaviness that is worse than your usual brain fog. A sense of being actively unwell rather than just depleted.
EBV reactivation has been specifically associated with neurological symptoms and cognitive dysfunction in Long COVID, and elevated EBV antibody levels have been linked to increased severity and number of symptoms.
Post exertional worsening is particularly relevant here. Overexertion is one of the most consistent triggers of viral reactivation, because pushing past your energy limits stresses the immune system in precisely the way that allows latent viruses more room. Many people describe a pattern where they had a good few days, did too much, and then hit a wall that felt specifically viral rather than just depleted. This may be exactly what is happening, and it is worth reading alongside our article on post exertional malaise if this pattern sounds familiar.
Herpes simplex reactivation, meaning cold sores or genital herpes outbreaks, is more straightforward to recognise because it is visible. Cold sores appearing more frequently than before COVID, triggered by fatigue, stress, exertion or illness rather than the occasional sunburn. In a well regulated immune system these are contained quickly. In an immune system under ongoing strain, they can appear more easily and heal more slowly.
Shingles is varicella zoster reactivating along a nerve pathway. It is painful, often described as burning or stabbing along one side of the torso, face or limbs, and is accompanied by a distinctive blistering rash. It is more common in people over 50 or those with compromised immunity. Its appearance in younger people after COVID is one of the cleaner signals that immune disruption is genuinely happening.
The question everyone actually wants answered: am I contagious?
This is the worry that sits underneath everything else, particularly for people with children, elderly relatives, or colleagues they see daily.
For EBV reactivation, the honest answer is that in most everyday situations, no, you are not meaningfully contagious. EBV spreads through saliva, which is why glandular fever is sometimes called the kissing disease. During reactivation, viral levels in saliva are usually far lower than during primary infection. Talking to someone, being in the same room, sharing a sofa, or handling the same objects does not meaningfully transmit EBV in reactivation. Avoiding sharing drinks, cutlery or kissing directly during periods of active symptoms is a reasonable and sufficient precaution.
For herpes simplex, the rules are clearer and more important. The virus is contagious when a cold sore or lesion is visible, and also during the prodrome phase, the tingling or itching that arrives before a blister appears. Reactivated virus switches from latent to active replication and travels along nerve pathways to skin cells, where it can either cause a visible lesion or shed without obvious symptoms, as described in this review of HSV and other herpesviruses reactivating after COVID. Outside of active outbreaks, risk is low though not zero, since asymptomatic shedding can occasionally occur. This is worth being straightforward about with close contacts.
Shingles cannot be spread as shingles to another person. Someone who has never had chickenpox or been vaccinated could, theoretically, contract chickenpox from direct contact with an open shingles blister, but this requires contact with the actual fluid in the blister, not casual proximity. Keeping the rash covered until it has crusted over is the standard and effective precaution.
Does Viral Reactivation Cause Long COVID or Result From It?
This is one of the biggest unanswered questions in Long COVID research.
Scientists currently have three main theories.
The first is that viral reactivation contributes directly to Long COVID symptoms. Reactivated viruses may increase inflammation, stimulate the immune system and worsen fatigue, brain fog and neurological symptoms.
The second is that viral reactivation is a consequence of Long COVID. In this theory, COVID disrupts normal immune surveillance, allowing dormant viruses to become active without being the primary cause of the illness.
The third—and increasingly favoured—possibility is that both processes occur together. SARS-CoV-2 may trigger immune dysregulation, leading to viral reactivation, which then further amplifies inflammation and prolongs symptoms.
Current evidence cannot yet prove which explanation is correct, but it is likely that viral reactivation forms one piece of a much larger biological puzzle rather than being the sole explanation for Long COVID.
Why Doesn’t Everyone With Long COVID Experience Viral Reactivation?
One of the most important questions is why viral reactivation affects some people but not others.
Researchers believe several factors may influence this, including:
- Differences in the way each person’s immune system responds to COVID.
- Previous exposure to viruses such as EBV or HSV.
- Genetic factors affecting immune regulation.
- The severity of the original COVID infection.
- Existing autoimmune or inflammatory conditions.
- Physical and psychological stress during recovery.
This variability is one reason why Long COVID looks so different from one person to another. Two people may have very similar symptoms while the biological mechanisms driving those symptoms are not exactly the same.
Rather than thinking of viral reactivation as something that happens to everyone with Long COVID, it is better understood as one of several overlapping processes that may contribute to persistent illness.
Reading your blood tests
If your doctor has run EBV or herpes antibody tests, the results can be confusing.
IgG antibodies reflect past exposure. Almost everyone who has had EBV will have positive IgG for life. A positive EBV IgG on its own tells you that you have had EBV, not that anything is currently active.
IgM antibodies are the ones that rise during recent or reactivated infection. A positive EBV IgM suggests recent activity, though in Long COVID and post viral states, IgM patterns can be complex. Results need to be interpreted alongside your actual symptoms and clinical context, not treated as a verdict in isolation.
EBV early antigen, specifically the EA D IgG, is a more specific marker of reactivation and the one used in several of the key Long COVID studies. If this is elevated alongside symptoms, it carries more weight as evidence of active reactivation than standard IgM alone.
What actually helps
There is no established antiviral treatment protocol for EBV reactivation in Long COVID. Antivirals such as valacyclovir and acyclovir are effective for herpes simplex and shingles, reducing duration and severity when started early. Their role in EBV is less clear and most of the case evidence comes from individual clinical decisions rather than large trials. This is an area where research is genuinely still developing.
For herpes simplex, starting antivirals at the first sign of prodrome, before the blister appears, makes a meaningful difference to how severe and prolonged the outbreak is. If you are having frequent cold sores since COVID, it is worth discussing suppressive therapy with your GP, meaning a daily low dose antiviral to reduce reactivation frequency overall.
For all viral reactivation, the most consistent and most evidence grounded approach is treating it as a signal rather than a separate problem. Your immune system is under strain. The reactivation is the visible sign of that strain. The management that matters most is the same management that helps Long COVID overall: rigorous pacing to avoid the post exertional crashes that stress immunity further, sleep prioritised as genuinely non negotiable, and reducing additional immune demands where possible.
Supplements such as lysine are sometimes used for herpes management, with mixed evidence, and monolaurin has been studied in laboratory settings without convincing human trial data. Neither should be treated as a substitute for medical advice, and both are worth discussing with a clinician if you are considering them alongside prescribed treatment.
This is not failing. It is information.
Finding cold sores appearing more often, or recognising the fatigue of EBV reactivation, or working out that the shingles in your thirties was not a coincidence, can feel like things are getting worse. Sometimes they are. But these are also diagnostic signals with a biological logic behind them.
Viral reactivation tells you something specific about where your immune system is and what it is managing. That information is more useful than alarming. It points toward what needs support and confirms that what you are experiencing is physiological rather than imagined.
The research connecting viral reactivation to Long COVID symptom patterns is still developing. But the direction is consistent: this is a real mechanism, it affects a significant proportion of people with Long COVID, and it deserves to be taken seriously rather than dismissed as incidental.
Common Questions About EBV, Herpes and Long COVID
Can COVID reactivate Epstein-Barr virus (EBV)?
Yes. Research increasingly suggests that COVID-19 can disrupt the immune system in ways that allow dormant viruses such as Epstein-Barr virus (EBV) to reactivate. Several studies have found evidence of recent EBV reactivation in a significant proportion of people with Long COVID, although researchers are still investigating whether this directly causes symptoms or contributes to ongoing illness.
What are the symptoms of EBV reactivation in Long COVID?
EBV reactivation may cause profound fatigue, swollen lymph nodes, recurrent sore throat, brain fog, poor concentration, muscle aches and a general feeling of being unwell. Many people describe the symptoms as feeling similar to glandular fever (infectious mononucleosis). However, these symptoms can overlap with Long COVID itself, so blood tests and clinical assessment are important.
Why do I keep getting cold sores after COVID?
Cold sores are caused by herpes simplex virus (HSV), which remains dormant in nerve cells after the initial infection. COVID can temporarily weaken immune surveillance, making HSV more likely to reactivate. Many people with Long COVID notice that cold sores occur more frequently after physical overexertion, poor sleep, emotional stress or post-exertional malaise.
Can COVID cause shingles, even in younger adults?
Yes. Shingles occurs when the varicella-zoster virus (the virus that causes chickenpox) reactivates. Although shingles is more common in older adults, studies and case reports have described shingles developing in younger people after COVID-19, probably because of temporary immune dysregulation.
Does viral reactivation cause Long COVID?
Scientists do not yet know for certain. Current evidence suggests viral reactivation may contribute to Long COVID in some people by increasing immune activation and inflammation. It is also possible that viral reactivation is a consequence of Long COVID rather than the original cause. Many researchers believe both processes may occur together.
Can post-exertional malaise (PEM) trigger viral reactivation?
Possibly. Physical, cognitive and emotional overexertion place additional stress on the immune system. Researchers believe this may reduce the immune surveillance that normally keeps dormant viruses under control, making viral reactivation more likely in susceptible individuals. Although more research is needed, many people report that viral symptoms flare after episodes of post-exertional malaise.
What blood tests can show EBV reactivation?
Doctors may request an Epstein-Barr virus antibody panel, which can include EBV IgG, EBV IgM, Early Antigen (EA-D) and EBV Nuclear Antigen (EBNA). Positive IgG usually indicates past infection rather than active disease, while Early Antigen antibodies may provide stronger evidence of recent viral reactivation. Blood test results should always be interpreted alongside symptoms and medical history.
Does a positive EBV IgG mean my virus has reactivated?
No. A positive EBV IgG simply shows that you have been infected with Epstein-Barr virus in the past, which is true for around 90–95% of adults worldwide. On its own, IgG does not indicate active viral reactivation.
Am I contagious if Epstein-Barr virus or herpes reactivates?
Usually not in everyday situations. EBV reactivation rarely produces the same level of viral shedding seen during the initial infection. Cold sores caused by HSV are most contagious while blisters are present or during the tingling stage before they appear. Shingles can spread chickenpox not shingles to someone who has never had chickenpox through direct contact with the blister fluid.
Do antiviral medications help viral reactivation in Long COVID?
Antiviral medications such as aciclovir and valaciclovir are effective treatments for herpes simplex and shingles when started early. Their role in treating EBV reactivation during Long COVID is much less certain, and there is currently no established antiviral treatment protocol supported by large clinical trials. Treatment decisions should always be made with your healthcare professional.
Will viral reactivation stop as Long COVID improves?
For many people, yes. Viral reactivation appears to become less frequent as immune function stabilises and Long COVID symptoms gradually improve. Good sleep, careful pacing, avoiding repeated crashes and managing overall health may help reduce the likelihood of future viral reactivation, although recovery varies from person to person.
Is herpes contagious without visible sores?
Risk is substantially lower outside active outbreaks, but asymptomatic shedding can occur, meaning the virus can occasionally be present on the skin surface without visible signs. The highest risk period is when lesions are present, including during the prodrome tingling before a blister appears.
Should I isolate from family during viral reactivation?
or EBV reactivation with no lesions, normal family contact is generally fine with standard precautions around saliva sharing. For active herpes or shingles lesions, covering affected areas and avoiding direct skin contact is the relevant precaution. Full isolation is not necessary or recommended
Will viral reactivation keep happening?
Frequency tends to track with overall immune stability. As Long COVID improves and immune dysregulation settles, reactivation episodes often become less frequent. Consistent pacing, sleep and avoiding immune stressors are the most durable way to reduce their frequency.
Can my GP test for viral reactivation?
Yes. EBV antibody panels including IgM, IgG and early antigen can be requested. HSV antibody testing is also available. If you suspect viral reactivation is contributing to your symptom pattern, it is worth asking specifically for these rather than waiting for them to be offered routinely.
This article is for general information and education. It does not replace personalised medical advice. If you are experiencing frequent viral reactivation, worsening symptoms, or are unsure about your blood test results, please speak with your GP or a clinician familiar with Long COVID.
Sources and further reading
EBV reactivation in Long COVID patients, Pathogens 2021: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8233978/EBV reactivation review, Consensus Research Library 2025: https://topics.consensus.app/news/literature-review-indicates-recent-ebv-activity-in-two-thirds-of-long-covid-patients-evidence-review Herpesvirus dysregulation in Long COVID, Bateman Horne Center: https://batemanhornecenter.org/herpes-virus-dysregulation-in-long-covid/ COVID and vaccines as herpesviridae reactivation triggers, ScienceDirect 2023: https://www.sciencedirect.com/science/article/pii/S0365059623000235 Viral suspects fuelling Long COVID, ScienceDaily December 2025: https://www.sciencedaily.com/releases/2025/12/251214100911.htm
About Long Covid Journey
Long Covid Journey is an independent educational resource dedicated to explaining the science of Long COVID in clear, balanced and accessible language. Our articles combine peer-reviewed research with the lived experience of people affected by Long COVID, helping patients, families and healthcare professionals better understand this complex condition.
This article has been developed using published research on viral reactivation, Epstein-Barr virus (EBV), herpesviruses, immune dysregulation and Long COVID. Because this field is evolving rapidly, we distinguish between findings supported by multiple studies and areas where evidence is still emerging.
Our goal is to provide evidence-informed information—not certainty where none exists. We regularly review and update our content as new research becomes available, ensuring readers have access to the most current understanding of Long COVID and related conditions.
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