If you've been diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), or you suspect you might have it, you already know the frustration of being told “your labs look fine” while you're barely able to get off the couch. You know the loneliness of an illness that most people can't see. And you may have wondered, more times than you can count: What is actually causing this?
As a functional medicine physician who has personally navigated the devastating terrain of chronic illness (including Crohn's disease and mold toxicity), I understand the profound and often isolating experience of being sick with something that conventional medicine doesn't fully understand or acknowledge. That's exactly why research like the landmark 2020 paper from Dr. Robert Naviaux at UC San Diego and Dr. Bhupesh Prusty in Germany fills me with such hope. Because now, for the first time, we have a compelling mechanistic explanation for what many of us have long suspected: a common, ubiquitous herpesvirus, Human Herpesvirus 6 (HHV-6), may be playing a central role in triggering and perpetuating ME/CFS through a cascade of mitochondrial damage and immune dysregulation.
Let's unpack what this means, what the science says, and, most importantly, what you can actually do about it.

What Is HHV-6, and Why Should You Care?
Human Herpesvirus 6 (HHV-6) is not some exotic pathogen. In fact, by the time you were three years old, there's a 90–100% chance you had already been infected with it. HHV-6 is the virus responsible for roseola, that common childhood illness with the high fever and distinctive pink rash. Like all herpesviruses (think EBV, CMV, HSV), HHV-6 never truly leaves the body. It integrates its DNA into your chromosomes and goes dormant, silently hitchhiking inside your cells for the rest of your life.
There are two variants: HHV-6A and HHV-6B. HHV-6B is the one that causes roseola in children. HHV-6A appears to have a stronger neurotropic (brain-seeking) profile and has been more consistently linked to neurological and autoimmune conditions, including ME/CFS, multiple sclerosis, and Hashimoto's thyroiditis. HHV-7, a close viral cousin, also plays a supporting role in this drama.
Here's the critical question: if nearly everyone carries HHV-6, why do only some people develop ME/CFS? The answer lies in what happens when this sleeping giant wakes up.
The Breakthrough Science: What Naviaux and Prusty Discovered
The 2020 paper published in ImmunoHorizons, titled “Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome,” is one of the most significant papers in ME/CFS research of the past decade. Here's what makes it so groundbreaking.
The Two-Edged Sword of HHV-6 Reactivation
The researchers showed that when HHV-6 reactivates, even partially in just a small number of cells, those cells begin secreting signals that trigger what Dr. Naviaux calls the Cell Danger Response (CDR). The CDR is an ancient, evolutionarily conserved survival mechanism. Think of it as your body's equivalent of declaring a state of emergency. When the CDR is activated, cells shift from “normal operations” into a defensive, hypometabolic lockdown.
On one level, this is brilliant biology. The study demonstrated that when ME/CFS patient serum was added to healthy cells in the laboratory, those cells became remarkably resistant (up to 99% protected) against both RNA viruses (influenza-A) and DNA viruses (HSV-1). This explains something that has long puzzled researchers and patients alike: many ME/CFS patients report dramatically fewer colds and other common infections after developing the illness. Their cells are in a constant state of antiviral alert.
But here is the devastating trade-off: this antiviral protection comes at the cost of your mitochondria.
What Happens to Your Mitochondria
Mitochondria are the powerhouses of your cells, generating the ATP (adenosine triphosphate) that fuels every function in your body, from thinking to moving to digesting food. When HHV-6 reactivates, the researchers found that mitochondria fragment, breaking apart from their normally elongated, networked form into fragmented, dysfunctional particles (the “M1” pro-inflammatory state).
This fragmentation has profound downstream consequences:
- ATP production crashes. Without intact mitochondrial networks, cells can't generate adequate energy. Even when glucose was replaced with galactose (which forces cells to rely entirely on mitochondrial respiration), ATP remained depleted, confirming this is a true mitochondrial failure, not a simple metabolic shift.
- Pyruvate dehydrogenase is suppressed. This critical enzyme converts pyruvate (from glucose) into the fuel your mitochondria need to run. Its suppression is also found in ME/CFS patients' muscle biopsies and blood samples, creating a kind of metabolic traffic jam at the cellular level.
- Superoxide dismutase 2 (SOD2) drops. SOD2 is your mitochondria's primary antioxidant enzyme. When it falls, reactive oxygen species (ROS) accumulate, generating the oxidative stress and “oxidative shielding” signature that has been documented in ME/CFS for decades.
- The effects are transmissible. Perhaps the most stunning finding: the researchers transferred cell culture supernatant from HHV-6-reactivated cells to healthy cells with NO viral DNA, and those healthy cells developed the same mitochondrial fragmentation and ATP depletion. When serum from ME/CFS patients (but not healthy controls) was added to healthy cells, the same thing happened. Something circulating in ME/CFS patients' blood, not the virus itself, is spreading this hypometabolic signal throughout the body.
As Dr. Naviaux himself stated: “Our results show that cellular bioenergetic fatigue and cellular defense are two sides to the same coin in ME/CFS. When energy is used for cellular defense, it is not available for normal cell functions like growth, repair, neuroendocrine and autonomic nervous system functions.”
This is the biological explanation for post-exertional malaise (PEM), the hallmark symptom of ME/CFS where any exertion causes a prolonged, sometimes devastating crash. The cells simply don't have the energy reserves to recover from normal activity.
Why Standard Testing Often Misses HHV-6
One of the most frustrating clinical realities in ME/CFS is that standard HHV-6 testing often comes back negative or “normal” even in severely ill patients. The Naviaux/Prusty study helps explain why. Their PCR testing of blood found HHV-6 DNA in only 16% of ME/CFS patients. But when they used a more sensitive technique, fluorescence in situ hybridization (FISH) to detect HHV-6 small noncoding RNA (sncRNA-U14) as a marker of viral reactivation, the positivity rate jumped to 40%.
This matters clinically. The virus doesn't need to be in full “productive” replication mode to cause damage. Even partial, incomplete reactivation (in which only a tiny fraction of cells produce a few viral RNA molecules, with no actual viral proteins being made) is enough to trigger the whole cascade. This is also why standard antiviral drugs that target the HHV-6 DNA polymerase (like ganciclovir and foscarnet) don't work well in some ME/CFS patients: there's no active polymerase to block.
What Testing to Consider
If you or your clinician wants to evaluate HHV-6's role in your illness, consider:
- HHV-6 IgG and IgM antibody titers. Elevated IgG (particularly greater than 4x normal range) can suggest reactivation, though high IgG is ubiquitous in the general population.
- HHV-6 PCR from blood (whole blood or PBMC). This can detect active viral DNA; a positive result is meaningful, but a negative does not rule out tissue-level reactivation.
- HHV-7 DNA testing. The Naviaux/Prusty study found HHV-7 DNA in 36% of ME/CFS patients; combined HHV-6/HHV-7 infection may be additive.
- Metabolomics testing. Naviaux's lab has demonstrated that ME/CFS has a reproducible chemical signature across 20 metabolic pathways; this is not yet commercially standard but represents a frontier of objective diagnosis.
- Functional mitochondrial testing. Organic acids testing and CoQ10 levels can help identify mitochondrial dysfunction.
The HHV-6 Foundation (hhv-6foundation.org) maintains an excellent clinician guide on testing options.
The Connection to the Cell Danger Response Theory
To truly understand ME/CFS through the lens of this research, we need to spend a moment with Dr. Naviaux's broader framework: the Cell Danger Response (CDR). Think of the CDR as your body's most fundamental survival instinct operating at the cellular level.
When a cell encounters a threat (a virus, a toxin, psychological trauma, or physical injury), mitochondria detect the danger first. They shift from energy production into defense mode, releasing a cascade of chemical signals (including extracellular ATP via purinergic signaling). This alarm system is supposed to be temporary: fight the threat, heal, and return to normal. But in ME/CFS, this healing cycle gets stuck. The CDR stays chronically activated long after the original trigger (HHV-6 reactivation, a bacterial infection, mold exposure, trauma) has passed.
This is why ME/CFS overlaps with so many other complex chronic conditions, including Long COVID, post-treatment Lyme disease syndrome, fibromyalgia, and mast cell activation syndrome (MCAS). They all represent variations of a stuck CDR, perpetuated by persistent low-level immune activation and mitochondrial dysfunction. It's also why a holistic, root-cause approach (not just chasing one virus with one drug) is so essential.
As I've explored in my previous articles on Long COVID and Chronic Fatigue and Post-Viral Chronic Fatigue, the pattern of viral infection triggering lasting immune dysregulation and energy depletion is one of the most important frontiers in modern medicine.
What Triggers HHV-6 Reactivation?
If HHV-6 is sleeping in most of us without causing problems, what wakes it up? Understanding the triggers is critical for both prevention and treatment:
- Physical or emotional stress. Elevated cortisol and stress hormones suppress immune surveillance, giving latent viruses an opening.
- Other infections. Co-infections can trigger immune dysregulation that provokes HHV-6 reactivation; COVID-19 in particular has been shown to reactivate multiple herpesviruses.
- Mold and mycotoxin exposure. Environmental triggers that activate the CDR can push cells with latent HHV-6 into reactivation, something I see regularly in my clinical practice with mold-ill patients.
- Heavy metal toxicity. Mercury and other metals impair immune function and mitochondrial integrity.
- Hormonal changes. Puberty, pregnancy, perimenopause, and thyroid dysfunction can all shift immune balance.
- Immune suppression. Any cause of lowered immune function creates conditions for reactivation.
- Sleep deprivation. Chronic poor sleep is both a trigger for and a consequence of viral reactivation.
- Overtraining or physical exhaustion. This is why pushing through ME/CFS symptoms almost always makes them worse.
Conventional Medical Treatments
It's important to understand what the current medical evidence supports, and where it falls short, so you can have an informed conversation with your healthcare provider.
Antivirals
Valganciclovir (Valcyte) is the most studied antiviral for HHV-6-associated ME/CFS. In a randomized, double-blind, placebo-controlled trial by Dr. Jose Montoya's group at Stanford, ME/CFS patients with elevated HHV-6 and EBV antibody titers who received 900 mg/day of valganciclovir for 6 months showed statistically significant improvements in mental fatigue, Fatigue Severity Scale scores, and cognitive function. They were 7.4 times more likely to be classified as responders compared to placebo. A retrospective study of 61 patients showed 52% responded, with 81% of responders showing cognitive improvement.
A 2022 comparative study found that artesunate (100 mg/day for 3 months), traditionally used as an antimalarial, may be more effective than valaciclovir or valganciclovir for chromosomally-integrated HHV-6, precisely because artesunate has an alternative mechanism of action that does not require the viral DNA polymerase to be active. This is significant given Naviaux and Prusty's finding that incomplete HHV-6 reactivation (without polymerase expression) is what drives ME/CFS in many patients.
Valaciclovir (Valtrex) and acyclovir have shown more modest benefit for HHV-6 specifically (they are better suited for HSV and some EBV-related conditions), though some clinicians use them as part of broader antiviral protocols.
Foscarnet is used in severe HHV-6 encephalitis cases, particularly in immunocompromised patients, but its toxicity profile limits use in ME/CFS.
Important caveat: Antiviral therapy is not appropriate for all ME/CFS patients. Work with a knowledgeable physician to evaluate your specific situation, test appropriately, and weigh risks versus benefits. These medications carry real side effects and require monitoring.
Low-Dose Naltrexone (LDN)
LDN (1.5–4.5 mg at bedtime) is increasingly recognized as an important tool in ME/CFS management. It modulates immune function, reduces neuroinflammation, and may help interrupt the abnormal microglial activation seen in ME/CFS. While not specifically anti-HHV-6, LDN targets the downstream neuroinflammatory consequences of persistent CDR activation.
Rintatolimod (Ampligen)
This immunomodulatory drug has FDA Breakthrough Therapy Designation for ME/CFS and works by enhancing natural killer cell activity and normalizing immune function. It represents a different approach: rather than targeting the virus, it targets the immune dysfunction that allows viral persistence.

A Functional Medicine Approach: Natural Strategies
While pharmaceutical interventions have their place, a comprehensive functional medicine approach addresses the terrain (the underlying immune function, mitochondrial health, and inflammatory state) that allows HHV-6 to perpetuate illness. Here is my integrative framework:
1. Support Mitochondrial Function (The Root of the Energy Crisis)
Given that mitochondrial fragmentation is the central mechanism linking HHV-6 to ME/CFS symptoms, mitochondrial support is foundational:
- CoQ10 (ubiquinol form, 200–400 mg/day). Essential for electron transport chain function; deficiency is common in ME/CFS. Our Activated CoQ10 delivers a highly bioavailable ubiquinol form for maximal mitochondrial support. CoQ10, PQQ, and NT Factor are also combined in our ATP Boost formula.
- PQQ (pyrroloquinoline quinone, 10–20 mg/day). PQQ promotes mitochondrial biogenesis, meaning the creation of new mitochondria, helping your body rebuild the fragmented mitochondrial network. Found in ATP Boost.
- NT Factor (phosphatidylcholine-rich lipid complex). Specifically designed to repair mitochondrial membranes, with clinical evidence in ME/CFS. Part of the ATP Boost formulation.
- D-Ribose (5–15 g/day). A sugar that bypasses the damaged energy pathways and directly feeds ATP regeneration; particularly helpful for post-exertional crashes.
- Magnesium glycinate (300–400 mg/day). A critical cofactor for over 300 enzymatic reactions including ATP synthesis, and the glycinate form is exceptionally well-tolerated and absorbed. Our Magnesium Glycinate is an excellent foundation for anyone with ME/CFS.
- Alpha-lipoic acid (200–600 mg/day). This nutrient regenerates other antioxidants (including vitamins C and E and glutathione), supports mitochondrial function, and crosses the blood-brain barrier to combat neuroinflammation. Our Alpha Lipoic Acid 200mg provides a flexible, titratable dose.
2. Restore Glutathione and Reduce Oxidative Stress
The drop in SOD2 (superoxide dismutase 2) seen in HHV-6 reactivation means oxidative stress runs unchecked. Replenishing antioxidant defenses is critical:
- NAC (N-acetyl cysteine, 500–1,200 mg/day). The most direct precursor to glutathione, our master antioxidant, NAC also has direct antiviral properties of its own. Our NAC 500 provides pharmaceutical-grade NAC. For sustained release throughout the day, the Jarrow N-A-C Sustain is an excellent option.
- Glutathione (liposomal or S-acetyl form). Direct glutathione supplementation for those who need more robust replenishment than NAC alone can provide. Our Glutathione Essentials delivers a highly absorbable form.
- Vitamin C (buffered, 1–3 g/day orally; IV vitamin C for more acute situations). A powerful antioxidant and immune modulator, high-dose IV vitamin C has been used successfully in acute and chronic viral illness. Our Buffered C Caps provide a gentle, non-acidic form that is easy on the gut.
- Resveratrol. This polyphenol inhibits herpesvirus replication and NF-κB activation in both cell culture and animal studies, and powerfully activates the Nrf2 antioxidant pathway. Our ResveraMax combines resveratrol with TrueBroc™ broccoli extract, turmeric, and andrographis for broad Nrf2 activation and antioxidant support.
3. Antiviral Botanicals and Natural Compounds
These natural compounds have evidence for broad-spectrum antiviral activity against herpesviruses, including inhibiting viral replication and modulating host immunity:
- Monolaurin (glycerol monolaurate from lauric acid). Monolaurin disrupts the lipid envelope of enveloped viruses, including herpesviruses. In-vitro studies demonstrate broad virucidal activity against multiple herpesvirus family members. I've used this clinically for years in patients with herpesvirus-related conditions, as I discuss in my Epstein-Barr Virus blog. Our Monolaurin C combines monolaurin with vitamin C for synergistic antiviral and immune support.
- Lysine (1,000–3,000 mg/day). Lysine interferes with herpesvirus replication by competing with arginine, an amino acid herpesviruses require for protein synthesis. Pair with a lower-arginine diet (reducing nuts, chocolate, and seeds during active flares). Our Lysine 1000 delivers a therapeutic dose in each capsule.
- Olive leaf extract. Rich in oleuropein, olive leaf has well-documented antiviral properties against enveloped viruses including herpesviruses. Our Olive Leaf 500 provides a potent standardized extract. Monolaurin and olive leaf are frequently used together for synergistic antiviral support. For a convenient all-in-one herpesvirus protocol, our EBV Energy Bundle, which combines Monolaurin C, Olive Leaf 500, Lysine 1000, and adrenal support, is precisely designed for this purpose and applies directly to HHV-6 reactivation as well.
- Quercetin (500–1,000 mg/day). A powerful flavonoid with documented anti-herpesvirus activity, quercetin inhibits NF-κB, reduces viral-induced inflammation, and also stabilizes mast cells, an important co-benefit for ME/CFS patients who also have MCAS. Found in our Hist Assist formula.
- Berberine (500–1,000 mg/day). Berberine has been shown to inhibit herpesvirus replication via NF-κB inhibition and apoptosis induction in infected cells. It is also powerfully anti-inflammatory and antimicrobial, addressing the co-infections that commonly fuel HHV-6 reactivation. See our Berberine 1000.
- EGCG (green tea extract). EGCG has demonstrated antiviral activity against multiple herpesvirus family members, in part through polyphenol disruption of viral envelope integrity.
- Medicinal mushrooms (Reishi, Cordyceps). These are potent immunomodulators that enhance natural killer cell activity, which is critical for controlling herpesvirus reactivation. NK cell dysfunction is a hallmark of ME/CFS.
- Licorice root (as glycyrrhizin). Glycyrrhizin specifically inhibits HHV-6 replication in vitro and has meaningful immune-modulating and anti-inflammatory properties. For those who also have adrenal fatigue and low cortisol, both common in ME/CFS, AdreCor with Licorice Root offers dual adrenal and antiviral botanical support. Use with caution in those with elevated blood pressure.
4. Support Immune Function at the Foundation
- Vitamin D3 (5,000 IU/day with K2; optimize serum 25-OH vitamin D to 60–80 ng/mL). A critical regulator of innate and adaptive immunity, vitamin D deficiency is strongly correlated with herpesvirus reactivation and disease severity. Our Daily D3 provides pharmaceutical-grade D3 in a highly absorbable softgel form.
- Zinc (15–30 mg/day). Essential for T-cell function, zinc also has direct antiviral activity against multiple herpesvirus family members. Our Activated Zinc uses a highly bioavailable chelated form for superior absorption and immune support.
- Vitamin A. This nutrient maintains mucosal immunity and modulates T-regulatory cell balance, working synergistically with vitamin D in immune regulation.
- Immune Essentials. Our comprehensive Immune Essentials formula brings together key immune-supporting nutrients in a single, convenient formula.
- Probiotics. A healthy gut microbiome is essential for systemic immune regulation and immune surveillance. Our Spore Probiotic Plus IgG offers dual immune and gut support with resilient spore-based organisms plus immunoglobulins.
5. Address the Nervous System and Adrenal Axis
The autonomic nervous system dysfunction in ME/CFS is not secondary. It is part of the same CDR-driven pathology. Supporting the HPA axis and helping the nervous system step down from survival mode is essential for recovery:
- Adaptogenic herbs (ashwagandha, rhodiola, holy basil). These help regulate cortisol rhythms and build stress resilience; consider our Adrenal Essentials. For those with low cortisol and adrenal exhaustion, AdreCor with Licorice Root adds botanical cortisol support.
- Phosphatidylserine. This nutrient helps regulate HPA-axis activity and blunts pathological cortisol elevations that suppress antiviral immunity.
- Sleep optimization. Deep, restorative sleep is when viral immune surveillance is most active and when mitochondrial repair occurs. Our Dream Powder supports healthy sleep architecture with magnesium and calming botanicals.
- Mind-body practices. Gentle yoga, breathwork, heart rate variability (HRV) biofeedback, and trauma-informed therapy directly modulate the autonomic nervous system, reduce purinergic signaling, and help interrupt the stuck CDR loop that perpetuates ME/CFS.
Prevention: Keeping HHV-6 Dormant
For those who have HHV-6 or who want to reduce their risk of reactivation, prevention is about maintaining immune resilience and minimizing triggers:
- Prioritize sleep. Aim for 7–9 hours of quality sleep consistently, as this is when immune surveillance is most robust.
- Manage stress actively. Chronic psychological stress is one of the most potent triggers for herpesvirus reactivation.
- Avoid immune-suppressing factors. Limit alcohol, minimize processed foods, and address nutritional deficiencies.
- Support detoxification. Mold, heavy metals, and environmental toxins can trigger CDR activation. Explore our Detox Bundle if you have significant toxic burden.
- Treat infections promptly. Other infections (respiratory viruses, tick-borne illness, bacterial overgrowth) can trigger HHV-6 reactivation through immune perturbation.
- Limit high-arginine foods during vulnerable periods. During times of stress or active viral symptoms, reducing nuts, seeds, chocolate, and high-arginine grains may be helpful.
- Maintain optimized vitamin D. Year-round vitamin D optimization is one of the simplest, most evidence-backed immune-support strategies.
A Note on ME/CFS and MCAS
Many of my patients with ME/CFS also have mast cell activation syndrome (MCAS), and there is growing evidence that HHV-6 itself can trigger mast cell activation. Mast cells have been shown to be activated by herpesviral proteins, and the resulting histamine release and inflammatory mediators can worsen post-exertional malaise, cognitive symptoms, and neuroinflammation. If you're dealing with both conditions, targeted MCAS support (including quercetin, vitamin C, and histamine-lowering interventions) becomes even more important. See our MCAS Bundle.
A Message of Hope and Faith
If you or someone you love is living with ME/CFS, I want you to know this: your suffering is real, it has biological underpinnings that science is finally beginning to map, and healing, while often slow and nonlinear, is possible.
I have sat with patients who have been dismissed, disbelieved, and told “there's nothing wrong with you” for years. I have also witnessed remarkable recoveries when we find and address the true root causes: viral triggers like HHV-6, mitochondrial dysfunction, toxic burden, and trauma held in the nervous system.
The CDR theory teaches us something profound: your body is not broken. It is protecting itself, brilliantly and desperately, at enormous cost. Our job as healers, and your job as your own advocate, is to create the conditions under which your body feels safe enough to step down from that state of emergency, repair its mitochondria, and return to healing.
I believe in the power of science and the power of prayer, and I've seen both work in ways I cannot fully explain. You are not alone on this journey. May you find the answers, the practitioners, and the community that help you reclaim your life.
Summary: Key Action Steps
For patients navigating HHV-6 and ME/CFS, I recommend working with a knowledgeable functional medicine physician to:
- Test appropriately. HHV-6 IgG titers, PCR, HHV-7, and metabolic markers.
- Evaluate and treat mitochondrial dysfunction. CoQ10 (ubiquinol), PQQ, NT Factor, D-ribose.
- Replenish glutathione and antioxidants. NAC, vitamin C, alpha-lipoic acid.
- Consider targeted antiviral strategies. Both natural (monolaurin, lysine, quercetin, berberine) and pharmaceutical (valganciclovir, artesunate, LDN) based on your individual case.
- Address immune foundations. Vitamin D3, zinc, probiotics, medicinal mushrooms.
- Support the nervous system and HPA axis. Adaptogens, sleep hygiene, trauma-informed care.
- Remove triggers. Mold, toxins, stress, other infections, pro-inflammatory diet.
References
- Schreiner P, Harrer T, Scheibenbogen C, Lamer S, Schlosser A, Naviaux RK, Prusty BK. Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. ImmunoHorizons. 2020;4(4):201–215. doi:10.4049/immunohorizons.2000006. https://www.immunohorizons.org/content/4/4/201
- Naviaux RK, Naviaux JC, Li K, et al. Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci USA.2016;113(37):E5472–E5480. doi:10.1073/pnas.1607571113. https://www.pnas.org/doi/10.1073/pnas.1607571113
- Naviaux RK. Metabolic features and regulation of the healing cycle: a new model for chronic disease pathogenesis and treatment. Mitochondrion. 2019;46:278–297. doi:10.1016/j.mito.2018.08.001. https://pubmed.ncbi.nlm.nih.gov/30099167/
- Montoya JG, Kogelnik AM, Bhangoo M, et al. Randomized clinical trial to evaluate the efficacy and safety of valganciclovir in a subset of patients with chronic fatigue syndrome. J Med Virol. 2013;85(12):2101–2109. doi:10.1002/jmv.23713. https://pubmed.ncbi.nlm.nih.gov/23959519/
- Watt T, Oberfoell S, Balise R, et al. Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers. J Med Virol. 2012;84(12):1967–1974. doi:10.1002/jmv.23411. https://pubmed.ncbi.nlm.nih.gov/23080504/
- Maltsev DV, Bidovanets L. A comparative study of valaciclovir, valganciclovir, and artesunate efficacy in reactivated HHV-6 and HHV-7 infections associated with chronic fatigue syndrome/myalgic encephalomyelitis. Microbiol Immunol. 2022;66(4):193–199. doi:10.1111/1348-0421.12966. https://pubmed.ncbi.nlm.nih.gov/35102619/
- Ablashi DV, Eastman HB, Owen CB, et al. Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. J Clin Virol. 2000;16(3):179–191. https://pubmed.ncbi.nlm.nih.gov/10738144/
- Chapenko S, Krumina A, Kozireva S, et al. Activation of human herpesviruses 6 and 7 in patients with chronic fatigue syndrome. J Clin Virol. 2006;37(Suppl 1):S47–S51. https://pubmed.ncbi.nlm.nih.gov/17276366/
- Fluge Ø, Mella O, Bruland O, et al. Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome. JCI Insight. 2016;1(21):e89376. doi:10.1172/jci.insight.89376. https://pubmed.ncbi.nlm.nih.gov/27882347/
- Prusty BK, Gulve N, Govind S, et al. Active HHV-6 infection of cerebellar Purkinje cells in mood disorders. Front Microbiol. 2018;9:1955. doi:10.3389/fmicb.2018.01955. https://pubmed.ncbi.nlm.nih.gov/30233512/
- Sokolovska L, Cistjakovs M, Matroze A, Murovska M, Sultanova A. From Viral Infection to Autoimmune Reaction: Exploring the Link between Human Herpesvirus 6 and Autoimmune Diseases. Microorganisms.2024;12(2):362. doi:10.3390/microorganisms12020362. https://www.mdpi.com/2076-2607/12/2/362
- Naviaux RK. Oxidative shielding or oxidative stress? J Pharmacol Exp Ther. 2012;342(3):608–618. doi:10.1124/jpet.112.194167. https://pubmed.ncbi.nlm.nih.gov/22738794/
- Kasimir F, Toomey D, Liu A, et al. Tissue specific signature of HHV-6 infection in ME/CFS. Front Mol Biosci.2022;9:1044964. doi:10.3389/fmolb.2022.1044964. https://pubmed.ncbi.nlm.nih.gov/36741957/
- West AP, Shadel GS, Ghosh S. Mitochondria in innate immune responses. Nat Rev Immunol. 2011;11(6):389–402. https://pubmed.ncbi.nlm.nih.gov/21597473/
Related Reading on DrJillCarnahan.com
- The Sleeping Giant: Tips to Treat Reactivation of Epstein-Barr Virus
- Is a Hidden Infection Causing Your Chronic Fatigue?
- Long COVID: A Fascinating Look at This New Epidemic's Similarities to Chronic Fatigue Syndrome
- Post-Viral Chronic Fatigue: A Fascinating Look at the Link to COVID-19
* These statements have not been evaluated by the Food and Drug Administration. The product mentioned in this article are not intended to diagnose, treat, cure, or prevent any disease. The information in this article is not intended to replace any recommendations or relationship with your physician. Please review references sited at end of article for scientific support of any claims made.












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