When it comes to virus and ME/CFS there are several schools of belief.
- A Virus caused ME/CFS and thus eliminating the virus should cause remission
- Virus are re-activated (or no longer suppressed) by the immune changes associated with ME/CFS
- De-activating the virus may improve (but not cure) ME/CFS
Past Posts on Virus
- EBV, HHV5 and other virus in CFS [2016]
- Viruses, Retrovirus and Chronic Fatigue Syndrome [2016]
- Antivirals and ME/CFS: Paxlovid, Tamiflu etc [2023]
Quick Summary
The literature is below:
- 1. Epstein-Barr Virus (EBV)
EBV, which causes infectious mononucleosis, is one of the most frequently implicated viruses in ME/CFS. Studies show that 8–15% of people who develop infectious mononucleosis go on to meet ME/CFS criteria, and a subgroup of ME/CFS patients show evidence of EBV reactivation or immune response abnormalities related to EBV5 7. - 2. Human Herpesvirus 6 (HHV-6)
Reactivation of HHV-6, another common herpesvirus, has been hypothesized to contribute to ME/CFS symptoms, particularly in combination with EBV reactivation7. - 3. Enteroviruses
Historical and contemporary evidence links enteroviruses (a group that includes polioviruses, coxsackieviruses, and echoviruses) to ME/CFS. Outbreaks of ME/CFS have coincided with enteroviral epidemics, and some researchers consider enteroviruses a likely culprit, especially in cluster cases1. - 4. Influenza Viruses
Influenza infection has been associated with a more than two-fold increased risk of developing ME/CFS in the years following infection17. - 5. SARS-CoV-2 (COVID-19)
Many individuals with long COVID meet criteria for ME/CFS, and SARS-CoV-2 is recognized as a trigger for ME/CFS in some cases67. - 6. Other Herpesviruses
Varicella zoster virus (which causes chickenpox and shingles) and other herpesviruses have also been reported as potential triggers7. - 7. Ross River Virus
This mosquito-borne virus has been linked to ME/CFS onset, likely through immune system dysregulation3. - 8. Retroviruses (e.g., XMRV)
Early studies suggested an association between the retrovirus XMRV and ME/CFS, but this link has been discredited by subsequent research and retraction of the original findings2.
Model
It is well known that virus will alter the microbiome. This alteration is to trick/hijack the microbiome to produce chemicals/metabolites that the virus needs (and to reduce those that hurt it) [SEE BOTTOM FOR CLARITY]. Once the virus is eliminated, then sometimes the microbiome gets “stuck” in this state. People have symptoms of the virus (symptoms caused by the metabolites!) but do not have the virus any more.
It is this persistent change of the microbiome: dysbiosis; that I believe is the path to relief and possible remission.
Virus and Microbiome Treatment
Using herbs know to be both anti-viral and anti-bacterial is my favored approach. You may get severe die-off from these (along with a herxheimer effect). Die off will usually start to ebb by day 10-14 after starting.
My personal favorites are:
- Tulsi
- Haritaki
- Neem
- Wormwood (Artemisia)
- Olive Leaf
The list of Anti-viral herbs
| Herb | Notable Antiviral Actions |
|---|---|
| Tulsi (Holy Basil) | Herpes, hepatitis, influenza, coronaviruses Inhibits viral replication and modulates immunity28. |
| Neem | Herpes simplex virus (HSV-1 and HSV-2)27, Influenza viruses:10, Dengue virus:58, Hepatitis C virus (HCV)6, Coxsackie virus, polio, and HIV57, SARS-CoV-2 (COVID-19)49. |
| Olive Leaf | Inhibit viruses such as herpes simplex virus (HSV), influenza virus, hepatitis B and C, human papillomavirus (HPV), HIV, and notably, SARS-CoV-2 (the virus causing COVID-19)125678. |
| Haritaki (Terminalia chebula) | Antiviral activity against a range of viruses, including SARS-CoV-2 (the virus responsible for COVID-19), herpes simplex virus type 2 (HSV-2), and influenza A virus. In particular, Haritaki demonstrated inhibition of the SARS-CoV-2 main protease in laboratory assays, suggesting it may halt viral replication15. |
| Curcumin (from turmeric): | Antiviral against influenza, HIV, hepatitis, and coronaviruses8. |
| Ginseng: | Traditional use for immune support and antiviral activity5 |
| Sage | HIV-1, herpes simplex, Indiana vesiculovirus Rich in safficinolide and diterpenoids; active against HIV-1, herpes simplex virus, and Indiana vesiculovirus157. |
| Oregano | Rotavirus, norovirus, general antiviral Contains carvacrol and thymol; effective against rotavirus, norovirus, and other viruses1578. |
| Fennel | Herpes, respiratory viruses Contains trans-anethole; shown activity against herpes viruses and respiratory viruses27. |
| Peppermint (Mentha piperita): | Contains menthol and rosmarinic acid; antiviral against herpes simplex and influenza viruses2. |
| Lemon balm | Herpes simplex, respiratory viruses Contains flavonoids and essential oils; active against herpes simplex and respiratory viruses7. |
| Ginger | Influenza, RSV, calicivirus Contains gingerols and zingerone; effective against influenza, RSV, and feline calicivirus5. |
| Garlic | Influenza, HIV, HSV-1, rhinovirus Contains allicin; antiviral against influenza, HIV, HSV-1, viral pneumonia, and rhinovirus53. |
| Echinacea | Colds, respiratory infections Boosts immune function and reduces duration of colds and respiratory infections8. |
| Elderberry | Influenza, cold viruses Traditionally used for influenza and cold viruses1. |
| Astragalus | General antiviral, immune boost Immunomodulatory and antiviral properties1. |
| Aloe vera | Coronaviruses, herpes, influenza, HPV Contains compounds effective against coronaviruses, herpes, influenza, HPV, and more2. |
| Thyme | Herpes, influenza, general antiviral Contains thymol and carvacrol; antiviral and antimicrobial7. |
| Andrographis | Influenza, hepatitis C, dengue Contains andrographolide; active against influenza, hepatitis C, and dengue8. |
| Artemisia annua (Wormwood) | Hepatitis B & C, malaria Used for malaria; also shows antiviral activity against hepatitis B and C48. |
My Personal Protocol
Do one at a time for 7-14 days, then move to the next one. Take notes on die-off or symptom changes with each. Constant rotation is strongly encouraged. Repeat but with only that cause a die-off or change.
You may or may not have a virus or re-activated virus. Most ME/CFS patients are not tested for all of the candidates virus listed above. Prescription antivirals with ME/CFS are very sensitive to which virus that a person has.
Appendix
Viruses lack their own metabolic machinery and rely entirely on host cell metabolites and metabolic pathways to reproduce. While viruses do not carry out metabolism independently, they hijack and reprogram the host cell’s metabolic processes to obtain the energy, nucleotides, lipids, and amino acids required for replication. Key findings include:
Metabolic Reprogramming by Viruses
- Aerobic glycolysis (Warburg effect): Most viruses induce glycolysis to rapidly generate ATP and intermediates like pyruvate/lactate, even in oxygen-rich conditions12. This provides energy and substrates for viral genome replication (e.g., nucleotides from glucose metabolism)13.
- Fatty acid synthesis: Enveloped viruses (e.g., herpesviruses, SARS-CoV-2) upregulate lipid biosynthesis to create viral envelopes136.
- Nucleotide production: Viruses like HSV-1 redirect the pentose phosphate pathway and TCA cycle to boost purine/pyrimidine synthesis for genome replication3.
Host Dependency Examples
- Human cytomegalovirus (HCMV) increases glycolytic flux, TCA cycle intermediates, and fatty acid synthesis to support its 96-hour replication cycle13.
- Herpes simplex virus (HSV) prioritizes nucleotide synthesis over glycolysis, reflecting its faster 24-hour replication timeline3.
- SARS-CoV-2 hijacks folate metabolism and one-carbon pathways to facilitate RNA synthesis6. Inhibiting these pathways reduces viral replication.
Experimental Evidence
- Glycolysis inhibitors like 2-deoxyglucose (2-DG) block late-stage herpesvirus assembly1.
- Adenovirus activates Myc oncogene signaling to drive glycolysis and nucleotide synthesis1.
- Vaccinia virus is an exception, showing minimal glycolysis dependence and instead utilizing alternative carbon sources like sorbitol1.
In summary, viruses co-opt host metabolites by reprogramming cellular metabolism to meet their replication demands. This metabolic hijacking is a nearly universal feature of viral reproduction, making host metabolic pathways potential therapeutic targets126.
CFS Remission 