The viral origin to that infection we never recovered from may have looked something like this:
Step 1 Virus attaches to our cells
Step 2 Virus penetrates our cell membranes
Step 3 Virus takes over our cellular machinery
- Makes its own viral proteins
- Inserts its genetic information into our own
- Makes new viral nucleic acids (RNA & DNA)
Step 4 Virus destroys the host cell and looks for the next unlucky candidate
It is still unclear if ME/CFS is defined by a post-viral epigenetic trigger, an undiscovered mystery virus, or if there are genetic susceptibilities in place that make patients immunocompromised. In all likelihood more than one of these reasons, if not all, are at play in this complicated illness.
Anti-viral drugs are the mainstay of ME/CFS treatment, yet the results are not as promising as one would hope. I believe this is due to a couple factors:
- Many anti-viral drugs are non specific to viruses
- If a virus mutates, the anti-viral drug will no longer be effective
- Viruses can form a protective phospholipid layer around itself
- Viruses may hide deep in tissues where medications or immune cells cannot access
Instead of giving up when the anti-viral drug stops working, there are several strategies patients can use to intervene in blocking viral penetration and replication (1).
Here are 5 evidenced-based approaches
Proteins found in many Herpes family viruses, including HSV-1 and CMV, are rich in the amino acid L-arginine. In vitro, when viruses are deprived of L-arginine, viral replication is halted. An amino acid that is analogous to L-arginine, L-lysine, has been shown to also block the activity of L-arginine (2).
Studies show that when the ratio of L-lysine to L-arginine is high, viral replication is inhibited. Unlike arginine, lysine is an essential amino acid—meaning it can only be obtained through diet or supplementation. Several studies have showed positive results with a dosage of 3 grams throughout the day (1,3).
Lipoic Acid & NAC
The cell signaling molecule NF-kB has been termed THE central mediator of the immune system. Activation of NF-kB occurs immediately following exposure to a viral infection. Viruses that trigger NF-kB include HIV-1, EBV, HCV, HBV, influenza, and HTLV-1 (4).
Persistent activation of NF-kB has been linked to neurodegenerative diseases as well as certain cancers. In fact, it is believed to be chronically up-regulated in ME/CFS, resulting in a vicious cycle of events (Maes & Twisk).
Getting a handle on NK-kB is likely key to undoing much of the continuous destruction of this illness. Several NF-kB inhibitors have been established in the literature: lipoic acid and NAC are 2 such nutrients.
Lipoic acid has been shown to completely block HIV-1 replication via inhibition of NF-kB. It also acts synergistically with antiretroviral drugs and has been studied extensively in clinical trials of HIV infected patients (5).
N-acetlycysteine (NAC) plays multiple physiological roles in the immune system—glutathione precursor, T-helper cell proliferator, chelator, etc. It has been used for decades as a natural antiviral strategy to reduce symptoms of influenza (6). In a cross-over study using diabetic patients, oral NAC supplementation showed significant reduction of NF-kB activity after 1 month that returned to baseline following discontinuation (7).
Vitamin D is all the rage for uses ranging from cancer prevention to bone health. However, it also plays a key role in viral infections. Like NAC and lipoic acid, it inhibits NF-kB to reduce the inflammatory state that occurs with infection.
Vitamin D can also stimulate the production of anti-viral peptides—specifically those necessary to attack enveloped viruses. The mechanism of 2 such peptides has been found in cathelicidin and human beta defensin-2. These peptides work by inhibiting replication of HSV-1, retroviruses, and adenoviruses (8).
There is also speculation that vitamin D inhibits EBV infection due to the correlation between low vitamin D levels and MS—an illness closely linked to latent EBV infection.
In a state of chronic oxidative stress and mitochondrial dysfunction, as is seen in ME/CFS and Fibro, selenium is depleted at a rapid pace. This leads to impaired immune responses to RNA viruses and may even lead to viral mutation (9). An increased virulence of otherwise benign viruses has been seen in the literature as well. This increased virulence seems to be worsened when Vitamin E is also depleted.
Specifically, enteroviruses such as coxsackie virus B3 proliferate and become more virulent in the absence of adequate selenium; as well as its analog vitamin E (10). Enteroviruses such as these have long been implicated in many cases of ME/CFS according to the extensive work of Dr. Chia (11).
2 Souki SK, Gershon PD, Sandri-Goldin RM. (2009) Arginine methylation of the ICP27 RGG box regulates ICP27 export and is required for efficient herpes simplex virus 1 replication. J Virol. 2009 Jun;83(11):5309-20. http://www.ncbi.nlm.nih.gov/pubmed/19321610
3 Rubey, RN (2010) Could lysine supplementation prevent Alzheimer's dementia? A novel hypothesis. Neuropsychiatric disease and treatment. 6:707–710. http://www.dovepress.com/getfile.php?fileID=7998
4 Hiscott J, Kwon H, Génin P. (2001) Hostile takeovers: viral appropriation of the NF-kappaB pathway. J Clin Invest. 107(2):143-51. http://www.ncbi.nlm.nih.gov/pubmed/11160127
5 Patrick, L. (2000) Nutrients and HIV: part three - N-acetylcysteine, alpha-lipoic acid, L-glutamine, and L-carnitine. Altern Med Rev. 5(4):290-305. http://www.ncbi.nlm.nih.gov/pubmed/10956377
6 De Flora S, Grassi C, Carati L. (1997) Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur Respir J. 10(7):1535-41. http://www.ncbi.nlm.nih.gov/pubmed/9230243
7 Amore A, et al (2013) N-Acetylcysteine in hemodialysis diabetic patients resets the activation of NF-kB in lymphomonocytes to normal values. J Nephrol. 26(4):778-86. http://www.ncbi.nlm.nih.gov/pubmed/23065916
8 Hansdottir S, et al (2010) Vitamin D decreases respiratory syncytial virus induction of NF-kappaB-linked chemokines and cytokines in airway epithelium while maintaining the antiviral state. J Immunol. 184(2):965-74. http://www.ncbi.nlm.nih.gov/pubmed/20008294
9 Harthill M. (2011) Review: micronutrient selenium deficiency influences evolution of some viral infectious diseases. Biol Trace Elem Res. 143(3):1325-36. http://www.ncbi.nlm.nih.gov/pubmed/21318622
10 Levander OA Beck MA. (1999) Selenium and viral virulence. Br Med Bull. 1999;55(3):528-33. http://www.ncbi.nlm.nih.gov/pubmed/10746343
11 Chia JK (2005) The role of enterovirus in chronic fatigue syndrome. J Clin Pathol. 58(11):1126-32. http://www.ncbi.nlm.nih.gov/pubmed/16254097