Monday, April 27, 2009

Rheumatoid Arthritis

I originally wrote this post in 2004 at This post is for information only. It represents the observations, views and opinions of the author, but is not a recommendation for treatment. Anyone reading it should consult his/her physician before considering treatment.
Rheumatoid Arthritis (RA) affects mainly the joints of the hands and feet, although it can extend to other tissues. Of all the forms of arthritis, RA is most likely to lead to crippling disabilities. It is the most common "autoimmune" disease, affecting three times more women than men. It is characterized by inflammation and destruction of cartilage in the joints, often causing deformities in the fingers. Despite continued research, the cause of RA is unknown. Some researchers believe that an infectious microbe (mycoplasma or virus) is the cause and others believe it is simply the immune system has started to recognize the normal cells as foreign and attacks them ("Microbiology, Principles and Explorations" 5th Edition, by Jacquelyn G. Black, 2002, pg. 495.) In either case, it is recognized that the inflammatory immune response causes the bulk of the damage. In general, the drugs that treat the disease are anti-inflammatories. Since an inflammation response is an immune response, such anti-inflammatories can be viewed as immune suppressants. Some of my friends with the disease have told me that some of the drugs are reasonably effective at keeping their RA in control. However, there are others where the drugs have failed to control the disease. My view is that they may be helpful for many, but are limited in effectiveness because they do not address the root, viral cause.

I have long believed that most if not all autoimmune diseases, where the immune system attacks and damages normal cells, have an infectious agent as the root cause. The immune system is attacking the infectious agent with its usual inflammatory response, which is not very specific to the infectious agent. In doing so, it also damages surrounding normal cells as collateral damage. From the statements from the book referenced above, it appears that I am not alone in this suspicion. The big question is: What is the infectious agent?

For a long time I have been suspicious that it might be a herpes virus. As discussed in the above referenced book, there are a wide variety of herpes viruses that can be responsible for a number of different health issues. I won't attempt to list them here. In general, herpes viruses have the characteristic of infecting nerve cells. Once in the cell, they create a "provirus" that takes up permanent residence in the body of the nerve cell, where the immune system will not attack it. It then serves as a template to produce active viruses. It can be dormant for long periods of time and when triggered, by an unknown cause, it will start to produce active viruses. These viruses will move along the axons of the nerve cells and exit at the terminal synaptic contacts. At this exit point the viruses can damage cells, creating the well recognized lesion which is called a "cold sore" or fever blister" in the case of herpes simplex. The damage can be due to the virus or due to the inflammation response. In other types of herpes infections the herpes damage can be internal and not visible on the skin. Six variations of the herpes virus have been identified so far and that is certainly not the end. The infection usually cycles from dormant to active and back to dormant again.

Upon a closer look, it can be seen how this mechanism of virus production and dispersal serves to protect the source, provirus, in the body of the nerve cell. The immune system's inflammation response will attack the active viruses that are exiting at the synaptic contacts, which are spatially removed from the nerve body. Thus the nerve body, which is the host for the source provirus, is protected from the immune system's inflammation response. Since nerve cells have a long life, a herpes infection does also, essentially the life of the person.
If this is a cause of RA, then there must be infected nerve cells that have axons with terminal synaptic contacts in the joints where the inflammation is observed.

Historically, the common treatment for a herpes virus is the amino acid L-lysine. It appears that the mechanism of the lysine is to encourage the provirus to become dormant again stopping the production of more viruses. There are also drugs designed specifically to attack the herpes virus, which appear to be effective. If it is the cause, I reasoned that L-lysine as well as the drugs targeting the herpes virus should be effective in treating RA.

At this point in my thinking, I was reading the journal: The Scientist, Nov. 17, 2003, V. 17, No 22, pg.8. The article is titled "Natural Is Not Necessarily Better". It is primarily focused on breast milk sometimes transmitting viruses to the infant. As part of the discussion it also states that "A study conducted on patients with rheumatoid arthritis showed that the prevalence of HTLV-1 Tax positivity is at least three times higher in such patients than in healthy individuals." It also concludes that the virus was acquired transplacentally or by breast milk. HTLV-1 is a retrovirus discussed in the above referenced book on pg. 262. Could this be the cause of RA and not the herpes virus? Because it is a retrovirus, it is similar to the HIV virus responsible for AIDS. If that is the case, lysine and herpes drugs may be ineffective. There is no clear evidence that they are effective for retroviruses. Retroviruses are very different than herpes viruses. They are RNA viruses while herpes viruses are DNA viruses so one would not expect them to respond the same to the same treatments.

I then happened to read the book: "The Virus Within, A Coming Epidemic" by Nicholas Regush, 2000. This book mainly addresses HIV and AIDS. As part of this, it was found that, in the case of AIDS, there appeared to always be a co-infection with the herpes virus, Human Herpes Virus No. 6 (HHV-6). The evidence also indicated that HHV-6, not HIV, was the primary cause of cell damage and thus death. It occurred to me that if there was a HTLV-1 infection in RA, similar to HIV, there might also be a herpes co-infection. Similar to HIV, the herpes virus might be the primary cause of cell damage. If this was the case, then herpes treatments might be effective in treating RA.