Viral-induced heart damage is the single cause of CFS according to over a decade of research by Dr. A. Martin Lerner, a board certified internist who recently presented his findings at The American Society of Microbiology. Since 1988, Lerner has investigated the theory that two viruses belonging to the same viral family damage the heart muscle, resulting in CFS.
In an interview with ImmuneSupport.com, Lerner, who practices at William Beaumont Hospital in Royal Oak, Michigan, explained that his findings “are remarkable. The viruses that seem to be involved are two very sophisticated members of the herpes virus family, gamma and beta virus, also known as Epstein-Barr Virus and cytomegalovirus.”
Lerner is emphatically not referring to the herpes virus known as HHV-6, or HHV-8. In fact, contrary to several other avenues of research currently being explored, Lerner states that, “I do not believe that HHV-6 is important in any major way at all. Certainly not in the subset of patients my collaborators and I have studied.”
Several studies support Lerner’s theory, the first of which was published in the peer-reviewed journal Chest. This study observed that patients with CFS all had abnormal cardiac readings. From there, open studies were conducted with control groups, which were then repeated in a double-blind study in 1997. In this study, which Lerner himself was not involved in, 60 CFS patients with no known heart disease blindly had halter monitors read by independent cardiologists. Over 95% of the patients with CFS had abnormal halter monitors, meaning that they had heart damage.
At the same time, another study led by Lerner and published in Clinical Nuclear Medicine, found that CFS patients had left ventricular dysfunction and several other serious cardiac abnormalities. Later the researchers learned that the longer the patient has CFS, the greater the heart damage.
But why does the virus lead to CFS in some people and not others? Lerner described how: “In a CFS patient, the mechanism of the disease is completely different. The whole virus is not produced, and often, there is evidence of past infection. The virus stays in the DNA of the cell forever. When the virus infects a CFS patient, it tries to ‘make’ itself completely and is unsuccessful. The classical means of making a viral diagnosis fail – the (usual) tests cannot find the rising antibody.”
He adds that it is possible for CFS to result from one or other of the viruses, or from both in combination. He says that the work he’s doing strongly implicates the heart in the development of CFS – “The heart is definitely weakened.” That may be why when physically active people are struck down with the disease, they feel the effects dramatically. He theorizes that these people who are used to exercising sense their inability to exercise at prior levels earlier than people who do not exercise.
If proven, Lerner’s theory is hugely significant for the way CFS could be treated. In fact, Lerner, a CFS patient himself, was the first to try high doses of potent anti-viral drugs, such as valacyclovir (brand name Valtrex) and ganciclovir (Cytovene).
He is now involved in a double-blind placebo controlled study of valacyclovir’s effects on Epstein-Barr Virus. The pharmaceutical company Glaxo Wellcome is funding the study, and Lerner predicts it will conclude in about a year.
Although Lerner was unable to comment on the treatment protocol being tested, he did affirm that he is himself now well. “I’ve been able to work full-time, exercise and swim. I’m on maintenance Valtrex, and I’m living fine.” He agrees, however, that these kinds of drugs can have serious side effects such as kidney stones, renal failure and gastrointestinal upset, and he stressed the need to be very careful in using these powerful drugs.
Despite Dr. Lerner’s long academic career, including a 20-year stint as Head of Infectious Diseases, it has been a difficult struggle for his research to be taken seriously. He readily admits that the studies have had “very, very little impact to date,” in the medical community. He says it has been “rather lonely these many years.”
However, Lerner remains optimistic and believes that the tide is now turning in his favor. “The work we’re presenting at the present time in particular having to do with the mechanism (of the virus) is compelling. Incomplete herpes virus multiplication is exciting and scientifically valid.”