Lerner's response to glutathione depletion.-methylation cycle block hypothesis

[Guest guest]

Hi, all.

One of the people I met for the first time at the IACFS meeting was

Dr. A. Lerner. As you may know, he is the doctor from

Michigan who has specialized in treating viral infections of the

heart, producing cardiomyopathy in CFS. He had this condition

himself some years ago.

At the meeting, I gave him copies of my poster papers, and in

particular told him that I would like to have his comments on my

pathogenesis paper (posted in the files of this list at GD-MCB etc.)

I saw him again later in the conference, and he told me that he had

read my paper. His comment was, " It makes sense. " I was really

happy to hear this from a person who has focused on the viral

infection aspect of CFS, since I expected that he would believe that

the viruses were the " first cause. " But he was willing to accept the

chain of events as I presented them.

In the paper, I discuss viral infections, including why the viral

infections that are present initially in CFS are the ones that are

observed, what causes latent viruses to reactivate, how the immune

system responds to them, including the low activity of the NK cells,

the activation of the RNase-L system, the shift to Th2 immune

response, why the infections aren't knocked out, and why more

infections accumulate over time in a PWC's body. I discuss why

sackie seems to be more prevalent in PWCs in the UK. I also

discuss intracellular bacterial infections, and why Chlamydia

reactivates. Furthermore, I discuss why inflammation is more of a

problem later in the course of the illness.

I invite everyone to take a look at this paper. There really is

something in there for everyone, since I pulled together essentially

all the observed features of CFS into a common cause-effect tree. I

would appreciate your comments.

Rich