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Last updated January 1, 2014

Stealth Virus Encephalopathy

Dr. W. John Martin, Center for Complex Infectious Diseases. Lecture Transcript 3/9/1997

I must say I have been working on Chronic Fatigue Syndrome or viruses that can cause, or infect, not only chronic fatigue but a whole series of neuropsychiatric illnesses from autism in children, Attention Deficit, manic depression, schizophrenia and so forth, and this work proceeds slowly. All of a sudden, I had a call from Donovan to say that he's had an outbreak up here, would I be interested in looking at some of the samples to see if, in fact, we could see a similar virus to the virus that we have been studying called the Stealth virus. He sent the samples and I'm thrilled to say that, yes, we do have some positive cultures, and I really think we do have now an opportunity for a major advance in understanding this illness, not only to the benefit to the local people here, but hopefully to the benefit of large numbers of people throughout this country, and perhaps throughout the world, who are neurologically impaired, [have] dysfunctional brain syndrome, [who are] being shunted from psychiatrists to neurologists, often finishing up in institutions and very much being dropped by the medical system.

It was on the idea of sharing this work that I established or founded a center for complex infectious diseases to emphasize the complexity of these illnesses and the need for hard, solid research to understand what is going on, hopefully to lead to a cure.

Dr. Anderson was kind enough to visit us in the laboratory. It occupies half of the top floor. We have really excellent space. One of the laboratories of the offices is occupied by a Dr. Zacky Salahuden (sp?) who is the first person to describe a major human virus, called Human Herpes Virus 6. We have facilities for electron microscopy, chemistry, tissue culture and so forth. So we have the location and we have the equipment to proceed to study a class of viruses, the diseases that are associated with these viruses, and hopefully we can extend this to therapeutic endeavors. And again, I really want to emphasize the opportunity that this epidemic that Dr. Anderson has described, in terms of making substantial progress, is really here and now, and I am thrilled to be here and hope there will be additional visits, and certainly additional samples to look at, and perhaps to work through Dr. Anderson in terms of evaluating some of the potential therapies.

As with any research we have to start from the beginning. I want to describe the viruses, then the diseases and then something about the therapies. The viruses were termed Stealth viruses essentially because of this line. [Note: copies of the slides Dr. Martin used to illustrate his lecture are available for viewing at the CCID website.]


Stealth Viruses
By nature [the stealth viruses] evoke very little inflammation or cellular information in the body. So, they're not so virulent in the sense that they don't grow so aggressively in the test tube, but they have this enormous advantage [in] that they're not seen by our immune system. They have deleted those components that our immune system would ordinarily engage the virus. So, something like the stealth bomber avoiding radar, these viruses have adapted themselves to avoid the cellular inflammatory reaction. They're cytopathic in that they can damage cells and we can see that, both in the test tube, in vitro, and also in patients, in vivo.

There is a very broad range of cell permissiveness and, what's important as far as epidemics are concerned, is that they grow equally well in animal cells and in animals, in fact, as they do in humans. So, this is an exception to the usual barriers that exist between viruses jumping species, that these viruses can, in fact, grow in animals and are potentially transferable from humans to animals and back into humans.

One important piece of science that's evolving is an understanding of how these viruses have learned to adapt to avoid the immune system. The basic premise is that, rather than having a completely intact, fully formed genome, they exist in a fragmented, unstable form. The fragments have essentially deleted away from themselves those parts that the immune system might recognize. That's an important concept because it goes against the conventional wisdom that viruses are complete entities and if you had a fragment it couldn't grow and produce damage.

There were a number of these viruses being molecularly heterogeneous. The other point which I'll focus on a lot today is we know that some of these viruses undoubtedly have come from African green monkey cytomegaloviruses. The relevance of that will appear later since we use African green monkeys, still use them, and certainly have used them in the past, to make polio vaccines at a time when it was considered appropriate to use fresh animal tissues to make vaccines, a practice that nobody would ever initiate again today. So, those are the generalizations and the general comments I wanted to make about these viruses.

Essentially, these viruses are defined by the fact that, if we put them in tissue culture in a test tube with indicator cells, they will damage the cells. This shows kind of an essentially near-normal cell culture, but you can see appearing in this cell culture these few abnormal cells picked up by differential staining. One can see what a normal culture essentially looks like without those cells or if exposed to blood cells from a normal person. If we take that same culture from a patient that has one of these neuropsychiatric illnesses and watch it over time, we can see this absolutely spectacular formation of foamy vacuolated cells that fuse together, and you can see this bizarre looking cell.

This type of virus is very damaging to these cells, providing we make the effort to allow it to grow in culture with these cells. So, the viruses, even though they are not seen by the immune system, under the appropriate conditions can be very damaging to the cells that they infect.

I'll mention that we've been working on this for a long time. Back in 1991, we had such a culture from a patient who still has Chronic Fatigue Syndrome. This was a lady in Los Angeles who worked as a health care worker and basically became sick with a typical chronic fatigue-like illness. Her virus was fortunate in the sense that it was more intact than many of the viruses you do see, and by using an electron microscope and looking at the infected cells from cultures, we could begin to see particles that were indicative of a virus.

These are pretty typical viruses that generally look like the herpes virus, that would include cytomegaloviruses, Herpes Virus 6, Herpes Simplex Virus. These other, larger units are the types of viral materials that viruses use to assemble themselves. So here we had a culture from a patient and it looked as if it might be a herpes virus, yet when we did all the various tests for [HHV], it did not show to be a normal human herpes virus. Rather, we found it was something different. We proceeded to do molecular studies on that virus and essentially this summarizes some of the studies on it as well as results of the molecular studies.

It produced, as I said, vacuolated cytopathic effects in humans and as I indicated earlier, even in animal cell lines—cat cells, even some insect cell lines. It looked like herpesvirus-like particles. This polymerase chain reaction is a very sensitive molecular technique that was used and that gave us portions of the virus genome and when we sequenced one portion it showed some relatedness to human cytomegalovirus, partial--50%--similar but not really human cytomegalovirus. When we extended that study and the sequence analysis, and had sequence analysis available for African green monkey Simian cytomegalovirus, it was apparent that we had 90 - 95% relatedness of parts of that virus to this African green monkey-derived cytomegalovirus. For those people who can appreciate the numbers, this is a kind of quantitative analysis that shows a measure, either by FASTA score or BLASTN score, a measure of the relative relatedness of this virus to human cytomegalovirus. The FASTA score was 348. More closely related to the cytomegalovirus from Rhesus monkeys, a score of 1000. But the highest of all with African green monkey viruses, referring to the simian cytomegalovirus. The BLASTN score shows powers to the tenfold, and 10 to the 245 is an unbelievably high number. Without any equivocation then, we can say that this virus came from African green monkeys, simian cytomegalovirus.

It was not the same because it had changed [mutated, evolved], but essentially, that is where it came from. I was able to publish this in this article, definitively stating [that] the African green monkey origin of the stealth virus isolated from this patient was the Chronic Fatigue Syndrome. It was on this basis that I could make the understatement, if you want, that concern should be given to the fact that we have been using African green monkeys to make polio vaccines and that should be looked into as a potential source of these viruses in the community.

The whole issue of using monkeys relates to the issue of the prevention, which has been effective, of polio. As you can all recall in your lifetime, the polio vaccine program began around 1954. Dr. Jonas Salk devised a protocol for developing an inactivated polio vaccine. He used Rhesus monkeys at the time and his vaccine was inactivated. Competing with Dr. Salk was Dr. Albert Sabin and his approach was to use live attenuated or modified polio virus that was grown as live virus whereas Dr. Salk was using formaldehyde to inactivate his virus and required large amounts. It had to be injected and took some time to work. Dr. Sabin had the advantage of using live virus required only to be taken on a sugar cube, worked very fast and was clearly a preferable vaccination protocol from the point of view of inducing anti-polio immunity.

About 1960, it was realized that the choice of Rhesus monkeys had a major problem. They were commonly infected with a virus called Simian Vacuolating Virus, SV-40 or Simian Virus 40, a type of small DNA virus. Realizing this, a major switch was made very abruptly to move from Rhesus monkeys to African green monkeys. At the same time, the switch was being made to go from an activated vaccine to a live vaccine, whereas in the initial choice of Rhesus monkeys--the initial evaluation of vaccines--there was a major concern of potential contaminants and so forth. That concern was not addressed as aggressively because people do not want to interrupt the vaccination program, yet throughout the 1960's there were repeated reports to raise concerns that the use of fresh animal monkey kidney cells with no inactivation process was going to potentially lead to problems.

I've taken three quotations from eminent people here. Dr. Hilary Kroprowsky [said] "As monkey kidney tissue is host to innumerable simian viruses, the number found varying in relation to the amount of work expanded to find them, the problem presented to the manufacturer is considerable, if not insuperable. As our technical methods improve, we may find fewer and fewer lots of vaccines that can be called free of simian virus." This was dated in 1961 and it was the concern at that time that there could be atypical viruses.

This concern was discarded in some regard because the vaccines were in production, the children were receiving it, there was a push into this program. [The concerns] continued, however,. [They were addressed] in 1968 by Lederle (which has now become American Cyanamid or now American Home Products). The person representing the vaccine manufacturer was referring to a discussion with Dr. Roderick Murray, who was then the head of the Food and Drug Administration Regulatory Affairs, that there were some concerns at Lederle about a possible requirement barring the use African green monkey kidneys as a substrate for the growth of attenuated polio viruses. Dr. Murray had stated that the adventitious agents that Dr. Kendall Smith [wa]s presumably detecting by his technique was of little consequence for an oral preparation in that such a large experience exists with the use of oral polio vaccine without any evidence of trouble relating to these agents.

So, politically, the process at that time was essentially to say, look we've been using these vaccines, people could raise concerns that there might be contaminants but clearly nobody is getting acutely sick as a result of these vaccines, so let's not trouble the system, let's not pursue it. That attitude was in 1968 still persisted. People like Dr. Kendall Smith were identifying agents, other people were identifying viruses in these vaccines and it came to an issue in 1972 when 11 monkeys were put aside [in a joint FDA-Lederle study], not to make polio vaccine, but to see what might grow out from the kidneys that might otherwise be used for polio vaccine. All 11 monkeys studied demonstrated the presence of CMV like agents. These monkeys all originated from Kenya over a short period of time, and 7 of those monkeys would have passed their existing test standards.

In other words, only 4 of those CMV viral isolates would be detected using their standard detection system. So, it was clear that they had a finding and most of the rest of this contingency plan dealt with what response Lederle would take if in fact the FDA were to disclose this information and require some change in the use of African green monkeys.

Unfortunately, there was no response at all from FDA, but more pertinent to the issue, there was no disclosure of this to the scientific community. Again, for various reasons which I don't need to go into, but it was still a persistent issue because one year later in 1973, correspondence from American Cyanamid, being concerned that the [FDA] was taking longer with their vaccine approval and perhaps were going to give preference to an alternative vaccine made in the human cell lines, the argument was, if the bureau wanted to restrict us, they should bring up the subject of cytomegalovirus in our substrate (i.e. African green monkey kidney tissue) which they have not done even though they have told us the monkeys in the collaborative study performed in 1972 were all positive for this agent.

So we have, unfortunately, this clear demonstration of something going wrong in the public health system. Primarily what went wrong was an unwillingness in the regulatory system to bring this information to the scientific community. If society as a whole had endorsed the continued use of monkeys even though they had cytomegaloviruses in them, one would expect that, that society's perspective and can suffer the consequence. It's when this information is withheld and not disclosed that one has reason to be concerned. One can now look back with some real concern at what has occurred over the last 30 years or more using this kind of vaccine with this information not being openly discussed.

It's not that easy; I can tell you that if it were just a straight forward virus perhaps one could detect it. There are differences between the stealth viruses and regular viruses. I've had continued discussions with people at FDA, American Cyanamid, [and] recent communications with people doing the testing in American Cyanamid. To quote them specifically, they still not infrequently detect cytomegaloviruses, but they certainly take concerns now to avoid cytomegaloviral contamination - but it may be a little bit too late. The horse is already out of the barn. The viruses are in the community.

There are other concerns about the issues that we have raised about fragmented genomes. The representative from FDA even a few weeks ago was saying that, no, they still do not want to test the vaccines for cytomegalovirus because if they find a fragment, they won't know how to interpret it and they prefer to do nothing. There is a basic difficulty with these viruses. To show it here, if this is our friend, Human Herpes Virus 6, we can see in this cell relatively intact viral particles that develop before the cell undergoes a major cytopathic or damaging effect. When we look at a typical stealth viral infected cell we often see this appearance which is very degenerate, foamy vacuolated cell. There's a lot of material that is virus like but it hasn't formed itself into an intact, complete virus. And you get rather these incomplete viral forms. Still enough to cause cytopathic effects, and one would have thought that this would certainly be of cause or concern. [But] to be told that one does not want to look at vaccines because one might see only a fragment of a virus is not particularly satisfying.

There have been public health approaches to this problem, primarily to recommend a switch from live polio vaccine to split protocols, inactivated followed by live, to increase the production of inactivated, then bringing the inactivated one in totally, but this is a very slow non-response to what could be considered a much more urgent public health problem in terms of vaccines, or even a much larger problem in terms of the nation's blood supplies, individuals who can get infected from other individuals and so forth.


What I'd like to do in the second phase is emphasize to you some of the diseases that can be associated with these viruses.

Now I've purposely chosen some of the more severe cases. I can certainly talk to you about the young children we see that have Attention Deficit, Turret Syndrome, failing in school, who have signs of a modest encephalopathy. We don't get the occasion with those individuals to look at the brain tissue and so forth, and also, since I've presented these cases to CDC and FDA I want to put you in the same situation as they've been put in to see cases that I think any one of [which] is so compelling that they ought to evoke a major public health response and, yet, each of these cases has been discarded as something fitting for a wastebasket. They are unusual cases, but why bother [seems to be the CDC's and FDA's attitude].

The first case in this area is a lady from Palm Springs, a school teacher. I use this word "dysphasia", difficulty in speaking, but that underestimates her initial problem and her later problem. So, she worked in the school in Palm Springs and, I guess, in early 1989 she made spelling mistakes in sending a note home with her pupils and this led to the school administration getting on to her case. She was under a lot of stress. She saw therapists and basically had to switch schools, became a part-time kindergarten teacher, later still had difficulties and was somewhat relieved when she finally went to a neurologist and the neurologist, though not finding any major signs, found that she lost her sense of smell and went ahead and did some other tests. At that stage though, she started to really deteriorate in her ability to speak, identify things, and she also lost her ability to draw clearly and this was her attempt as a person who, I think, she was in her thirties at the time, all of a sudden found herself unable to draw a clock, a house and so forth. She was then subjected to neurologic examination. This technique called magnetic resonance imaging—you can see the heightened white area around that ventricular part of her brain. It was clearly abnormal. Another way of looking at the brain, you can see the same white areas around the ventrical regions. So she was referred to USC to try to understand what was the process occurring in this poor lady.

They went ahead and did a biopsy of that area. This shows where a very fine needle, and there is a small black area which is some small air entrapment and for those in the front you may see a very small rounded black area also, a small piece of brain tissue was removed and referred to us to look to see if there was a leukemic process, if there was some kind of conventional viral infection, what was going on. This was tissue that came to the lab and, the first comment to make, even at this level, is that it doesn't show the typical inflammatory reaction of lymphocytes, which, if it did, it'd be essentially a blue looking tissue because lymphocyte stains blue. On higher magnification there was essentially nothing very much to pick out by light microscopy—no cancer, no inflammation, would be perhaps discarded as essentially normal.

But using that molecular technique I referred to, polymerase chain reaction, we had evidence, that there was some kind of virus in this lady's brain, and when we spent a lot of time doing electron microscopy, we could see, and this is a glial cell, glial fibers, on the top there you can see those vacuoles of lipid filled vacuoles as in the bottom, a lot of lipofuscin type material, which is degenerate material from an aging cell and a few viral particles that we could see in other parts of the section. So, it was very clear that this lady did, in fact, have a viral infection, but it was not a typical, conventional virus. This lady became ill in 1989. She has steadily deteriorated over the last several years and for the last 2 years has been in a nursing home in Palm Springs. This is now her MRI and her brain is markedly atrophied, degenerated and she's quadriplegic, essentially requiring feeding, assisted ventilation. Only her husband has stayed by her and when comments are made, the neurologist doesn't like to visit the nursing home. One can see how these patients, from being so prominently worked up, hav[ing] brain biopsies in a major medical center, finish up falling through the cracks to lay abandoned in nursing homes.

If there was only one patient, one could say, yes, well, things happen, we don't know about it. But there were many. I have presented 12 cases to FDA. Another one, once again from this area, was a 30-year-old dentist who worked in Bakersville, she—I guess I could date it back to mid-1995—she changed in her whole personality, from a vibrant young person to somebody suffering personality disorder, had severe headaches, tried to do so many things to revitalize herself: joining clubs, lost her job at one position where she was working, got another job at a dental practice but failed to turn up for work, and only towards the nine months or so into her illness did she finally call her mother for help. Her mother had her go to various physicians and, as with so many of these people when there's alteration in the level of consciousness and there's this abnormal behavior, the first diagnosis is a psychiatric illness and they're admitted to a psychiatric hospital. She deteriorated further there and it was clear that she had organic brain disease. She actually went ahead and had a brain biopsy and it showed again this lack of any inflammatory reaction. By regular microscopy though we could see these markedly vacuolated cells with degenerate nuclei, so we again had clear evidence of some pathology and the electron micrograph again showed these very characteristic vacuolated degenerate cells. Now this lady became so comatose that she was unresponsive to pain stimulation. I would see her, she would spend only moments trying to engage who I was, what I might be doing. I'm happy to tell you that she has shown quite remarkable recovery from that. I can discuss with her things, though she still has many of the features that we associate with Chronic Fatigue Syndrome, particularly poor memory. It's very unlikely that she will ever go back to work and, again, nobody can fully evaluate who she was before to where she is now.

I could go through more and more of these cases but I wanted to present this one. This one's a gentleman who came into to Los Angeles County hospital with a two week acute illness with behavioral changes. He was reluctant to come in. Again, in the emergency room, they decided that he probably had a psychiatric illness. They sent him to a medical ward, there were abnormalities in his MRI at the time. He did go through the process of slow recovery, rehabilitation convalescent hospital, told to come back for rehabilitation. When he came back he was told he was still too sick, stay at home . He basically would have a number of episodes--just to recount two of them--he came back to the emergency room complaining of pain; they asked when he'd last gone to a bathroom and, since it was a few days, was given an enema for constipation; another time he would drive his car and get totally lost and finally, 45 minutes beyond his expected exit, he crashed the car. He just gave up. Admitted to a hospital, they would suture his lacerations, but nobody would ask why this 30-year-old person was in such a state. How could he have ever been there and why wasn't somebody caring for him? He finally had an exacerbation, became comatose, was taken to the hospital, again had a brain biopsy, and died. His brain biopsy showed the same characteristic cells and, what was interesting in this person as an additional complication, around the blood vessels there were damaged blood vessels and he had evasculitis. Again, I don't want to be overly critical, but his death certificate read heart failure because they thought they might have missed something in terms of neurologic exam. The people that were most concerned were the nursing staff on the ward because they realized that medicine didn't have anything to offer this individual and that this poor individual slipped through the cracks, having died from what is essentially an unexplained illness [though] every indication is that he had a viral infection.

There's only one other patient whom I have this in vitro culture showing viral particles. This is a lady who, I think, when she was 19, came into County Hospital. They saw her and admitted her because they thought she was schizophrenic. She showed some response. They changed the diagnosis to manic depression. Four years later she became acutely comatose and was admitted to County Hospital. Primarily because of cerebral spinal fluid, the fluid surrounding the brain and the spine, did not show any evidence of inflammation, they ascribed her illness not to a viral infection, but to a drug overdose. This woman became comatose and has never recovered from her coma. And if one needs any justification for doing the work we're trying to do, it's to go and see these people who have been essentially been year after year in a comatose stage with every indication of having a viral infection and yet not meeting current criteria and not fitting into established existing diagnoses.

Now all of these papers have been subject to publications. There is this top one, the Genetic Instability, the Fragmentation of the Viral Genome. There's this person who died—fatal case. The other ones where these, actually three patients but having a severe stealth virus encephalopathy following a chronic fatigue like illness. And this last lady with a bipolar psychosis. So they've been presented out there. These cases along with several others, one would have thought would have been sufficiently compelling to evoke a major public health concern, particularly since in two of them we have very clear evidence that the virus is African green monkey cytomegalovirus and therefore can be linked directly to the use of vaccines. But, unfortunately, we're still having an uphill battle, which, again, as I stated, this talk is real encouragement I have that Dr. Anderson has, in fact, identified another group of patients who will come through with some of this illness.

I think for those who may be having this illness or having friends with it, I'd like to provide a couple of explanations that will give you a sense of the broad basis of this dysfunctional brain syndrome and why I see Chronic Fatigue Syndrome as just part of a very broad spectrum.

Essentially the hypothesis we're working on is that stealth viruses can be implicated as contributing factors to a wide range of neuropsychiatric illnesses: Autism, Attention Deficit, Occupational Defiance, Turret's Syndrome in children, Chronic Fatigue Syndrome, fibromyalgia, Multiple Sclerosis where it can initiate the illness and then complicated by autoimmune responses, and so forth. The reason that this would make sense is because the brain, unlike other organs in the body, has a very selective localization of its functions and the brain's function is essentially to respond to different stimuli.

And if we take a normal brain, we get appropriate responses. In an abnormal brain we can have inappropriate response, for example, with a lot of brain illnesses, it can trigger a sense of fatigue. If that's a predominant symptom, people will be classified as Chronic Fatigue Syndrome. Fibromyalgic patients have a lower threshold for pain and so they'll feel pain in their back and their jaw and muscles and joints, so they'll be the predominant symptoms in what we call our affect—our mood. If we become depressed, then it will become depression. If we don't think clearly and we can no longer make rational thought processes, then having cognitive deficits, then people will use labels, like schizophrenia, and if we have parts of our body normally regulated by the brain and now being dysregulated, for example, bowel function, we can have things like Irritable Bowel Syndrome. What is clear as I get a chance to see these various patients is that very few patients fit into a single category and many of these patients, if you look at them, have a range of these symptoms and often they vary with time and it depends on who they see.

If they see a psychiatrist, they'll be called one thing, a neurologist something else and it's clear that this type of illness process in the brain, clinical neuropsychiatry has a long way to go to understand that, in many of these patients, viruses may be involved and [I am] particularly concerned for those people who are given a psychiatric diagnosis because unfortunately nobody ever recovers from a diagnosis of schizophrenia. So, if I go on a little bit more about this disease process, obviously we're trying to learn a lot about it.

I mentioned these viruses can grow in animals. We don't see any obvious personality changes in a mouse or a rat, but we do see it if we take cats. We chose cats because a number of the Chronic Fatigue Syndrome patients reported that their household pets were showing behavioral changes, with neurological illness or other changes that were confusing to the veterinarian and they wondered if the disease may have passed between them. So we actually took the virus that we had grown from our chronic fatigue patient and put the virus into the cats and wondered what would happen, and I can tell you, from friendly, frisky, happy-go-lucky animals they became reclusive, irritable, shied away from bright lights, rubbed their backs and necks against the cage making those areas quite hairless, were very difficult to handle, and so forth. We looked in the brain, and again we find the subtle changes but not obvious inflammation in the brain. If we looked at it by electron microscopy we can see viral particles causing this brain illness. And the benefit from the cat model was that we could see what else was going on in the animal. And this gave a clear indication that the illness was not confined to the brain. If we looked at the animals, many of them would have this gingivitis and it's an unfortunate point of our Chronic Fatigue Syndrome patients. Many of them do in fact have their teeth excised, they get a gingivitis. We've seen people with large salivary glands where the virus can be resident. It comes out and seems to find a little nidus in the soltace between the gum and the tooth. We see this being very important in terms of transmission. We've even given patients toothbrushes and then taken the toothbrush and cultured viruses from it. Again, you get the sense that I see this as a very severe potential spreading disease that I'm not really surprised at all that Dr. Anderson has come up with evidence of direct transmission when you see this kind of occasion in animals.

If we look at the various [cat] organs, we know that there is infection in the liver and in the bowel. We know that the liver is not dysfunctional in the sense that there's not a lot of cellular destruction. They don't become jaundiced but we also realized that the ability of the liver to detoxify—the normal toxins that would come from the bowel—were being impaired, that the bowel would have leaky bowel syndrome, that we could aggravate the brain damage as a result of added toxins coming though the bowel not being fully detoxified. So we have a good understanding of this disease process in the animals.


Now, with all that I want to talk a little bit about the spread of infection and then a little bit about the therapy. As I mentioned, Dr. Anderson now has examples of people that, over the last five or six years, unfortunately have come across the same type of situation without being able to molecularly define the virus. We had a family in Florida where the wife has Chronic Fatigue Syndrome and she attends various groups. She knows, but her husband doesn't admit, the fact that he has Chronic Fatigue Syndrome also. Their mother, the grandparent, has Parkinson's disease, and their son is called schizophrenic. They know, as a family, they have the same pervasive illness. When I talked to the neurologist, he will be apologetic about the diagnosis of Parkinson's, it's just a label. He knows that. I did not get an apology, though, from the psychiatrist; it was basically the argument, "well, the person benefits from being called schizophrenic," but the other one is that medicine demands that we categorize people with disease-related groups and there is no [insurace] reimbursement if we start saying we do not know what's going on. Very sad. Fortunately, this child has pulled out from schizophrenia and I got a card from him that he got married, probably a year ago.

This idea of diverse clinical manifestations is confusing to the typical clinician who would expect the same symptoms in husband and wife as opposed to appreciating the fact that brains are different, [and that] locations in brains that can be infected can be [affected in] different [ways]. This whole issue of why some people get infected and others don't, I think we can relate to the presence of antibodies that cover a much broader range of antigens in the cellular immune system. I'm keen on observing and trying to prevent the spread of infection, if it's already in an infection in a family, by seeing who else in the family has antibodies that could neutralize the virus and those who don't have it. I think that something should be done to protect those individuals.

We know from animals as well from human studies that [viruses] can be passed orally, sexually and transplacentally. We're looking at the moment at two twins in Tarzana Hospital who were born premature with brain damage


I come to this one and again I think I've emphasized to you the sense there's a big problem here. There's a problem in its recognition, its acceptance and so forth. It's not very pleasant to be told that there are problems, that people made mistakes and so forth. I'm optimistic and hopeful that the unconventional nature of these viruses holds them open to therapeutic endeavors that conventional viruses may have resisted. So, I do therefore have a real interest working with Dr. Anderson and others to evaluate different therapies. If I list the approaches here, they certainly begin with antiviral therapies. There's a lady I['m going to visit] in Palm Springs who is on gangcyclovir. Some of the sick patients have had foscarnet. So, we're trying to evaluate how useful these compounds are. And we also have in the test tube an inhibitor which I gave the name Epione. We do not yet have an antiviral agent.

What can people do? It's clear that sensory input can aggravate certain symptoms and they should be avoided. Other sensory input can ameliorate some of the symptoms, and patients soon work out what they can take and what they can't take, what's useful and not useful. Even this placebo benefit to some patients is quite useful to at least try to boost themselves beyond what medicine can do. Reducing exposure to toxic factors and food adjustments is clearly important and people soon realize this. The number of patients with this illness who will move away from alcohol and so forth is very clear. The detoxification pathways, if they're not working, the liver is impaired, I think one can help reduce the added burden of these toxic agents. Though I haven't emphasized it too much, as a systemic illness, there are other organs that can be damaged, oftentimes altering immune responses against the thyroid, the pancreas, other organs, and they need to be looked into by a clinician. It's very hard to find the appropriate clinician who can address all of these problems for these patients and oftentimes it's the patients who can learn more about this illness than any one particular physician. I did want to go through these because one reason for being here is to say, "What kind of response can be made to Dr. Anderson's description and finding of this situation?"

I think it's clearly very important that we extend beyond the four patients that we have so far and culture many more people. Those whom we have cultured we'd like to reculture. We'd like to see how many people have no symptoms and those who do have symptoms, to understand this whole process so that we can understand how somebody might be infected without symptoms and so forth.

We need, because so far I can tell you that a cytopathic infected culture is very convincing but it doesn't have the hard currency that sequencing of a virus has. A major challenge for us it to take the viruses that we have cultured and clone out a portion of that virus and sequence it. I mention that we have the facility, we don't have resources yet but that's a very high priority because, once we can establish where the virus with this outbreak has occurred, what its portions of genetic sequences are, we can than have a molecular probe that we can do a much wider survey with then we can just through cultures.

I mentioned the idea of testing family members. Again, I am very sensitive having seen this illness. I think that many of you should be tested to know where you stand in relationship to this kind of an epidemic. I think we should go back, though again, they are expensive, difficult, painful for the animals and for the animal caretakers, I think it's important to look at this particular virus and see what it does do in animals and have the animal model available for evaluating antiviral therapies and finally, since there were so many patients that Dr. Anderson has seen, I think it's appropriate to create the treatment groups so that we could have two people in the one family and have one person take one type of therapy and see what happens to the other person by comparison. I think this in an important opportunity to make some real headway with this kind of an illness.

I want to acknowledge Dr. Anderson. It was very gratifying for me when first he identified the outbreak and then made contact and secondly when he came to the lab and saw the need to make a move in this direction. I think we have the instincts and the ability to do it though we certainly, absolutely need your help if we can benefit, not only this community, but truly a much larger community out there. We do need a lot of help with this kind of an illness.

The original transcripts of this videotaped lectuer were prepared by Carolyn Viviani and appear at the CCID website.

Melissa Kaplan comments:
The outbreak referred to by Dr. Martin is the recent stealth virus cluster outbreak in the Mojave desert area on Southern California. Despite the continuing incidences of such clusters, the CDC continues to insist that:

    a) CFS is not a virus;

    b) CFS is not contagious (ignoring the fact that they also consider it a Priority One emerging disease);

    c) CFS does not have a very high prevalence in the general population (ignoring the fact that they also consider it a Priority One emerging disease);

    d) CFS does not occur in clusters; and

    e) CFS does not run in families.

Does it bother anyone else besides me that the FDA is the arbiter of which vaccines, drugs and additives are safe and which are not, and that the CDC is the arbiter of who is sick and who is not?




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