rational expectations for chelation: thimerosal & ethylmercury

[Guest guest]

The concept of ASD "subgroups" seems especially important. Here are some

subgroups that come to mind this morning:

1. There are genetic autisms, and I'm sure that not all of them have

been identified.

2. There are infection-related autisms wherein the child has lab-test

signs of chronic-active infections, often accompanied by signs of impaired

hematopoietic processes, occasionally accompanied by worrisome plasma &

urinary amino-acid profiles.

3. As first elaborated by Edelson, there are autisms related to heavy

metals and to chronic detox.

4. As elaborated in the recent thimerosal/autism paper, there are (likely

to be) autisms caused by ethylmercury injections during vaccinations. As

a co-author of that paper and as an analyst of ASD immune panels, my own

hunch is that many thimerosal-damaged kids also partake of item-2 and/or

item-3 hereinabove.

5. Some thimerosal-damaged ASD-children are likely to have been transiently

susceptible (eg, by an infection that caused low-glutathione at the time

of one or several thimerosal injections).

These considerations have implications for chelation therapies. We shall

be learning what proportions of chelated kids:

(a) show no improvement;

( show perhaps a little improvement;

© show significant improvement but remain very ASD;

(d) show wonderful, even amazing improvement.

The immune panels I have critiqued indicate that a size-unknown subset

of ASD kids are in category-2 hereinabove. Such kids seem likelier to have

been susceptible to ethylmercury neurotoxicity when injected with thimerosal

and likelier, via hepatobiliary dysregulation, to also participate as category-3

kids. The extent of their improvement in response to chelation may depend

upon having successfully addressed the child's underlying infections and/or

burdens of other heavy metals.

There may be a thimerosal-injured subgroup that does not respond to

chelation. This subgroup is probably linked to category-5 hereinabove;

and the ASD traits would have been induced as a result of extreme susceptibility

at the time of thimerosal injections -- in conjunction with ethylmercury

impairments of microtubule function during critical periods of synaptogenesis.

This subgroup of kids may be unresponsive to chelation therapy even though

their ASD-related CNS-lesion was induced by physician-injected ethylmercury.

I have a vision: 10,000 parents will soon have tried chelation. There

will be a distribution of responses in accord with categories a

thru d hereinabove. Most parents will not be so lucky as to have

a category-d child. Parental expectations -- their hopes about chelation,

their comparison of costs versus potential benefits -- ought be tempered

by a realistic appraisal of ASD subgroups and how those subgroupings (i)

point towards etiological processes that affected how the infant or toddler

handled his or her ethylmercury, and (ii) also point towards rational expectations

of what chelation therapy may do for any given ASD child.

[Guest guest]

Science is DEFINED as the simplest theory consistent with the facts.

Since this discussion is headed away from that into the byzantine complexity

characteristic of unscientific AMA medicine I'll let others continue it.

Personally I stick to science and its practical applications.

Andy Cutler

[Guest guest]

[ ] rational expectations for chelation: thimerosal & ethylmercuryThe concept of ASD " subgroups " seems especially important. Here are some subgroups that come to mind this morning: 1. There are genetic autisms, and I'm sure that not all of them have been identified. 2. There are infection-related autisms wherein the child has lab-test signs of chronic-active infections, often accompanied by signs of impaired hematopoietic processes, occasionally accompanied by worrisome plasma & urinary amino-acid profiles. 3. As first elaborated by Edelson, there are autisms related to heavy metals and to chronic detox. 4. As elaborated in the recent thimerosal/autism paper, there are (likely to be) autisms caused by ethylmercury injections during vaccinations. As a co-author of that paper and as an analyst of ASD immune panels, my own hunch is that many thimerosal-damaged kids also partake of item-2 and/or item-3 hereinabove. 5. Some thimerosal-damaged ASD-children are likely to have been transiently susceptible (eg, by an infection that caused low-glutathione at the time of one or several thimerosal injections). These considerations have implications for chelation therapies. We shall be learning what proportions of chelated kids: (a) show no improvement; ( show perhaps a little improvement; © show significant improvement but remain very ASD; (d) show wonderful, even amazing improvement. The immune panels I have critiqued indicate that a size-unknown subset of ASD kids are in category-2 hereinabove. Such kids seem likelier to have been susceptible to ethylmercury neurotoxicity when injected with thimerosal and likelier, via hepatobiliary dysregulation, to also participate as category-3 kids. The extent of their improvement in response to chelation may depend upon having successfully addressed the child's underlying infections and/or burdens of other heavy metals. There may be a thimerosal-injured subgroup that does not respond to chelation. This subgroup is probably linked to category-5 hereinabove; and the ASD traits would have been induced as a result of extreme susceptibility at the time of thimerosal injections -- in conjunction with ethylmercury impairments of microtubule function during critical periods of synaptogenesis. This subgroup of kids may be unresponsive to chelation therapy even though their ASD-related CNS-lesion was induced by physician-injected ethylmercury. I have a vision: 10,000 parents will soon have tried chelation. There will be a distribution of responses in accord with categories a thru d hereinabove. Most parents will not be so lucky as to have a category-d child. Parental expectations -- their hopes about chelation, their comparison of costs versus potential benefits -- ought be tempered by a realistic appraisal of ASD subgroups and how those subgroupings (i) point towards etiological processes that affected how the infant or toddler handled his or her ethylmercury, and (ii) also point towards rational expectations of what chelation therapy may do for any given ASD child.

[Guest guest]

Re: [ ] rational expectations for chelation:

thimerosal & ethylmercury

>

>In a message dated 7/18/00 9:04:30 AM, aspergerian@... writes:

>

><< 2. There are infection-related autisms wherein the child has lab-test

>signs of chronic-active infections, often accompanied by signs of impaired

>hematopoietic processes, occasionally accompanied by worrisome plasma &

>urinary amino-acid profiles. >>

>

>These are likely secondary to heavy metal intoxication and thus curable by

>proper chelation, e. g. with lipoic acid for mercury.

>

><< The immune panels I have critiqued indicate that a size-unknown subset

>of ASD kids are in category-2 hereinabove. Such kids seem likelier to have

>been susceptible to ethylmercury neurotoxicity when injected with

thimerosal

>and likelier, via hepatobiliary dysregulation, to also participate as

>category-3

>kids. The extent of their improvement in response to chelation may depend

>upon having successfully addressed the child's underlying infections and/or

>burdens of other heavy metals. >>

>

>This begs the question of cause and effect.

>

>Cause: heavy metal tox.

>

>Effect: messed up immune system.

>

>This is the way it is with adults (many of whom have before and after detox

>immune panels showing great improvement) so it is the scientific hypothesis

>for children until such time as someone runs immune panels before

vaccination

>and after on children who turn autistic and verifies which comes first.

>

>Andy Cutler

>

>------------------------------------------------------------------------

>Missing old school friends? Find them here:

>1/7079/9/_/705339/_/963938628/

>------------------------------------------------------------------------

>

>

[Guest guest]

Theresa

Am curious about genetics of autism. Lots of moms say since birth. I have a friend who swares pitocin did them in, so this would make that connection. Does pitocoin in IV drips contain thimersol?

Kathy

[ ] rational expectations for chelation: thimerosal & ethylmercuryThe concept of ASD " subgroups " seems especially important. Here are some subgroups that come to mind this morning: 1. There are genetic autisms, and I'm sure that not all of them have been identified. 2. There are infection-related autisms wherein the child has lab-test signs of chronic-active infections, often accompanied by signs of impaired hematopoietic processes, occasionally accompanied by worrisome plasma & urinary amino-acid profiles. 3. As first elaborated by Edelson, there are autisms related to heavy metals and to chronic detox. 4. As elaborated in the recent thimerosal/autism paper, there are (likely to be) autisms caused by ethylmercury injections during vaccinations. As a co-author of that paper and as an analyst of ASD immune panels, my own hunch is that many thimerosal-damaged kids also partake of item-2 and/or item-3 hereinabove. 5. Some thimerosal-damaged ASD-children are likely to have been transiently susceptible (eg, by an infection that caused low-glutathione at the time of one or several thimerosal injections). These considerations have implications for chelation therapies. We shall be learning what proportions of chelated kids: (a) show no improvement; ( show perhaps a little improvement; © show significant improvement but remain very ASD; (d) show wonderful, even amazing improvement. The immune panels I have critiqued indicate that a size-unknown subset of ASD kids are in category-2 hereinabove. Such kids seem likelier to have been susceptible to ethylmercury neurotoxicity when injected with thimerosal and likelier, via hepatobiliary dysregulation, to also participate as category-3 kids. The extent of their improvement in response to chelation may depend upon having successfully addressed the child's underlying infections and/or burdens of other heavy metals. There may be a thimerosal-injured subgroup that does not respond to chelation. This subgroup is probably linked to category-5 hereinabove; and the ASD traits would have been induced as a result of extreme susceptibility at the time of thimerosal injections -- in conjunction with ethylmercury impairments of microtubule function during critical periods of synaptogenesis. This subgroup of kids may be unresponsive to chelation therapy even though their ASD-related CNS-lesion was induced by physician-injected ethylmercury. I have a vision: 10,000 parents will soon have tried chelation. There will be a distribution of responses in accord with categories a thru d hereinabove. Most parents will not be so lucky as to have a category-d child. Parental expectations -- their hopes about chelation, their comparison of costs versus potential benefits -- ought be tempered by a realistic appraisal of ASD subgroups and how those subgroupings (i) point towards etiological processes that affected how the infant or toddler handled his or her ethylmercury, and (ii) also point towards rational expectations of what chelation therapy may do for any given ASD child.

[Guest guest]

In a message dated 7/18/00 3:45:25 PM, aspergerian@... writes:

<< Andy,

I take it you agree with me, ie, that a genetic predisposition towards

chronic infection and immune impairment is easily and accurately documented

by PCR and need not be befuddled by a " discount the genetic influence,

think only about mercury " . Thnx for the clarification.

>>

, please stop the sophistry.

After you add up the known genetic incidence of these conditions and show

that it is similar to the current incidence of autism I will discuss the

issue. Until then, the ball is in your court to do some homework, and the

only scientifically valid theory I know of is that the immune impairment of

autism is caused by the thimerosal rather than being causal of thimerosal

poisoning.

I try not to put words in other people's mouths and I would appreciate the

same courtesy in return. We may end up disagreeing profoundly on this issue

or we may surprisingly end up in agreement but let us get there through

proper collegial debate, not the kind of stuff QuackWatch tries to pass off

as legitimate argument.

Andy Cutler

[Guest guest]

I cannot agree with the idea that all postnatal immune impairments are

initiated as a result of heavy metal exposure. Some immune impairments

have genetic substrates (eg, 1,3), even as postnatal Hg exposure might

exacerbate tendencies towards impaired immunity. Here are several examples

of genetic predispositions towards chronic infection.

1. The first cite links several MHC alleles with effects from EBV.

2. The second citation links several of those alleles with autism.

3. The third cite links a certain HLA genotype with seizures and CMV

infection.

4. The fourth cite links chronic CMV with "common variable immune deficiency"

and is followed by a comment about genetic and/or non-genetic (ie, acquired)

forms of CVID.

5. The fifth cite links another HLA allele with tendencies to avoid

a certain chronic infection.

Also, whenever I hear inquiries about pitocin, my first reaction is,

Why was the pitocin necessary? In other words, what was occurring (or what

had occurred) so that pitocin was necessary?

1: Arthritis Rheum 1999 Jul;42(7):1485-96

Synovial Epstein-Barr virus infection increases the risk of rheumatoid

arthritis

in individuals with the shared HLA-DR4 epitope.

Saal JG et al.

OBJECTIVE: To investigate the presence of the Epstein-Barr virus (EBV)

in

rheumatoid arthritis (RA) synovium and its correlation with the HLA

genotype in

an attempt to elucidate the role of EBV in the pathogenesis of RA.

METHODS: EBV DNA/RNA was investigated by polymerase chain reaction

(PCR) analysis of synovial tissue from 84 patients with RA and from 81

patients with non-RA arthritis

(controls) and was correlated with the patients' HLA genotype.

RESULTS: EBV DNA and EBV-encoded RNA 1 transcripts were significantly

more frequently present in synovial tissue from the RA patients (29 of

84) than in that from the non-RA

patient controls (8 of 81). EBV DNA-positive individuals had a 5.47

times higher

risk of presenting with RA than did EBV DNA-negative individuals. In

HLA-DRB1*0401,0404,0405,0408-positive or shared epitope-positive

patients, the

risk was further increased (odds ratio for EBV and HLA-DR4 approximately

41, for

EBV and the shared epitope approximately 15) compared with those who

lacked both

EBV DNA and RA-linked HLA genotypes.

CONCLUSION: EBV seems to function as an environmental risk factor for

RA, particularly in patients with the RA-linked HLA-DRB1 alleles.

2. J Neuroimmunol 1996 Jul;67(2):97-102

Strong association of the third hypervariable region of HLA-DR beta

1 with autism.

Warren RP et al.

We reported that the major histocompatibility complex (MHC) including

the null

allele of the C4B gene and the extended haplotype B44-C30-DR4 is associated

with

autism. We report now that the third hypervariable region (HVR-3) of

certain DR

beta 1 alleles have very strong association with autism. The HVR-3

of DR beta 1*

0401 or the shared HVR-3 alleles DR beta 1* 0404 and DR beta

1* 0404 and DR

*0101, was expressed on extended haplotypes in 23 of 50 (46%)

autistic subjects

as compared to only 6 of 79 (7.5%) normal subjects. Another HVR-3 sequence,

the

DR beta 1* 0701 allele, was carried on extended haplotypes in 16 (32.0%)

of the

autistic subjects as compared to 8 (10.1%) of the normal subjects.

3: Brain Dev 1988;10(4):256-8

HLA antigens, epilepsy and cytomegalovirus infection.

Iannetti P et al.

Thirty-one epileptic patients, selected from among 900 children with

previous

febrile convulsions and subsequent epilepsy, were typed for HLA antigens.

In 16

of the 31 patients CMV was isolated from the urine shortly after the

appearance

of spontaneous fits; in the remaining 15 patients the virus was never

detected.

All the examined children were typed for 14 HLA-A, 23 HLA-B, 7 HLA-C

and 9

HLA-DR specificities, and compared with a group of healthy subjects.

The HLA-A11 antigen was present in 25% of the children with chronic

CMV

infection and epilepsy, and absent in patients with epilepsy but

without CMV infection

(p less than 0.02). The possibility that the A11 antigen is a marker

of the predisposing

genes for CMV infection in children with epilepsy following FC is proposed.

4: Nihon Rinsho Meneki Gakkai Kaishi 1995 Apr;18(2):247-55

[Chronic cytomegalovirus infection that present specific clinical course--a

case

of a boy with common variable immunodeficiency]. [Article in Japanese]

Wada Y et al.

We describe an 8-year-old boy with CVID and chronic CMV infection. Although

at

onset he was diagnosed as IgA deficiency, 4 years after his clinical

manifestations because compatible to CVID. During his clinical course

he had

suffered from various disorders as follows; AIHA, interstitial pneumonia,

hemophagocytic syndrome, chronic gastroenterocolitis and so forth.

At the age of

8 the PCR of CMV-DNA of biopsy specimen from colon, lung and bone marrow

were

confirmed to be positive. Hematological examinations revealed abnormal

cellular

immunity such as decreased CD 4/8 ratio with increased HLA- DR+ CD

8+ T cell,

decrease of absolute blood lymphocytes count and reduced response of

lymphocytes

to blastogenetic agents. These findings brought us to diagnose him

as having

CVID complicated with chronic CMV infection. This case gives us some

impact to

speculate what role CMV infection plays in CVID, Whose etiology

is unknown.

[if a person ventures forth into medical articles about CVID, then

he or she soon

finds that most, but not all such articles focus upon rare genetic-glitches

known

to cause CVID. However, a gung-ho articles junkie soon finds -- after

lots of searching, photocopying, and reading -- that some researchers refer

to acquired CVID. My own research-readings in autism prompted the notion

that many ASD kids may have an

acquired CVID. I've an URL with citations at: http://www.jorsm.com/~binstock/cvid.htm

]

5: Tissue Antigens 2000 Mar;55(3):195-8

HLA haplotypes are associated with differential susceptibility to Trypanosoma

cruzi infection.

Nieto A et al.

We explored a possible role of HLA class II genes in determining the

susceptibility to Trypanosoma cruzi infection as well as in the development

of

chagasic heart disease in a rural mestizo population from Arequipa

(Southern

Peru). HLA-DRB1 and DQB1 polymorphisms were determined in 85 seropositive

(asymptomatic, n=52; cardiomyopathic, n=33) and 87 seronegative individuals.

We observed that the DRB1*14-DQB1*0301 haplotype correlates with

not having T.

cruzi infection in a highly endemic area (OR= 0.26 (0.124.63);

Pc=0.01).

This protective association is a dominant trait. We found no differences

in the

allelic or haplotypic distributions we examined between asymptomatic

and

cardiomyopathic patients in this population. Our data offer indirect

but

compelling evidence that polymorphism in HLA region is involved in

a

differential susceptibility to T. cruzi chronic infection.

[Guest guest]

---Also, whenever I hear inquiries about pitocin, my first reaction is, Why was the pitocin necessary? In other words, what was occurring (or what had occurred) so that pitocin was necessary?---

Well, being the total birth junkie that I am, I have to say that MOST of the time, pitocin isn't necessary at all. It is used in over 50% of births, mostly because of hospital liability issues, and doctors wanting birth to happen on a schedule (M-F, 8-5), which it was never designed to do. I am on a few lists with unassisted birthers (birth at home , no paid attendant), and in the over 100 birth stories I have collected, there is prodromol labor for up to a week before the birth takes place. There is NO way that an ob wants to deal with the uncertainty of mother natures clock. So they blast the babies out before they are done cooking. Also, in over 90% of the births that finish in God's time that I have collected, the babies are born at 42-43 weeks gestation. We are forcing these children to be born TOO early!!! And then injecting them with toxins on top of it immediately following their premature birth.

In all of medicine, I have to say that ob's are the worst, interfering with nature in a way that is despicable. They don't even know what normal birth is anymore.

(proud to have delivered her last babe at home unassisted 5 1/2 months ago, and a 9 1/2 pounder at that :-)

rochester@...--------"Before many can know something, one must know it. I am in revolt against the old lie that the majority is always right." -- Henrik Ibsen--------

[Guest guest]

<< Would this theory then go bye bye in your mind? Andy or Theresa?

Complements being affected by mercury? >>

No. It isn't byzantinely complex. It is plausible but underconstrained by

data, so I would leave it in the realm of possibility but not use it

diagnostically or therapeutically except as a last resort until I found more

information on it one way or the other.

BTW, essentially all proteins in your body have sulfur in them. It isn't

unique to a few special ones.

Andy

[Guest guest]

Andy,

I take it you agree with me, ie, that a genetic predisposition towards

chronic infection and immune impairment is easily and accurately documented

by PCR and need not be befuddled by a "discount the genetic influence,

think only about mercury". Thnx for the clarification.

AndyCutler@... wrote:

Science is DEFINED as the simplest theory consistent

with the facts.

Since this discussion is headed away from that into the byzantine

complexity

characteristic of unscientific AMA medicine I'll let others continue

it.

Personally I stick to science and its practical applications.

Andy Cutler

[Guest guest]

Would this theory then go bye bye in your mind? Andy or Theresa?

Complements being affected by mercury? It does affect the thiols in the complement system.....Dr REed Warrens Study, I was involved in through OHSU. I was told this is a protein of some sort that encodes something to warn the body or to have the body eliminate something like a viral, toxin or fungal that needs to be eradicated, but that this protein is either absent or subnormal or fragile? IT is an AUTOIMMUNE GENE, one of a series of them I was told. Hmmmmmm?

If so, then my husband and I who have null alleles on the c4b are ACTUALLY MERCURY poisined as well OR this is very genetic for us? This then was " inherited " or passed on so to speak to my children with c4b complement FULL aLLELES, but could that be a reflection of OUR POISINING and of OUR COMPLEMENTS being messed with mercury or other metals or other perterbers? To let you know, I have a mouthful of poisin, so does my husband, I was exposed ALL MY LIFE to mercury salts in malathion. When does genetics really come into play here, is this a genetic predispostition to have damage or is this a viral/environmental load that no ones genes will be able to handle? So for instance our scores which were indicitve of the null allele on c4b are actually indicitive of a generational poisining OR this is ALL HEREDITARY? I hope I stated that right, in other words, man's doing vs God's plan? Andy says a score of ABSOLUTELY ZERO was a mistake at the lab, but I have rehearsed this with Dr Burger, and he says, it says what it says, it is a gene that is completely nullified in my son and (possibly) daughter, not working, at all. If with this information I had this before their vaccine series of damages, I would have had every right to refuse vaccines for them ON A MEDICAL BASIS. (not saying everyones case isn't), But particularly them. Notice it says, VIRALS, TOXINS and FUNGALS....these are in vaccines or create the condition becuase of the vaccine. I am frustrated, I want to know really so that my other children without autism will have this information for their reproductive health. No one seems to know, and I am going to find out I guess, the best I know how. I have already told my other daughters without autism to get tested for null allele on c4b before they get married, as well as their partners, now is that fair, or should they never ever visit the dentist or ever get their kids vaccined(of course grandma will say no).

Kathy

[ ] Re: rational expectations for chelation: thimerosal & ethylmercuryI cannot agree with the idea that all postnatal immune impairments are initiated as a result of heavy metal exposure. Some immune impairments have genetic substrates (eg, 1,3), even as postnatal Hg exposure might exacerbate tendencies towards impaired immunity. Here are several examples of genetic predispositions towards chronic infection. 1. The first cite links several MHC alleles with effects from EBV. 2. The second citation links several of those alleles with autism. 3. The third cite links a certain HLA genotype with seizures and CMV infection. 4. The fourth cite links chronic CMV with " common variable immune deficiency " and is followed by a comment about genetic and/or non-genetic (ie, acquired) forms of CVID. 5. The fifth cite links another HLA allele with tendencies to avoid a certain chronic infection. Also, whenever I hear inquiries about pitocin, my first reaction is, Why was the pitocin necessary? In other words, what was occurring (or what had occurred) so that pitocin was necessary? 1: Arthritis Rheum 1999 Jul;42(7):1485-96 Synovial Epstein-Barr virus infection increases the risk of rheumatoid arthritis in individuals with the shared HLA-DR4 epitope. Saal JG et al. OBJECTIVE: To investigate the presence of the Epstein-Barr virus (EBV) in rheumatoid arthritis (RA) synovium and its correlation with the HLA genotype in an attempt to elucidate the role of EBV in the pathogenesis of RA. METHODS: EBV DNA/RNA was investigated by polymerase chain reaction (PCR) analysis of synovial tissue from 84 patients with RA and from 81 patients with non-RA arthritis (controls) and was correlated with the patients' HLA genotype. RESULTS: EBV DNA and EBV-encoded RNA 1 transcripts were significantly more frequently present in synovial tissue from the RA patients (29 of 84) than in that from the non-RA patient controls (8 of 81). EBV DNA-positive individuals had a 5.47 times higher risk of presenting with RA than did EBV DNA-negative individuals. In HLA-DRB1*0401,0404,0405,0408-positive or shared epitope-positive patients, the risk was further increased (odds ratio for EBV and HLA-DR4 approximately 41, for EBV and the shared epitope approximately 15) compared with those who lacked both EBV DNA and RA-linked HLA genotypes. CONCLUSION: EBV seems to function as an environmental risk factor for RA, particularly in patients with the RA-linked HLA-DRB1 alleles. 2. J Neuroimmunol 1996 Jul;67(2):97-102 Strong association of the third hypervariable region of HLA-DR beta 1 with autism. Warren RP et al. We reported that the major histocompatibility complex (MHC) including the null allele of the C4B gene and the extended haplotype B44-C30-DR4 is associated with autism. We report now that the third hypervariable region (HVR-3) of certain DR beta 1 alleles have very strong association with autism. The HVR-3 of DR beta 1* 0401 or the shared HVR-3 alleles DR beta 1* 0404 and DR beta 1* 0404 and DR *0101, was expressed on extended haplotypes in 23 of 50 (46%) autistic subjects as compared to only 6 of 79 (7.5%) normal subjects. Another HVR-3 sequence, the DR beta 1* 0701 allele, was carried on extended haplotypes in 16 (32.0%) of the autistic subjects as compared to 8 (10.1%) of the normal subjects. 3: Brain Dev 1988;10(4):256-8 HLA antigens, epilepsy and cytomegalovirus infection. Iannetti P et al. Thirty-one epileptic patients, selected from among 900 children with previous febrile convulsions and subsequent epilepsy, were typed for HLA antigens. In 16 of the 31 patients CMV was isolated from the urine shortly after the appearance of spontaneous fits; in the remaining 15 patients the virus was never detected. All the examined children were typed for 14 HLA-A, 23 HLA-B, 7 HLA-C and 9 HLA-DR specificities, and compared with a group of healthy subjects. The HLA-A11 antigen was present in 25% of the children with chronic CMV infection and epilepsy, and absent in patients with epilepsy but without CMV infection (p less than 0.02). The possibility that the A11 antigen is a marker of the predisposing genes for CMV infection in children with epilepsy following FC is proposed. 4: Nihon Rinsho Meneki Gakkai Kaishi 1995 Apr;18(2):247-55 [Chronic cytomegalovirus infection that present specific clinical course--a case of a boy with common variable immunodeficiency]. [Article in Japanese] Wada Y et al. We describe an 8-year-old boy with CVID and chronic CMV infection. Although at onset he was diagnosed as IgA deficiency, 4 years after his clinical manifestations because compatible to CVID. During his clinical course he had suffered from various disorders as follows; AIHA, interstitial pneumonia, hemophagocytic syndrome, chronic gastroenterocolitis and so forth. At the age of 8 the PCR of CMV-DNA of biopsy specimen from colon, lung and bone marrow were confirmed to be positive. Hematological examinations revealed abnormal cellular immunity such as decreased CD 4/8 ratio with increased HLA- DR+ CD 8+ T cell, decrease of absolute blood lymphocytes count and reduced response of lymphocytes to blastogenetic agents. These findings brought us to diagnose him as having CVID complicated with chronic CMV infection. This case gives us some impact to speculate what role CMV infection plays in CVID, Whose etiology is unknown. [if a person ventures forth into medical articles about CVID, then he or she soon finds that most, but not all such articles focus upon rare genetic-glitches known to cause CVID. However, a gung-ho articles junkie soon finds -- after lots of searching, photocopying, and reading -- that some researchers refer to acquired CVID. My own research-readings in autism prompted the notion that many ASD kids may have an acquired CVID. I've an URL with citations at: http://www.jorsm.com/~binstock/cvid.htm ] 5: Tissue Antigens 2000 Mar;55(3):195-8 HLA haplotypes are associated with differential susceptibility to Trypanosoma cruzi infection. Nieto A et al. We explored a possible role of HLA class II genes in determining the susceptibility to Trypanosoma cruzi infection as well as in the development of chagasic heart disease in a rural mestizo population from Arequipa (Southern Peru). HLA-DRB1 and DQB1 polymorphisms were determined in 85 seropositive (asymptomatic, n=52; cardiomyopathic, n=33) and 87 seronegative individuals. We observed that the DRB1*14-DQB1*0301 haplotype correlates with not having T. cruzi infection in a highly endemic area (OR= 0.26 (0.124.63); Pc=0.01). This protective association is a dominant trait. We found no differences in the allelic or haplotypic distributions we examined between asymptomatic and cardiomyopathic patients in this population. Our data offer indirect but compelling evidence that polymorphism in HLA region is involved in a differential susceptibility to T. cruzi chronic infection.