Nids

Ablashi et al provide further documentation of HHV6 in MS and CFS (1);
and their study is complementary to the recent findings of Knox,
Carrigan, et al (2). Together, when these studies are joined with V
Singh's HHV6 and MV findings (3), one wonders when neurologists and
psychologists will begin to request titer determinations and peripheral
viral-load quantifications in ASD kids -- especially since anti-HHV6
pharmaceuticals are available.
In regard to VK's study, I wonder if the "not quite significant"
difference between titers of controls and autistic kids arose because a
younger population would have more kids whose HHV6 infection was
somewhat recent. Regardless, although titers can provide a clue,
quantitation of viral load and of viral-activation status (2) seems a
more important determination.
Teresa
J Clin Virol 2000 May;16(3):179-91
Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic
fatigue
syndrome (CFS) patients.
Ablashi DV et al.
BACKGROUND: HHV-6 is a ubiquitous virus and its infection usually occurs
in
childhood and then becomes a latent infection. HHV-6 reactivation has
been shown
to play a role in the pathogenesis of AIDS and several other diseases.
OBJECTIVES: To determine what role HHV-6 infection or reactivation plays
in the
pathogenesis of multiple sclerosis (MS) and chronic fatigue syndrome
(CFS).
RESULTS: Twenty-one MS and 35 CFS patients were studied and followed
clinically.
In these patients, we measured HHV-6 IgG and IgM antibody levels and
also
analyzed their peripheral blood mononuclear cells (PBMCs) for the
presence of
HHV-6, using a short term culture assay. In both MS and CFS patients, we
found
higher levels of HHV-6 IgM antibody and elevated levels of IgG antibody
when
compared to healthy controls. Seventy percent of the MS patients studied
contained IgM antibodies for HHV-6 late antigens (capsid), while only
15% of the
healthy donors (HD) and 20% of the patients with other neurological
disorders
(OND) had HHV-6 IgM antibodies. Higher frequency of IgM antibody was
also
detected in CFS patients (57.1%) compared to HD (16%). Moreover, 54% of
CFS
patients exhibited antibody to HHV-6 early protein (p41/38) compared to
only
8.0% of the HD. Elevated IgG antibody titers were detected in both the
MS and
the CFS patients. PBMCs from MS, CFS and HD were analyzed in a short
term
culture assay in order to detect HHV-6 antigen expressing cells and to
characterize the viral isolates obtained as either Variant A or B.
Fifty-four
percent of MS patients contained HHV-6 early and late antigen producing
cells
and 87% of HHV-6 isolates were Variant B. Isolates from CFS, patients
were
predominately Variant A (70%) and isolates from HD were predominately
Variant B
(67%). Moreover, one isolate from OND was also Variant B. Persistent
HHV-6
infection was found in two CFS patients over a period of 2.5 years and
HHV-6
specific cellular immune responses were detected in PBMCs from ten CFS
patients.
CONCLUSION: In both MS and CFS patients, we found increased levels of
HHV-6
antibody and HHV-6 DNA. A decrease in cellular immune responses was also
detected in CFS patients. These data suggest that HHV-6 reactivation
plays a
role in the pathogenesis of these disorders.
2: Clin Infect Dis 2000 Oct;31(4):894-903
Human herpesvirus 6 and multiple sclerosis: systemic active infections
in
patients with early disease.
Knox KK, Brewer JH, Henry JM, Harrington DJ, Carrigan DR
By means of immunohistochemical staining, cells actively infected with
human herpesvirus 6 (HHV-6) were found in central nervous system tissues
from 8 (73%) of 11 patients with definite multiple sclerosis (MS).
Interestingly, 17 (90%) of 19 tissue sections showing active
demyelination were positive for HHV-6-infected cells compared with only
3 (13%) of 23 tissue sections free of active disease
(P<.0001).
Central nervous system tissues from 2 of 28 normal persons and
patients with other inflammatory demyelinative diseases were positive
for HHV-6-infected cells (P<.0001), and the 2 positive cases were
diagnosed as having HHV-6 leukoencephalitis.
By use of a rapid culture assay, blood samplesfrom 22 (54%) of 41
patients with definite MS were found to contain active HHV-6 infections,
compared with 0 of 61 normal controls (P<.0001).
No significant difference was found between HHV-6 viremia-positive
and HHV-6 viremia-negative MS patients with respect to type of disease
(relapsing/remitting or
progressive). In contrast, patients with active HHV-6 viremia were
significantly
younger and had shorter durations of disease than did HHV-6
viremia-negative
patients.
3. Clin Immunol Immunopathol 1998 Oct;89(1):105-8
Serological association of measles virus and human herpesvirus-6 with
brain
autoantibodies in autism.
Singh VK, Lin SX, Yang VC
College of Pharmacy, University of Michigan, Ann Arbor, Michigan,
48109-1065,
USA.
Considering an autoimmunity and autism connection, brain autoantibodies
to myelin basic protein (anti-MBP) and neuron-axon filament protein
(anti-NAFP) have been found in autistic children. In this current study,
we examined associations between virus serology and autoantibody by
simultaneous analysis of measles virus antibody (measles-IgG), human
herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP.
We found that measles-IgG and HHV-6-IgG titers were moderately
higher in autistic children but they did not significantly differ from
normal controls. Moreover, we found that a vast majority of virus
serology-positive autistic sera was also positive for brain
autoantibody:
(i) 90% of measles-IgG-positive autistic sera was also positive for
anti-MBP;
(ii) 73% of measles-IgG-positive autistic sera was also positive for
anti-NAFP;
(iii) 84% of HHV-6-IgG-positive autistic sera was also positive for
anti-MBP; and
(iv) 72% of HHV-6-IgG-positive autistic sera was also positive for
anti-NAFP.
This study is the first to report an association between virus
serology and brain
autoantibody in autism; it supports the hypothesis that a virus-induced
autoimmune response may play a causal role in autism.
ps: This post may be forwarded hither and yon.

Kathy,
thanks for your prompt and kind response. I do not check my messages
frequently, so if you send me anything and don't hear back soon, please
understand. our son, patrick, who was ten last month, wants me to put him to
bed and stay with him. by the time he goes to sleep, i am wiped out and our
older son or my husband are then monopolizing the computer. also, since we
got DSL, i encounter obtacles to signing on, as when DSL has been left on
overnight or for many hours.
As to your question on in-home allergens, we have not done much to date. We
have been using NAET treatments (both patrck and myself) for more than a year
and since then, patrick's eosinophils (as measured by blood work done by Dr.
G's office) have
come down and i believe this is largely due to the NAET treatments of food
and non-food allergies. Some of the non-food allergies we have worked on are
latex, which caused us to see that the continued presence of latex-backed
area rugs made clearing that allergy by NAET a prolonged experience. I have
kept the latex products out of patrick's room as much as possible. For
example, i put a small shelf into the hall outside of his room where i keep
his shoes, since they have latex soles. But there are small objects in his
room and elsewhere with latex and i have not removed then because he cleared
that allergy, meaning that it is, we hope, no longer a problem.
We have similarly treated p. for lead and copper using NAET. In case you are
not familiar with NAET, on children it involves accupressure while the child
holds a vial of the energy of the allergen. It is based on the meridians of
Chinese med. and is totally non-invasive. I have discussed this with Dr.
Goldberg, and I know he is sceptical but since P. is not ingesting any herbal
product, etc. with this, he does not object to it.
Back to the household allergen issue...our house is not clean and is
therefore full of dust, possibly molds, etc. I cannot keep up with the
housework and I gave up the once-a-week cleaning lady because we are so
buried by stuff that patrick pulls out of shelves, cupboards, etc. that i
feel i am the only one available to try to put the stuff back, and I can't
keep up with it enough to then do the kind of cleaning job I would like. It
so happens that i have been out looking at better vacuums and have my eye on
one of the Miele vacuums, which are sealed systems and have, in most models,
HEPA filters.
I do not allow any pesticides to be used in our house, even though we have
ant invasions when the weather is especially hot or rainy.
Maybe the above will spur your thoughts/suggestions. . thanks again for the
concern and for your work on the No. Cal. NIDS group.
mary n.

Kathy, sorry that referred to you as being part of the No. CAl. group...just
looked at your first message again and saw you are in N.Y. I attended the
first NIDS conference in May 1999. Do you know if a second such major
conference is planned?
mary n.

A parent asked: If a child has MV in intestinal tissue, might another virus
have established residency in intestinal tissue? Might such viruses be
treatable?
The answer is yes to both questions. Importantly, however, is the fact that
a number of immune regularities are associated with autism-spectrum
children, thus any specific autistic child may not be properly described as
"immunocompetent", even if his or her immune glitch is "subtle" (eg, null
allele of C4b gene or DRB1*0401 allele; RP Warren et al, series of studies).
The success of many anti-pathogen pharmaceuticals is dependent upon
pharmaceutical-pathogen specificity AND the host immune response against the
pathogen. Nonetheless, the presence of viruses in gastrointestinal tissue is
documented, and identifying and treating specific viruses in a specific
autistic child may be warranted (in a context of his/her immune portrait and
other medical data).
HSV, CMV, HHV6, & EBV have been identified in intestinal tissue (eg, 1,2);
in some instances, treatments have been effective (eg, 3-4).
As far as I know, when Andy Wakefield uses PCR to evaluate viral presence in
ASD intestinal tissue, he (i) generally has focused upon children whose
parents reported regression linked with the MMR and (ii) usually has not
conduced PCR screens for other viruses, especially in ASD children whose
regression is parentally reported as not linked with the MMR. (Of course,
this summary of Andy's PCR focus may need revision, correct me if my summary
is erroneous.)
Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
1: J Med Virol 1992 Nov;38(3):183-90
Detection of herpesvirus DNA in the large intestine of patients with
ulcerative
colitis and Crohn's disease using the nested polymerase chain reaction.
Wakefield AJ et al.
The prevalence of herpesvirus DNA was examined in inflammatory bowel disease
tissue. DNA was extracted from resection and biopsy specimens of the large
intestine from patients with ulcerative colitis (n = 21), patients with
Crohn's disease (n = 29), and patients with noninflammatory bowel disease
(controls)
(n = 21). The nested polymerase chain reaction was used to detect viral DNA
using primer pairs specific for either cytomegalovirus (CMV), herpes simplex
virus
1 (HSV1), human herpesvirus 6 (HHV6), varicella zoster virus (VZV), or Epstein
Barr virus (EBV). HSV1 and VZV DNA were not detected in any of tissue
samples. There was a high prevalence of CMV (81%), HHV6 (76%), and EBV (76%)
DNA in
ulcerative colitis tissue compared to Crohn's disease tissues (CMV 66%, HHV6
45%, EBV 55%). Control tissue had a relatively low frequency of CMV (29%)
and EBV (19%) DNA but a prevalence of HHV6 DNA similar to that of ulcerative
colitis (86%). However, the simultaneous presence of HHV6 and CMV and/or EBV
DNA in
ulcerative colitis tissue (76%) was much greater than in either Crohn's
disease
tissues (38%) or control tissue (29%) (P < 0.05). There was a low prevalence
of CMV, HHV6, and EBV DNA in peripheral blood mononuclear cells from all
patient groups. CMV and EBV are capable of reactivating HHV6: the high
prevalence of
coexistent HHV6 infection with either or both of these two viruses in
ulcerative colitis tissue suggests that they may play a synergistic role in
the
pathogenesis of this disease.
2. J Virol 1997 May;71(5):4103-6
Latent herpes simplex virus type 1 gene expression in ganglia innervating
the human gastrointestinal tract.
Gesser RM, Koo SC
Using in situ hybridization, we demonstrated that latent herpes simplex virus
type 1 (HSV-1) gene expression is prevalent in human adult nodose ganglia.
This suggests that infection of gastrointestinal sensory nerves, probably
through
swallowed virus-laden oral secretions, occurs commonly and that HSV-1
reactivating from this site may play a role in recurrent gastrointestinal
disorders.
3. 1: Chung Hua I Hsueh Tsa Chih (Taipei) 1996 Apr;57(4):289-92
Cytomegalovirus colitis in an immunocompetent old woman successfully treated
with ganciclovir: a case report.
Tsai HL, Huang CK, Cho G, Chen GH, Yang MD
Department of Internal Medicine, Taichung Veterans General Hospital, Taiwan,
R.O.C.
Cytomegalovirus (CMV) diseases occur almost exclusively in the
immunocompromised
hosts. Persons most commonly affected are patients with acquired
immunodeficiency syndrome (AIDS). On rare occasions, however, CMV diseases
can be seen in apparently immunocompetent persons. A CMV colitis in a
68-year old immunocompetent woman presenting with watery diarrhea, malaise,
and body weight loss of about 5 kg over a three week period is reported.
Colonoscopy and mucosal biopsy revealed CMV colitis involving the sigmoid
colon. Treatment for two weeks with ganciclovir (10 gm/kg/day I.V. in 2
divided doses) resulted in
resolution of colitis and clinical symptoms without any noticeable
side-effects. There was no relapse of infection by six months of follow-up.
The possibility of CMV colitis should be considered in any elderly person with
watery diarrhea, general debilitation, marked body weight loss and with
negative stool cultures. CMV colitis may be more frequent than is usually
believed. It has a favorable
response to ganciclovir without further relapse after the successful treatment
in patients with normal immune function.
4: Pediatr Infect Dis J 1989 Jul;8(7):436-40
Ganciclovir treatment of cytomegalovirus disease in immunocompromised
children.
Gudnason T, Belani KK, Balfour HH Jr
Department of Laboratory Medicine and Pathology, University of Minnesota,
Minneapolis 55455.
Twelve immunocompromised children were treated with 13 courses of
intravenously
administered ganciclovir for severe cytomegalovirus disease. All children were
allograft recipients; 6 received organ transplants (5 liver, 1 kidney) and 6
received bone marrow. They presented with one or more of the following forms
of cytomegalovirus disease: pneumonitis, 9; hepatitis, 3; colitis, 2;
peritonitis,
1; and retinitis, 1. Clinical improvement was observed in 7 (58%) of 12
patients during ganciclovir therapy. Cessation of active viral replication
during
therapy accompanied 69% of the treatment courses. Mild and transient increases
in
creatinine and liver function tests and/or decreases in neutrophil count
accompanied 77% of treatment courses but neutropenia (less than 1000
cells/mm3) did not occur. Transient decreases in platelet counts accompanied
therapy in
3 bone marrow allograft recipients, but greater than 50% decrease in
lymphocyte count was not seen. We conclude that ganciclovir is safe and
appears to have a beneficial effect on cytomegalovirus disease in some
pediatric transplant recipients.
ps: This post may be fowarded into other lists, shared with other
individuals.
{{And I tried sending this early this morning but had to dance quite a dance
with several computers in order to achieve outgoing mail.}}

Dear Mary,
I will pray for Patrick and for your family also. This will be no comfort but
in medicine no protocol works 100% for all patients. If they did my cousin,
whom we just buried in July, would have gone into remission as the majority
of people with her cancer have done. Having said that, research continues and
if the funding falls into place testing will start with the first
immunemodulators within the next few months AND there are several more after
that already in existence that have possibilities. Those drugs may be the
answer. You may have not seen dramatic improvement with your son but how much
worse would he have been had you done nothing medical? One question if I may?
How extensive have you gone into allergen removal in your home? Kathy R NIDS
Coalition-Northern New York

Thanx so much, Mary, for your info! I don't feel so all alone anymore with
our tough little case.
Tina M. Hendrix
CureNIDS2000@...
President, NIDS Coalition, Northern California
Neuro-Immune Dysfunction Syndromes
Autism Spectrum Disorder, ADD/ADHD, Learning Disorders, Hyperactivity, CFS,
etc.

there was no text in the message i received, just reference to a rumor in the
title.
mary

Tina,
We have been doing the Dr. Goldberg protocol for more than five years for our
son, Patrick, who turned 10 last month. Dr. G. refers to Patrick as one of
his tough cases, and I do mean extremely tough. We have not seen much
improvement but are more aware of his potential. We have been on too many
meds to list here, but are currently using Kutapressin, Paxil (I have not
seen any results from any of the SSRIs), occasionally iron (I need to hide it
in foods and he usually detects it) and, from Dr. Aguilar, we have been using
FGF-2. We stopped it for 3 months in an attempt to see if it was making our
son worse, but I am now sure that it is not. I suspect Dr. G will want us to
restart Diflucan or another anti-fungal next, since we have been off them
for approx. a year. I have been very confused about what the obstacle is.
We have behavior problems as well and I can't think straight, so we hang in
there meanwhile with the hope for improved immune modulators.
mary n.

there was no content or message re the languaga program you mentioned in your
title. where is the text?
mary nunan

http://www.pubmedcentral.nih.gov/picrender.cgi?artid=2478&pictype=5
keeping in mind, of course, that several prominent autism
specialists report (at conferences) that appx 1/3 of the docs'
ASD kids respond quite favorably to acyclovir.

full article (free) at:
http://www.pubmedcentral.nih.gov/picrender.cgi?artid=13311&pictype=5

Mark April 27th on your calendars now for the
2001 Autism Awareness Rally.
The Power of ONE!
If you aren't sure what one can do, turn your televisions to CNN
and watch the developing Presidential Election.
What a perfect year to celebrate the importance we have and contributions we
can make as one little person. As one person, you can make a difference in
your home, your neighborhood, your city, state and, yes, even the country.
As one community, working together, we multiply the strength of that one
little person exponentially!
Come and celebrate a day of autism awareness with Unlocking Autism at the
base of the Capitol Building in Washington, DC!
Friday, April 27, 2001
12pm to 5pm
By the way....did you make the deadline last year for the Open Your Eyes
project? It will be displayed again this year. So make sure you get those
pictures in early! Information regarding this project is on our website.
Please "knock" on the red door.
Unlocking Autism greatly appreciates any contributions you would like to make
to help us defray the cost of planning and producing this event and our other
awareness projects.
More information regarding the rally and other events to take place in DC
during that week will be coming in late December to our website:
http://www.unlockingautism.org.
PLEASE STAY TUNED.

the response I sent to the Washington Post regarding the "On the trail of Autism
" article.

NIDS is the possible answer. neuroimmunedr.com remember as you read the
articles that the gut does produce mast cells and that GI symptoms can
reflect a problem with the immune system. Kathy R NIDS Coalition-Northern New
York Chapter

The whole point of the 60 Minutes article on the MMR shots (aired Nov.
12, 2000) is to break up the shot, not get rid of it. Until it as been
further envestigated, they ought to break he shots up. It is feared
that the combination of the MMR shot triggers the autistic gene. One
can carry the gene, but not have the symptoms.

Hi all,
Did anyone see 60 min last night? Did anyone get the address for bill
Gates? Thanks, Lois

Has anyone heard of a Dr. Brewer in Kansas. One of my Mom's nighbors in
Chicago is very severely ill with a Neuro Immune like disease and is looking
for the e-mail addy or phone number for this doc.
Thanx!
Tina M. Hendrix
CureNIDS2000@...
Coordinator, NIDS Coalition, Northern California
Neuro-Immune Dysfunction Syndromes
Autism Spectrum Disorder, ADD/ADHD, Learning Disorders, Hyperactivity, CFS,
etc.
Tina M. Hendrix
CureNIDS2000@...
Coordinator, NIDS Coalition, Northern California
Neuro-Immune Dysfunction Syndromes
Autism Spectrum Disorder, ADD/ADHD, Learning Disorders, Hyperactivity, CFS,
etc.

Connie,
Here is all the info on the Ketogenic diet. My son was having petimal
seizures before we put him on the diet. By the way, it's been a full
month, and he has only had the one seizure.
There is a movie called "First do no harm" with Merryl Streep, about the
ketogenic diet. It is a true story of a mothers struggle to find out
why her son started having Grand-mal seizures, and the only thing that
worked was the diet. That is what inspired me to look into it for my
son.
8-)

Keeping in mind that rat neonatal may not be exactly equivalent
to human neonatal, the following study is important because it
demonstrates that HSV can affect startle responses.
This type of study sheds light upon individuals (such as myself)
who have difficulty acclimating to a constant sound and who can
JUMP! with startle to a sudden sound my synaptic networks ought
filter as irrelevant (1).
Teresa
1: Brain Res 2000 Apr 28;863(1-2):233-40
Neonatal herpes simplex virus type 1 brain infection affects the
development of
sensorimotor gating in rats.
Engel JA, Zhang J, Bergstrom T, Conradi N, Forkstam C, Liljeroth
A, Svensson L
Department of Pharmacology, Goteborg University, Box 431, SE 405
30, Goteborg,
Sweden.
The effect of neonatal brain infection of herpes simplex virus
type 1 (HSV-1) on
the development of sensorimotor function in the rat was
investigated using an
acoustic startle paradigm. Intracerebral inoculation of HSV-1 at
day 2 after
birth, but not at day 4, caused a significant delay in the
development of
prepulse inhibition of acoustic startle. A decrease in prepulse
inhibition was
shown at 37, 46 and 58 days of age in these rats compared to
control rats. No
evidence was obtained for other behavioural dysfunctions such as
differences in
sensorimotor reactivity, sensorimotor response habituation,
spontaneous
locomotor activity, rearing activity or stereotyped behaviour.
Prepulse
inhibition of acoustic startle is an accepted model of
sensorimotor gating in
the CNS, a function which has been shown diminished in
schizophrenic persons.
The present results suggest that early viral infections during a
neurone-susceptible period may contribute to the development of
this deficit.
PMID: 10773211, UI: 20237299
2: J Infect 1992 Sep;25(2):147-54
A 15-year surveillance study of antibodies to herpes simplex
virus types 1 and 2
in a cohort of young girls.
Christenson B, Bottiger M, Svensson A, Jeansson S
Department of Environmental Health and Infectious Diseases
Control, Karolinska
Hospital, Stockholm, Sweden.
A cohort of 839 young girls at the ages of 14 and 15 years was
screened for
total antibodies to herpes simplex virus (HSV) and, if positive,
for specific
antibodies to HSV-2, by means of a sensitive, enzyme-linked
immunosorbent assay
(ELISA). The cohort was followed from 1972-1987. Blood samples
were obtained on
six occasions during these 16 years. In total, 2270 blood samples
were taken.
The number of sero-converting girls was studied in relation to
calendar time.
Two methods were constructed for the statistical analyses. The
first of these
gave an estimate of the sero-prevalence at different points in
time. This
analysis showed that the sero-prevalence which was 23% against
HSV-1 in 1972 had
increased to 36% in 1976. At the end of the study in 1987, 50% of
the cohort had
sero-converted against HSV-1. The proportion of girls who had
sero-converted
against HSV-2 was 0.4% in the 14-15-year-olds and had reached 22%
by the end of
the study. The second statistical method used all the available
information
implicit in the observations so as to obtain a maximum-likelihood
(ML) estimate
of the prevalence. The ML estimates were slightly more precise,
but the two
estimates did not differ significantly. The observations were
further analysed
by the Mantel-Haenszel test in order to see if there was any
dependence between
positivity to HSV-1 and HSV-2 respectively but none was found.
PMID: 1331244, UI: 93056592

Note that we can include HSV, HHV6, MV, and other critters are
potential candidates for inducing chronic low-level infection
accompanied by chronic autoimmunity.
Each of these gems is available online at
http://www.neuroscion.com
Journal of Neuroimmunology
Volume 107, Issue 2
July 2000
Pages 201-204
Persisting viruses and autoimmunity
Marino Paroli a,b , Enrico Schiaffella a,b ,
Francesca Di Rosa c and Vincenzo Barnaba
a,b A barnaba@...
[a]Fondazione Andrea Cesalpino, Istituto di I
Clinica Medica, Università di Roma 'La
Sapienza', Policlinico Umberto I, viale del
Policlinico 155, I-00161 Rome,
Italy[b]Istituto Pasteur-Cenci Bolognetti,
I-00185 Rome, Italy[c]Istituto Regina
Elena, via delle Messi d'Oro 156, I-00158
Rome, Italy
A Corresponding author. Fondazione Andrea
Cesalpino, Istituto di I Clinica Medica,
Università di Roma 'La Sapienza', Policlinico
Umberto I, viale del Policlinico 155,
I-00161 Rome, Italy. Tel.: +39-6-445-399;
fax: +39-6-494-0594
Abstract
Viral infections can be responsible for the
onset and sustaining of autoimmune
processes. We discuss how chronic
inflammation associated with viral persistence is the
prerequisite for initiation of a multi-step
process leading to autoimmunity. Firstly, chronic
inflammation may favor the priming of
autoreactive T cells that have escaped thymic
selection and are specific for self-mimicking
viral peptides in the periphery. In addition,
viral persistence and inflammation can act
synergistically to induce and sustain
autoimmunity either unveiling cryptic
self-epitopes, or favoring determinant spreading, or
activating dendritic cells, or promoting
constant priming of new autoreactive T cells, or
contributing to the efficient generation of
effector cells, or, finally, restimulating memory T
lymphocytes.
Journal of Neuroimmunology
Volume 105, Issue 2
June 2000
Pages 145-153
Evidence for antigenic cross-reactivity between
herpesvirus and the acetylcholine receptor
Bryan M. GebhardtA bgebha@...
Lions Eye Research Laboratories, LSU Eye
Center, Louisiana State University Health
Sciences Center, 2020 Gravier Street, Suite
B, New Orleans, LA 70112-2234, USA
A Corresponding author. Tel.:
+1-504-412-1348; fax: +1-504-412-1315
Manuscript received 13 October 1999 Revised
14 January 2000 Accepted 18 January 2000;
Abstract
Herpes simplex virus (HSV) is neurotropic and
can pass from neuron to neuron at nerve
terminals. During the long evolutionary
relationship between HSV and vertebrates, this
virus may have evolved surface ligands that
mimic nerve cell receptors. The present
study was undertaken to determine if herpes
simplex virus type 1 (HSV-1) has an
antigenic relationship with the acetylcholine
receptor (AChR). Mice immunized with HSV-1
antigens or an AChR-expressing cell line were
tested for antibodies directed against the
AChR. By flow cytometry and ELISA, mouse
anti-HSV-1 sera were found to contain
antibodies that would bind to an epitope on
the plasma membrane of AChR-expressing
cells. Mice immunized with the
AChR-expressing cells were tested for their resistance to
HSV-1 infection. Statistically significantly
more of the animals immunized with
AChR-expressing cells resisted infection and
fatal encephalitis, compared to control
animals immunized with a cell line not
expressing the AChR. Sera from AChR-immunized
mice were tested for anti-HSV antibody by
ELISA and were found to contain antibodies
cross-reactive with HSV-1 antigens. These
sera also neutralized virus in a plaque
inhibition assay. The results indicate that
there are one or more antigenic epitopes
shared by herpesvirus and the AChR. Studies
are in progress to define the pathogenetic
significance of this molecular mimicry.
Journal of Neuroimmunology
Volume 105, Issue 1 June
2000 Pages 46-57
Mistaken self, a novel model that links
microbial
infections with myelin-directed autoimmunity
in
multiple sclerosis
Johannes M. van NoortA jm.vannoort@...,
Jeffrey J. Bajramovic, Arianne C.
Plomp and Marianne J.B. van Stipdonk
Division of Immunological and Infectious
Diseases, TNO Prevention and Health, P.O.
Box 2215, 2301 CE Leiden, The Netherlands
A Corresponding author. Tel.:
+31-71-518-1541; fax: +31-71-518-1901
Manuscript received 22 September 1999 Revised
24 November 1999 Accepted 15 December
1999;
Abstract
Several findings indicate that infectious
events play a role in the pathogenesis of multiple
sclerosis (MS). At the same time, T-cell
autoimmunity to myelin antigens is widely believed
to be crucial to the development of MS
lesions. Several mechanisms have been put
forward to explain the presumed link between
microbial infections and myelin-directed
autoimmunity. These include molecular
mimicry, bystander activation including epitope
spreading and superantigenic activation of T
cells. Evidence that either one of these
mechanisms actually occurs in MS patients,
however, is still weak. Also, none of the
above mechanisms explain why MS is unique to
humans. We propose an alternative link
between microbial infection and myelin
autoimmunity, which we refer to as 'mistaken
self'. In this mechanism, peripheral
microbial infections of lymphoid cells prime the human
T-cell repertoire not only to microbial
antigens but also to the stress protein alpha
B-crystallin that is expressed de novo in
infected lymphoid cells. Subsequently,
stress-induced accumulation of this self
antigen in oligodendocytes/myelin can provoke
pro-inflammatory responses as the recruited
memory T-cell repertoire then mistakes the
self protein for a microbial antigen. In this
paper we review the currently available
evidence that 'mistaken self' centering on
alpha B-crystallin represents a powerful source
of anti-myelin autoimmunity in a way that is
unique to humans.

Fetal and adult human CNS stem cells have similar molecular
characteristics and developmental
potential
Kaia Palm, Tuija Salin-Nordström, Michel
F. Levesque & Toomas Neuman Molecular Brain Research, 2000,
78:1-2:192-195
[Abstract] [SummaryPlus] [Full Text] [PDF
- 356K] Also: [ScienceDirect
Article is free at: http://www.neuroscion.com

Forgive me if this is redundant as I have not been keeping up with my emails
lately. What is a "ketogenic" diet, and what type of seizures did your son
have prior to the diet?
Thanks,
Connie

"Mild encephalitis/meningitis induced by HHV-6, a condition
sometimes not recognized as encephalitis/meningitis, may be one
of the most frequent causes of temporal lobe epilepsy." (1)
Perhaps the time has come for researchers and physicians to
contemplate that, in at least some autistic children, the
elevated anti-HHV6 titers reported by VK Singh (2) may represent
chronic, low-level infection that includes subclinical
encephalitis as described in Uesugi et al (1).
Importantly, when large groups are used in titer-based studies,
there is a built-in sloppiness because, unless properly-designed
pathogen-quantitation is enacted, there is no easy way to
differentiate (a) elevated titers from a somewhat recent
infection properly being immunosuppressed, from (b) a chronic,
low-level infection that is not being immunosuppressed.
Despite this cavaet, HHV6 is well worth considering in many ASD
kids, and appropriate lab-tests ought be performed. The use of
steroid-based pharmaceuticals may exacerbate HHV6 infections or
other chronic infections in an ASD child (3).
Teresa
ps: This post may be shared and posted into other listservs.
1. Psychiatry Clin Neurosci 2000 Oct;54(5):589-93
Presence of human herpesvirus 6 and herpes simplex virus detected
by polymerase
chain reaction in surgical tissue from temporal lobe epileptic
patients.
Uesugi H, Shimizu H, Maehara T, Arai N, Nakayama H
Department of Psychiatry, National Center Hospital for Mental,
Nervous, and
Muscular Disorders, Kodaira, Tokyo, Japan.
We investigated the presence of human herpesvirus 6 (HHV-6) and
herpes simplex
virus (HSV) in surgical tissue from temporal lobe epileptic
patients. A total of
17 cases were studied, including eight males and nine females.
The mean age was
24.9 +/- 11.1 years and the mean age of onset was 11.1 +/- 5.4
years. Five
patients were diagnosed as encephalitis/meningitis and another
three had a
history of suspected encephalitis/meningitis, but no patient
showed any obvious
neurological symptom or mental handicap. Mesial and lateral
temporal tissues
were examined by polymerase chain reaction. Among six patients
positive for
HHV-6 (35%), the mesial temporal lobe was positive in four and
the lateral
temporal lobe was positive in three. Herpes simplex virus was
positive in only
one patient. Three of the six patients positive for HHV-6 did not
show any
apparent causes. Mild encephalitis/meningitis induced by HHV-6, a
condition
sometimes not recognized as encephalitis/meningitis, may be one
of the most
frequent causes of temporal lobe epilepsy.
2. Clin Immunol Immunopathol 1998 Oct;89(1):105-8
Serological association of measles virus and human herpesvirus-6
with brain
autoantibodies in autism.
Singh VK, Lin SX, Yang VC
Considering an autoimmunity and autism connection, brain
autoantibodies to
myelin basic protein (anti-MBP) and neuron-axon filament protein
(anti-NAFP)
have been found in autistic children. In this current study, we
examined
associations between virus serology and autoantibody by
simultaneous analysis of
measles virus antibody (measles-IgG), human herpesvirus-6
antibody (HHV-6-IgG),
anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG
titers were
moderately higher in autistic children but they did not
significantly differ
from normal controls. Moreover, we found that a vast majority of
virus
serology-positive autistic sera was also positive for brain
autoantibody: (i)
90% of measles-IgG-positive autistic sera was also positive for
anti-MBP; (ii)
73% of measles-IgG-positive autistic sera was also positive for
anti-NAFP; (iii)
84% of HHV-6-IgG-positive autistic sera was also positive for
anti-MBP; and (iv)
72% of HHV-6-IgG-positive autistic sera was also positive for
anti-NAFP. This
study is the first to report an association between virus
serology and brain
autoantibody in autism; it supports the hypothesis that a
virus-induced
autoimmune response may play a causal role in autism.
3. Science 1995 Oct 13;270(5234):232-3
How the glucocorticoids suppress immunity.
Marx J

Limbic Circuitry in Patients With Autism Spectrum Disorders Studied With
Positron Emission Tomography and Magnetic Resonance Imaging.
Haznedar MM, Buchsbaum MS, Wei TC, Hof PR, Cartwright C, Bienstock CA,
Hollander
E
Am J Psychiatry 2000 Dec 1;157(12):1994-2001
OBJECTIVE: Cytoarchitectonic changes in the anterior cingulate cortex,
hippocampus, subiculum, entorhinal cortex, amygdala, mammillary bodies, and
septum were reported in a postmortem study of autism. Previously, the
authors
found smaller cingulate volume and decreased metabolism of the cingulate in
seven autistic patients. In this study, they measured the volume and glucose
metabolism of the amygdala, hippocampus, and cingulate gyrus in an expanded
group of 17 patients with autism spectrum disorders (autism [N=10] or
Asperger's
disorder [N=7]) and 17 age- and sex-matched healthy volunteers. METHOD:
Subjects
performed a serial verbal learning test during (18)F-deoxyglucose uptake.
The
amygdala, hippocampus, and cingulate gyrus were outlined on magnetic
resonance
imaging scans, volumes of the structures were applied to matching
coregistered
positron emission tomography scans, and three-dimensional significance
probability mapping was performed. RESULTS: Significant metabolic reductions
in
both the anterior and posterior cingulate gyri were visualized in the
patients
with autism spectrum disorders. Both Asperger's and autism patients had
relative
glucose hypometabolism in the anterior and posterior cingulate as confirmed
by
analysis of variance; regional differences were also found with
three-dimensional significance probability mapping. No group differences
were
found in either the metabolism or the volume of the amygdala or the
hippocampus.
However, patients with autism spectrum disorders showed reduced volume of
the
right anterior cingulate gyrus, specifically in Brodmann's area 24'.
CONCLUSIONS: Compared with age- and sex-matched healthy volunteers, patients
with autism spectrum disorders showed significantly decreased metabolism in
both
the anterior and posterior cingulate gyri.
PMID: 11097966

Please help...I am being given so many different messages by doctors my head
is spinning: The Royal Free said my son had 'Ileal lymphoid nodular
hyperplasia' the local gut-doc said' ulceritve colitis' ...my local GP
(after saying 'Crohns') said it is none of those, just some 'growths' and
severe constipation, and that he must be re-tested for 'EPILEPSY' ''s this
could be causing the pain''..? Excuse me? My son cannot control his bowels
...every 'diaper/nappy change' there is something ther and always 'sticky'
...and he is always pressing his lower abdomen area in pain...what the hell
do I do? I am lost....thanks in advance...I need all the advice I can get...
Love from Liz (and Jamie, 8, non-verbal-but getting there)

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Text&DB=PubMed
Two-Year Outcome of Preschool Children With Autism or Asperger's Syndrome.
Szatmari P, Bryson SE, Streiner DL, Wilson F, Archer L, Ryerse C
Am J Psychiatry 2000 Dec 1;157(12):1980-1987
OBJECTIVE: DSM-IV specifies that Asperger's disorder is a type of pervasive
developmental disorder without clinically significant cognitive or language
delay. There are no data, however, on the outcome of children with
Asperger's
disorder or on whether their outcome differs from that of children with
autism.
The objectives of this study were to compare the outcome of groups of
children
with these disorders over a period of 2 years on variables independent of
the
defining criteria and to identify variables that might account for these
differences. METHOD: All children 4-6 years of age who came for assessment
or
were currently in treatment at a pervasive developmental disorder service of
one
of several centers in a large geographic region were identified. Children
who
received a diagnosis of autism (N=46) or Asperger's syndrome (N=20) on the
basis
of a diagnostic interview and had an IQ in the nonretarded range were given
a
battery of cognitive, language, and behavioral tests. Families were
contacted
roughly 2 years after the date of their enrollment in the study, and many of
the
tests were readministered. RESULTS: Children with Asperger's syndrome had
better
social skills and fewer autistic symptoms 2 years after study enrollment
than
the children with autism. The differences in outcome could not be explained
by
initial differences in IQ and language abilities. Children with autism who
had
developed verbal fluency at follow-up were very similar to the children with
Asperger's syndrome at study enrollment. CONCLUSIONS: Although the exact
mechanism for the differences in outcome remain to be determined, it appears
that Asperger's disorder and autism represent parallel but potentially
overlapping developmental trajectories.
PMID: 11097964

Temporal Lobe Dysfunction in Childhood Autism: A PET Study.
Zilbovicius M, Boddaert N, Belin P, Poline JB, Remy P, Mangin JF, Thivard L,
Barthelemy C, Samson Y
Am J Psychiatry 2000 Dec 1;157(12):1988-1993
OBJECTIVE: The nature of the underlying brain dysfunction of childhood
autism, a
life-long severe developmental disorder, is not well understood. Although
researchers using functional brain imaging have attempted to contribute to
this
debate, previous studies have failed to report consistent localized
neocortical
brain dysfunction. The authors reasoned that early methods may have been
insensitive to such dysfunction, which may now be detectable with improved
technology. METHOD: To test this hypothesis, regional cerebral blood flow
was
measured with positron emission tomography (PET) in 21 children with primary
autism and in 10 nonautistic children with idiopathic mental retardation.
Autistic and comparison groups were similar in average age and developmental
quotients. The authors first searched for focal brain dysfunction in the
autistic group by using a voxel-based whole brain analysis and then assessed
the
sensitivity of the method to detect the abnormality in individual children.
An
extension study was then performed in an additional group of 12 autistic
children. RESULTS: The first autistic group had a highly significant
hypoperfusion in both temporal lobes centered in associative auditory and
adjacent multimodal cortex, which was detected in 76% of autistic children.
Virtually identical results were found in the second autistic group in the
extension study. CONCLUSIONS: PET and voxel-based image analysis revealed a
localized dysfunction of the temporal lobes in school-aged children with
idiopathic autism. Further studies will clarify the relationships between
these
temporal abnormalities and the perceptive, cognitive, and emotional
developmental abnormalities characteristic of this disorder.
PMID: 11097965

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Text&DB=PubMed
Personality traits of the relatives of autistic probands.
Murphy M, Bolton PF, Pickles A, Fombonne E, Piven J, Rutter M
MRC Child Psychiatry Unit and Social, Genetic and Development Psychiatry
Research Centre, Institute of Psychiatry, London.
Psychol Med 2000 Nov;30(6):1411-24
BACKGROUND: There is substantial evidence that the genetic liability to
autism
confers a risk for a range of more subtle social and communication
impairments,
as well as stereotyped and repetitive behaviours. Recent research suggests
that
increased expression of particular personality traits may be a manifestation
of
the liability to autism. METHODS: To investigate this we examined the
personality traits of the adult relatives of 99 autistic and 36 Down's
syndrome
probands, using the informant version of the Modified Personality Assessment
Schedule. RESULTS: There was significantly increased expression of the
traits
anxious, impulsive, aloof, shy, over-sensitive, irritable and eccentric
among
the autism relatives with evidence of different profiles for male and female
relatives and for parents and adult children. Factor analysis revealed three
broad groups of traits, two of which ('withdrawn' and 'difficult') appeared
to
reflect impairments in social functioning and a third group of anxiety
related
traits ('tense'). Each of these factors differed in their pattern of
associations with the factor we termed 'withdrawn' showing a similar pattern
of
association to that found for other autism related conditions. The 'tense'
factor appeared in part to be related to the burden of caring for an
autistic
child. CONCLUSIONS: This study confirms the finding that particular
personality
traits may aggregate in the family members of autistic individuals and
furthermore that some of these traits may be a manifestation of the
liability to
autism.
PMID: 11097081, UI: 20546823

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Text&DB=PubMed
Genetic Structure of Reciprocal Social Behavior.
Constantino JN, Todd RD
Am J Psychiatry 2000 Dec 1;157(12):2043-2045
OBJECTIVE: The study examined the genetic structure of deficits in
reciprocal
social behavior in an epidemiologic sample of male twins. METHOD: Parents of
232
pairs of 7-15-year-old male twins completed the Social Reciprocity Scale to
provide data on their children's reciprocal social behavior. Scale scores
were
analyzed by using structural equation modeling. RESULTS: Intraclass
(twin-twin)
correlations for scores on the Social Reciprocity Scale were 0.73 for
monozygotic twins (N=98 pairs) and 0.37 for dizygotic twins (N=134 pairs).
The
best fitting model of causal influences on reciprocal social behavior
incorporated additive genetic influences and unique environmental
influences.
CONCLUSIONS: For school-age boys in the general population, reciprocal
social
behavior is highly heritable, with a genetic structure similar to that
reported
for autism in clinical samples. Continuous measures of reciprocal social
behavior may be useful for characterizing the broader autism phenotype and
may
enhance the statistical power of genetic studies of autism.
PMID: 11097975

What about the other 60%?
Page

BELOW IS THE AUTOIMMUNE DISORDER LIST TO SEE IF YOU HAVE A FAMILY HISTORY OF
ANY OF THEM FOR THE POLLING PURPOSES.........
The Autism Bio Medical Discussion list has started a poll for Bio-Profiling
Purposes, which is wonderful I think!!
On the list Eric and I created, Autism-Awareness-Action@egroups.com ---- I
am duplicating those polls for the purposes of having even more responses -
as our list has different members than the ABMD list.......
Many of you are on the Autism-Awareness-Action or ABMD lists to participate
in the polls.......... for those who are not --- please consider joining
the Autism-Awareness-Action list to register your vote in the BioMedical
Polls!!
There are currently 4 polls to vote in, an AutoImmune Poll, a poll of family
history of Alcoholism, a poll for whether you received Pitocin in labor, and
a poll for whether you received a Rhogam shot. There will be additional
polls added - so join in no-mail mode so you can check in now and then and
see what other polls there are.
I know we can easily get more than 1000 votes!!!!!
Please encourage others to join to participate in the polling!
All responses at the conclusion of the polling will be forwarded to the ABMD
listowner.
The more responses we have, the better the Bio-Profile the ABMD list can
create!!
URL to join Autism-Awareness-Action:
http://www.egroups.com/group/autism-awareness-action
Subscribe: autism-awareness-action-subscribe@egroups.com
To go to the polls:::
http://www.egroups.com/polls/autism-awareness-action
AUTOIMMUNE DISORDER LIST FOR THE POLL::::

this article was in the Houston Chronicle Tuesday, Nov. 28. I checked
it out, it isn't a theory.
¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤
Researchers Identify Gene Common to Many Autism Cases
| Associated Press |
Researchers funded by the National Institutes of Health have identified
a gene that may predispose people to developing autism. The gene, known
as HOXA1, plays a crucial role in early brain development. The study was
conducted by a research team in NIH's Collaborative Programs of
Excellence in Autism and was published in the December issue of
Teratology.
"These findings strongly suggest that a gene controlling early brain
formation may underlie the development of autism in a large number of
cases," said Duane Alexander, M.D., Director of the National Institute
of Child Health and Human Development (NICHD) and chair of NIH's autism
coordinating committee.
The spectrum of disorders known collectively as autism frequently
involve problems in communicating with others and difficulty interacting
socially. Many people with autism exhibit repetitious hand and body
movements. Roughly one in 500 persons may be affected by some form of
the disorder. The research team was led by Jennifer Ingram, Ph.D., and
Christopher Stodgell, Ph.D., of the University of Rochester School of
Medicine and Dentistry in Rochester, New York. The research was
conducted as part of the NIH Collaborative Program of Excellence in
Autism (CPEA). This $42 million research initiative is an international
network of ten research teams seeking to unravel the mysteries of
autism. The network is co-funded by the NICHD, the National Institute of
Deafness and Other Communication Disorders, and the National Center for
Complementary and Alternative Medicine.
The researchers tested 57 people diagnosed with autism for a variant of
the HOXA1 gene. Of these, 22--about 40 percent-had one copy of the
variant. Only one person with autism carried two copies of the variant
gene, said the study's senior investigator, Patricia M.Rodier, Ph.D., of
the University of Rochester School of Medicine. When the researchers
tested hundreds of people without autism, they found that people who had
two copies of the variant were even less common. This suggests that
having two copies of the mutant gene interferes with survival. Moreover,
after testing the genes of parents and other family members of people
with autism, the researchers found that symptoms of autism were more
common in people who inherited the variant gene from their mothers than
in those who inherited the same gene from their fathers. Dr. Rodier said
that this agrees with several other studies of patterns of autism in
families; inheritance from the mother seems to play a strong role in who
develops the disorder.
Dr. Rodier and her coworkers first thought to investigate the HOXA1 gene
after reviewing the pattern of birth defects resulting from prenatal
exposure to thalidomide. Children born to mothers who took the drug
during pregnancy have sometimes been born with autism. Some of the
autistic children born to mothers who took thalidomide also had
misshapen ears, as well as abnormalities in the nerves of the head and
face.
Previous studies of these children suggest that the damage to the ears
and facial nerves resulted between the 20th and the 24th days after
conception. This time span marks the development of brain regions that
later control the muscles of the eyes, face, tongue, jaw, and throat.
Because mice engineered to lack the HOXA1 gene show similar patterns of
brain and ear abnormalities, the researchers tested autism patients for
abnormalities of the corresponding human gene. "One by one, we're
finding the genes responsible for the autism spectrum disorders," said
Marie Bristol-Power, Ph.D, NICHD special assistant for autism programs.
She noted that other NICHD-funded investigators previously have
discovered genes for two autism-related disorders, Rett syndrome and
Fragile X syndrome.
As is the case with such findings, the Rodier group's report must be
confirmed by other researchers. The other teams in the CPEA will seek to
reproduce the findings in the near future. Additional information about
autism is available on the NICHD autism page,
http://www.nichd.nih.gov/autism/

Hello all,
The Autism Bio Medical Discussion list has started a poll for Bio-Profiling
Purposes, which is wonderful I think!!
On the list Eric and I created, Autism-Awareness-Action@egroups.com ---- I
am duplicating those polls for the purposes of having even more responses -
as our list has different members than the ABMD list.......
Many of you are on the Autism-Awareness-Action or ABMD lists to participate
in the polls.......... for those who are not --- please consider joining
the Autism-Awareness-Action list to register your vote in the BioMedical
Polls!!
There are currently 4 polls to vote in, an AutoImmune Poll, a poll of family
history of Alcoholism, a poll for whether you received Pitocin in labor, and
a poll for whether you received a Rhogam shot. There will be additional
polls added - so join in no-mail mode so you can check in now and then and
see what other polls there are.
I know we can easily get more than 1000 votes!!!!!
Please encourage others to join to participate in the polling!
All responses at the conclusion of the polling will be forwarded to the ABMD
listowner.
The more responses we have, the better the Bio-Profile the ABMD list can
create!!
URL to join Autism-Awareness-Action:
http://www.egroups.com/group/autism-awareness-action
Subscribe: autism-awareness-action-subscribe@egroups.com
To go to the polls:::
http://www.egroups.com/polls/autism-awareness-action
Oh, and please only vote once in each poll..........
Thank you!
Michelle Guppy

Just a little note about my son who started the ketogenic diet for his
seizures three weeks ago.
He has had only one seizure, (very small absence seizure), and his
communication, social, and whole persona has changed. Tonight, I took
him (Cody) and his brother, (who is autistic) to look at christmas
lights around the neighborhood. Cody was saying, "Hey, look Mom, a
snowman... hey, look David, it's pretty lights!" Cody was diagnosed
with PDD-NOS last year, and just yesterday, his speech therapist said
she was astounded at the leaps and bounds that my son is making within
the past weeks.
It's as if a door was opened in his mind.
I'm still interested in what Dr. Goldberg can do for my son David. I
just thought I'd share this with you all cause I had read that some of
you have children who are having seizures, and I would feel awful if I
knew something might help your children, and not share it.

Hi all,
I will be having my ASA meeting Dec. 6. Anyone living in the md-DC-PA
area is welcome to come. Here is my ASA site.
http://www.alleganyinternet.net/autism.html If you need Directions or
more info please e-mail me and I will give them to you. Thanks a Lot!!!
lois (JJsmom)

I read the following post on the list. My question is
about Nancy Klimas. I know she is on the NIDS board,
but I have heard it through the rumor mill that
Nancy's research has centered more on cognitive
behavioral approaches, and that she has been opposed
to a name change for CFS. In light of what I hear,
can it be said that Nancy Klimas does not support a
viral etiology for CFIDS, and if so, how is it that
she could be supportive of Peptide T?
I look forward to hearing more from anyone who might
have better information.
Thanks,
Katherine Bradtke
Regarding recent questions on new immune modulators, I
believe most
of the interest surrounds the use of Peptide-T which
was developed by
Candace Pert and Michael Ruff at NIH. (Peptide-T has
primarily been
used for treatment of AIDs related issues.) Both
firmly believe that
Peptide-T will help virally affected autistic
children.
In addition, Drs. Jeff Galpin (UCLA) and Nancy Klimas
(U. Fla.?) also
believe Peptide-T holds much promise, as does Dr.
Andrew Zimmerman at
Hopkins. Most interesting is that all three groups of
folks have
arrived at their conclusions based on separate medical
approaches.
Unfortunately, Peptide-T has never received approval
from the FDA for
use of any kind, let alone pediatric use. A small rat
study showed
Peptide-T might affect the reproductive systems, so
another study
must be completed before the FDA will allow a
Peptide-T trial on
children. My understanding is this trial will take at
least another
6 months. Money for an autism trial has been raised
by MAT --
http://www.mat.org/

Regarding recent questions on new immune modulators, I believe most
of the interest surrounds the use of Peptide-T which was developed by
Candace Pert and Michael Ruff at NIH. (Peptide-T has primarily been
used for treatment of AIDs related issues.) Both firmly believe that
Peptide-T will help virally affected autistic children.
In addition, Drs. Jeff Galpin (UCLA) and Nancy Klimas (U. Fla.?) also
believe Peptide-T holds much promise, as does Dr. Andrew Zimmerman at
Hopkins. Most interesting is that all three groups of folks have
arrived at their conclusions based on separate medical approaches.
Unfortunately, Peptide-T has never received approval from the FDA for
use of any kind, let alone pediatric use. A small rat study showed
Peptide-T might affect the reproductive systems, so another study
must be completed before the FDA will allow a Peptide-T trial on
children. My understanding is this trial will take at least another
6 months. Money for an autism trial has been raised by MAT --
http://www.mat.org/
For more information about Peptide-T and Candace Pert go to:
http://www.mercola.com/2000/june/24/autism%20interview.htm
Hope this is helpful.
Jeff

Lisa - this is the first I've heard of the request for pictures. Can you give
more details; where to send them, what info to include, etc.....

Hey guys, I have had only very few responses for my request for NIDS kids
photos. I am not sure which ones we will use. We need kids in every stage of
NIDS, looking spacey and looking fine. color black and white. All the public
service announcement will say id that our kids are SICK, it is an EPIDEMIC, an
epidemic cannot only be GENETIC and we need some HELP. WE want to have this
ready to go in January and really need the photos. Lots of parents have already
worked very hard to raise money to pay for this and to get as far as we are.
Please help. E mail me off group and I will send you my address. We need
written permission as well. Thanks, lisa

The classification of autism, Asperger's syndrome, and pervasive
developmental
disorder.
Szatmari P
Department of Psychiatry and Behavioural Neursosciences, McMaster
University,
Hamilton, Ontario. szatmar@...
Can J Psychiatry 2000 Oct;45(8):731-8
OBJECTIVE: The current classification of the pervasive developmental
disorders
(PDDs) as conceptualized in both the DSM-IV and ICD-10 is deeply
unsatisfying to
many parents, front-line clinicians, and academic researchers. Is the
diagnostic
validity of the various disorders simply lacking empirical data for full
substantiation, or does the overall conceptualization of the category have
more
fundamental problems, not reflecting the "true" nature of the phenomena?
This
paper argues the latter hypothesis. I review the historical development of
the
classification of PDD, summarize recent empirical data on issues of
reliability
and validity, and suggest a new approach to classification and
understanding.
PMID: 11086556, UI: 20539131

Voice processing abilities in children with autism, children with specific
language impairments, and young typically developing children.
Boucher J, Lewis V, Collis GM
Department of Psychology, University of Warwick, Coventry, UK.
j.boucher@...
J Child Psychol Psychiatry 2000 Oct;41(7):847-57
It is well established that people with autism have impaired face
processing,
but much less is known about voice processing in autism. Four experiments
were
therefore carried out to assess (1) familiar voice-face and sound-object
matching; (2) familiar voice recognition; (3) unfamiliar voice
discrimination;
and (4) vocal affect naming and vocal-facial affect matching. In Experiments
1
and 2 language-matched children with specific language impairment (SLI) were
the
controls. In Experiments 3 and 4 language-matched children with SLI and
young
mainstream children were the controls. The results were unexpected: the
children
with autism were not impaired relative to controls on Experiments 1, 2 and
3,
and were superior to the children with SLI on both parts of Experiment 4,
although impaired on affect matching relative to the mainstream children.
These
results are interpreted in terms of an unexpected impairment of voice
processing
in the children with SLI associated partly, but not wholly, with an
impairment
of cross-modal processing. Performance on the experimental tasks was not
associated with verbal or nonverbal ability in either of the clinical
groups.
The implications of these findings for understanding autism and SLI are
discussed.
PMID: 11079427, UI: 20529793

Discovery of allelic variants of HOXA1 and HOXB1: Genetic susceptibility to
autism spectrum disorders.
Ingram JL, Stodgell CJ, Hyman SL, Figlewicz DA, Weitkamp LR, Rodier PM
Department of Obstetrics and Gynecology, University of Rochester School of
Medicine and Dentistry, Rochester, New York 14642.
Teratology 2000 Dec;62(6):393-405
BACKGROUND: Family studies have demonstrated that the autism spectrum
disorders
(ASDs) have a major genetic etiologic component, but expression and
penetrance
of the phenotype are variable. Mice with null mutations of Hoxa1 or Hoxb1,
two
genes critical to hindbrain development, have phenotypic features frequently
observed in autism, but no naturally occurring variants of either gene have
been
identified in mammals. METHODS: By sequencing regions of genomic DNA of
patients
with autism spectrum disorders, we detected a substitution variant at HOXA1
and
an insertion variant at HOXB1, both in coding regions of the genes.
Fifty-seven
individuals ascertained for a diagnosis of an ASD, along with 166 of their
relatives, were typed for these variants. Two non-ASD populations were
typed,
and the frequency of the newly identified alleles was determined in all
groups.
The genotypes of the ASD families were tested for conformation to
Hardy-Weinberg
proportions and Mendelian expectations for gene transmission. RESULTS: The
frequency of the variants was 10-25% in persons of European or African
origin.
In the ASD families, there was a significant deviation from the HOXA1
genotype
ratios expected from Hardy-Weinberg proportions (P = 0.005). Among affected
offspring, a significant deviation from Mendelian expectation in gene
transmission (P = 0.011) was observed. No statistically significant effects
were
detected when the same analyses were applied to the HOXB1 locus, but there
was
evidence of an interaction between HOXA1, HOXB1, and gender in
susceptibility to
ASDs. CONCLUSIONS: The results support a role for HOXA1 in susceptibility to
autism, and add to the existing body of evidence implicating early brain
stem
injury in the etiology of ASDs. Copyright 2000 Wiley-Liss, Inc.
PMID: 11091361

Lois
Don't know for sure, but one parent friend of mine mentioned something like
that with turkey and also with chicken. Nothing would surprise me when it
comes to our kids' whacky immune systems! Becky

Hi all,
JJ loves turkey! So everyday since thanksgiving he has wanted leftover
turkey. Fine, Except for the last couple of days he has been very cryie
and mean acting. He is on 0.25mg of Resperdal that has helped alot
before this. Does anyone know if the turkey has anything to do with
this?? thanks in advance! Lois (JJsmom)

Hi Guys:
Per a friend, Fox TV, on the news, is going to be talking about Autism.
I
don't know what the discussion will be about. At this point and thought
I
would let everyone know.
It will be on tonight and Monday night as well. I got this from another
list. Lois

I recently read an article on MSG in
the magazine LIVING WITHOUT
(which is a great magazine to get a subscription
to. Good article on a child with many food allergies
along with the MSG article)
The article talks about the hidden dangers and sources
of MSG. MSG is an excitotoxin.
WOW !! I didin't realize that MSG went by so
many names. My husband is allergic to MSG.
Our son Jacob is autistic and responding well to a combination
of ABA, NIDS and dietary changes. But now I'm wondering
what I'm feeding him. He's still 'responding to something'
but we can't place our finger on it.
Has anyone spoke with Dr Goldberg or their CAN doctor
about this hidden ingredient ??
Please email me
http://www.noMSG.com
Thank you!
Doris Smith
millersville MD

Hi
I read a book on this and I would defineitly avoid it. The basic
thing about msg , aspartame etc. is that it can have an effect on brain
cells. The brain cells can die from being flooded with too much glutamate.
The cells turn on and keep on going like an everyready battery until they get
exhausted and die. Certain things can predispose someone to this. Low
magnesium, maybe genes and others. It is really hard to avoid too, because
it has hidden names like yeast extract . All products do not label MSG, but
have hydrolyzed veg protein which is just another name. It may turn out to
be banned like phenelpropalanomine . It may take another ten years or so .
Things that are in and on are foods are said to be safe, deemed to be safe ,
but later turn out to be banned. I think the only way to be safe is too
check out everything for yourself. Not to accept all doctors words as
gospel. Trust your instincts. Look into everything. Check into everything
and continue to do so. kelly

This article is available online at the URL hereinbelow.
Vol. 96, Issue 22, 12708-12712, October 26, 1999
Immunology
Humoral response to herpes simplex virus is complement-dependent
Xavier J. Da Costa*, Mark A. Brockman*,
Elisabeth Alicot,, Minghe Ma,, Michael B.
Fischer,, Xioaning Zhou,, David M. Knipe*, and
Michael C. Carroll,,§,¶
Departments of * Microbiology and Molecular Genetics, Pathology,
and § Pediatrics, Harvard
Medical School, and The Center for Blood Research, 200 Longwood
Avenue, Boston, MA
02115
The complement system represents a cascade of serum proteins,
which
provide a major effector function in innate immunity. Recent
studies
have revealed that complement links innate and adaptive immunity
via
complement receptors CD21/CD35 in that it enhances the B cell
memory response to noninfectious protein antigens introduced i.v.
To
examine the importance of complement for immune responses to
virus infection in a peripheral
tissue, we compared the B cell memory response of mice deficient
in complement C3, C4, or
CD21/CD35 with wild-type controls. We found that the deficient
mice failed to generate a normal
memory response, which is characterized by a reduction in IgG
antibody and germinal centers.
Thus, complement is important not only in the effector function
of innate immunity but also in the
stimulation of memory B cell responses to viral-infected cell
antigens in both blood and peripheral
tissues.
http://www.pnas.org/cgi/content/full/96/22/12708
This post may be shared.

Seminar on Autism, or Neuro Immune Dysfunction Syndrome (NIDS)
Michael Goldberg, M.D., F.A.A.P, and President of the NIDS Medical Advisory
Board and Research Institute to speak on Autism/PDD
January 27, 2001
Presented by Northeast Medical Center Hospital and Northeast Hospital
Foundation, a half-day educational conference on
Autistic Syndrome
Humble Area Activity Center
(Houston)
2:00 - 6:00 pm
1401 South Houston Avenue
(Old Humble Road)
Humble, Texas 77338
Dr. Goldberg received his Medical Degree from UCLA and trained at LAC-USC
Medical Center. He is the President of the NIDS Medical Advisory Board and is
on the clinical teaching staff at both UCLA and Cedars-Sinai
Hospitals. He has seventeen years experience in evaluating and treating
children with disorders that fall within the evolving spectrum of "NIDS" (Neuro
Immune Dysfunction Syndromes), including Autism, ADD/ADHD, and Chronic Fatigue
Syndrome. Dr. Goldberg possesses a patient panel of over 400 with varying NIDS
conditions.
There is strong evidence that a large subset of children with 'acquired' autism,
where symptoms do not emerge until after the child's first few months to over a
year, suffer from a disease process that changes their immune system to a
dysfunctional level These children may appear normal in the first 15-18 months
of life. They crawl, sit up, walk, and usually hit normal milestones on
schedule. Suddenly, these children cease to progress - or begin to regress.
They become withdrawn, quiet sometimes, hyper at others. In the past, Autism
was considered a psychiatric disorder- some felt mentally retarded.
Dr. Goldberg proposes that NIDS is a medical condition, and is insurable, and
treatable and separates them from the 'hopelessness' associated with 'classic'
autism!
Come hear this foremost doctor in the field for over 17 years explain the new
directions we can take for these children! He has had tremendous success in
treating these children!
Conference Information:
January 27, 2001
Humble Area Activity Center
1401 South Houston Avenue
(Old Humble Road)
Humble, Texas 77338
2:00 - 6:00 pm
For more info:
Phone: 713-462-0607 (Bill or Julie Ehmling)
or e-mail : jehmling@...
Space is limited, so please register, and come early to get a good seat. You
will not want to miss this informative speaker as he tells us how to make a
difference for these children!

Michele Davies,
I have been reading your posts also, and I think you are doing a wonderful
job of explaining Dr. Goldberg's protocol, and giving information. I
appreciate your dedication.
I received your registration form for the upcoming conference! I am excited
that you will be there. I am sure that people will want to talk to you.
Since you mentioned that we are having a conference here, I thought I would
send the registration form as well, so that interested people can register!
I will do that in a separate e-mail.
If anyone has any questions regarding the conference,
jehmling@...
let me know!
Julie Ehmling

<A HREF="http://neuroimmunedr.com/Articles/Autism___PDD/autism___pdd.html"
Click here: Autism / PDD</A
Dear Michelle:
I thought that if I sent you this it would be very, very helpful and
informative.
There is a wealth of information in Dr. Goldberg's website. I have chosen
the What's new link for you to look through initially. You may chose to
click on articles and presentations, as well. Most of the answers to your
questions will be there.
You may also join our chatroom on Tuesday nites 10pm eastern standard
time, 7pm pacific time. Dr. Goldberg dedicates one nite a week for all
parents. He answers all questions and gives explanations of anything
you may need explained. He is wonderful.
As far as some of your concerns, in the last post I have received, I will
continue to answer to the best of my ability. I am certainly not a doctor,
nor am I educated in the medical field. I have a BA in Communications,
but my experiences as a single mother in raising my daughter Lindsey
has taught me plenty. She is my entire life. And I never believed that
she had no potential & would never speak, as I have been told, time and
time again.
Thank you for your compliment, I try to stay as positive as possible for
the sake of my daughter and of course, myself. We have been seeing
Dr. Goldberg since March 2000. Lindsey use to be in continual discom-
fort, pain and would cry for hours at a time. This is practically gone since
Dr. Goldberg took over. She is more attentive in school, listens better and
is finally starting to speak in 2-4 word sentences. It is more of a joy than
I can ever write. I live in Elmwood Park, NJ, just 10 minutes west of the
George Washington Bridge. My phone # is 201-703-1060. You may call
me anytime you want.
Dr. Goldberg has found that yes there are similarities in all our children's
blood, such as high viral counts, sometimes candida, and of course a lack
of blood flow in the temporal lobes of the brain. His protocol is also very
similar with each child. I am sure that he has some differences upon
treating each patient. But depending upon how long the child has been in
a dysfunctional state would depend how long the child will begin to make
progress. This is where the patience comes into play. His office number
is 818-343-1010. Best of luck to you and your son.
Where do you live? Would you like to attend one of Dr. Goldberg's seminars?
One is coming up in Dec at the Marriot in Bethesda, Maryland. And I know
of one in Jan at the Humble Activity Center in Humble, Texas. (I believe
that it
is not too far from Houston.) You may email Mrs. Julie Ehmling at:
ehmling@... and ask for a registration form.
Michele C. Davies
isoaa@...

Thanks Michele for your thorough reply. You give off such a positiveness in
your writing -too bad we can't meet. Anyway, how long have you been with
Dr.G? Yea, I agree ! When I do read the mail the parents do seem impatient,,
but I guess the attitude is that time is running out! Is his treatment
pretty much the same for each child? Does he pretty much assume that each
child has this viral infection? Do you know of anyone who had seen him and
the child has recovered? What test result did your child have that proved
that he/she had it? What behaviors did you see diminish once treated and did
the bowels change as well? The only behaviors that Richie has is limited
speech and social weakness even though he gets along so well with his
sister. He is a finicky eater, and he frequently wakes up at night.His bowels
are fine and rarely sick Lastly, these modulators,once approved how does one
get them? Thanks so much for replying, Michelle

Michele, you really feel confident with these immune modulators!! I keep
aasking what these things will do, but nobody answers me so I am going to ask
you. What are the names of these modulators and will they evenually help with
the bloodflow to the brain. I remember asking Dr. G about this and his answer
still confused me. I have yet made an appointment with him because my son is
improving with ABA and diet but I too pray everyday that something added will
help these guys become more typical. I am going to take your positiveness on
these modulators and make it my biggest hope as well. Please respond if you
can share more knowledge with me. Tak care, Michelle

Hi Michelle,
These immune modulators will expedite the healing process for our kids. Dr.
Goldberg's protocol involves healing the immune system. To do so, at this
point, we must only work with drugs/meds that are approved w/ FDA. These
drugs usually include, but are not limited to the following:
1-antivirals
2-antifungals
3-ssri (prozac, zoloft,etc.)
4-kutapressin
5-zyrtec (for sinus conditions)
These medications listed above help to eliminate the viruses, candida (excess
of
yeast) and improve bloodflow in the brain (temporal lobes) which should
enable the immune system to function more efficiently. It is sometimes an
extremely long process, could be anywhere from 1-5 years, and parents do seem
to lose their patience.
These immune modulators have been proven to be much more effective than
the medications listed above. These modulators will allow the body to not
only
function more efficiently but will maintain and regulate all the major
systems,
such as immune, central nervous system and blood flow in the temporal lobes
of the brain. The children will remain in a healthy balance, referred to as
homeostasis.
It is quite amazing how Dr. Goldberg linked this "New Type Of Autism", REALLY
SHOULD BE REFERRED TO AS NIDS, to the immune system. His wife was ill and
suffered from Chronic Fatigue Syndrome, similar abnormalities in her blood
and our children diagnosed with PDD/Autism were noted. Then he began to
realize that it was in fact a medical condition these kids suffer from. His
heart and soul has been in it from the get go. Nobody was listening to his
philosophy,etc. But he has hard, solid, scientific evidence of his
findings. He deserves to be acknowledged not only as a physician; but as a
human being that wants to see people healthy and fulfilling their lives. I
never met a doctor quite like him. Don't you wait, get a phone call to his
office asap. And remember these kids did not get to where they are overnite.
Give your son/daughter time, they will come out of this!!!
Sincerely and With Great Respect,
Michele C. Davies
isoaa@...

I'm hearing all about new immune modulators that might become
available soon. Where are they coming from and what are they exactly?
I don't get to get on here very much. Thanks for any info in advance.
Diane B.

Michelle:
Sorry for not getting back sooner. Yes, Dr. Goldberg starts children
usually on an anti-viral. Then an anti-fungal and then a ssri. I really
don't know if that would be the way he would start if the new immune
modulators were available.
Let's hope and pray that they become available real soon. It would
be the greatest Holiday gift for all of us. I pray for this more than
anything in the world.
Michele Davies
isoaa@...

Diane,
Wow, now I don't feel so bad. My son is 6 and that's ALL he does
when
he's not in school. He watches his favorite Disney videos and rewinds
one part for an hour or more and then goes on to another movie or part
and rewinds it for awhile. I try to keep him away from it but
sometimes
it just can't be done. :0)
Diane B.

Physician's Group Opposes Vaccine Mandates - The Association of
American Physicians and
Surgeons (AAPS), a leading national physician organization, is
calling for a moratorium on all
government mandated vaccines and has passed a resolution to that
end at their Annual Meeting.
The resolution calling for an end to mandatory childhood vaccines
passed without a single "no"
vote. This is a great organization of which I am proud to be a
member.
http://www.mercola.com/2000/nov/19/vaccine_mandate_opposition.htm

Not all cases of enterocolitis are caused by CMV. HHV6 is another
pathogen than can live in gastroinestinal tissue (Wakefield AJ et
al 1992) and is associated with subtly atypical epileptiform
activity (2). Nonetheless, Fox et al is interesting because an
antiviral treatment was successful (1).
A person wonders: how many children with chronic diarrhea are (or
are not) evaluated for pathogen presence in gastrointestinal
tissue? Especially since many infants acquire CMV, and an
infant's CMV infection can appear to be asymptomatic (eg, 3a-3b).
Furthermore, CMV-related cow's milk allergy and hepatobiliary
dysfunction are recognized (eg, 4-6), as are CMV-induced
impairments of immune function (eg, 7). Breast milk is another
source of CMV infection in an infant (8), and the connection
between CMV and some cases of autism has long been described (eg,
9-10).
Which prompts questions:
1. How many ASD children with early gastroinestinal problems
were/are experiencing "seemingly asymptomatic" CMV infection
within tissues related to digestion?
2. How many ASD children with mildly impaired immunity were/are
experiencing "seemingly asymptomatic" CMV infection within
certain immune-cell subsets?
3. How many ASD children being affected by chronic CMV would be
helped by an appropriate antiviral (in a context of
immune-restoration and sufficient nutrient-availability)?
Teresa
1. Pediatrics 1999 Jan;103(1):E10
Intractable diarrhea from cytomegalovirus enterocolitis in an
immunocompetent
infant.
Fox LM, Gerber MA, Penix L, Ricci A Jr, Hyams JS
University of Connecticut School of Medicine, University of
Connecticut Health
Center, Farmington, Connecticut, USA.
Infection with cytomegalovirus (CMV) in infants can be congenital
or perinatal.
Infected infants may be asymptomatic or present with pneumonia,
rash,
hepatosplenomegaly, or encephalitis.1 In the presence of an
immunodeficiency,
severe and sometimes fatal disease may occur. To our knowledge,
CMV has not
been identified previously as a cause of intractable diarrhea of
infancy. We
report the case of a 5-week-old immunocompetent infant with
intractable
diarrhea attributable to CMV-induced enterocolitis. Recognition
of this
infection and initiation of ganciclovir therapy was associated
with a rapid
improvement and resolution of the diarrhea.
2. Infant convulsions with mild gastroenteritis. Br & Dev
22.5.301-6 2000.
3a. Rev Inst Med Trop Sao Paulo 2000 May-Jun;42(3):129-32
Congenital cytomegalovirus infection in a neonatal intensive care
unit in brazil
evaluated by PCR and association with perinatal aspects.
Santos DV et al.
Cytomegalovirus (CMV) infection is the most common congenital
infection,
affecting 0.4% to 2.3% newborns. Most of them are asymptomatic at
birth, but
later 10% develop handicaps, mainly neurological disturbances...
3b. Obstet Gynecol 1999 Dec;94(6):909-14
Prenatal diagnosis of fetal cytomegalovirus infection after
primary or recurrent
maternal infection.
Nigro G, Mazzocco M, Anceschi MM, La Torre R, Antonelli G, Cosmi
EV
OBJECTIVE: To determine the reliability of prenatal diagnosis of
cytomegalovirus
infection in women with primary or recurrent infection. METHODS:
Amniotic fluid
(AF) samples from 117 pregnant women were evaluated for
cytomegalovirus culture
and cytomegalovirus-DNA detection. Neonatal and postnatal samples
also were
examined to confirm or exclude transmission of maternal-fetal
cytomegalovirus
infection. RESULTS: Of 25 women with primary cytomegalovirus
infection, 13 (52%)
had cytomegalovirus-positive AF samples by polymerase chain
reaction (PCR), nine
of which also were diagnosed by culture. All eight neonates born
to mothers
whose AF was cytomegalovirus-positive by PCR and culture were
cytomegalovirus
infected, and three were symptomatic. One aborted fetus had
cytomegalovirus-DNAemia. Of four women with
cytomegalovirus-positive AF samples
by PCR only, two delivered asymptomatic cytomegalovirus-infected
neonates and
two aborted (one fetus had cytomegalovirus encephalopathy). Of 45
mothers with
recurrent infection, two with AF cytomegalovirus-positive by PCR
and culture,
and another with cytomegalovirus-positive AF samples by PCR only,
aborted
cytomegalovirus-DNA-positive fetuses. Of the other seven women
with
cytomegalovirus-positive AF samples by PCR only, two delivered
asymptomatic
cytomegalovirus-infected neonates, two delivered neonates
cytomegalovirus-positive by PCR only (one was symptomatic), and
three delivered
infants cytomegalovirus-negative by PCR and culture. All 47
mothers with
nonactive cytomegalovirus infection and cytomegalovirus-negative
AF samples had
uninfected neonates... CONCLUSION: Prenatal diagnosis of
fetal cytomegalovirus infection should include PCR in addition to
viral culture,
particularly for congenital cytomegalovirus infections following
maternal
recurrence.
4. Arch Virol 1997;142(3):573-80
Ganciclovir therapy for cytomegalovirus-associated liver disease
in
immunocompetent or immunocompromised children.
Nigro G, Krzysztofiak A, Bartmann U, Clerico A, Properzi E, Valia
S, Castello M
Pediatric Institute, Rome, Italy.
Ganciclovir therapy was given intravenously to 20 children with
cytomegalovirus
(CMV)-associated liver disease, of whom 6 were immunocompetent
and 14 were
immunocompromised (9 had AIDS and 5 had solid tumors).
Immunocompetent children
had isolated liver disease diagnosed at birth (4 children), or
systemic
congenital CMV infection including liver disease (2 children).
Ganciclovir was
used following two regimens: A) 5 mg/kg twice daily for 8 to 86
days (mean 21);
B) 7.5 mg/kg twice daily for 14 days followed by 10 mg/kg three
times weekly
for three months. CMV infection was diagnosed by viral isolation,
detection of
viral antigens, and/or CMV DNA from blood and urine. All
immunocompetent
children had negative CMV culture and CMV DNA detection from
blood and/or urine
after 14 weeks of treatment. However, the three children who were
treated with
regimen B showed normal ALT levels at the end of the maintenance
course,
whereas the children who received ganciclovir with regimen A had
normal ALT
levels only after about 1 year. All children with tumors
initiated regimen B,
but only three, who had negative CMV detection and markedly
decreased ALT
levels, received full treatment; of the remaining two children,
one recovered
after only an initial course, and the other had therapy
interrupted because of
hepatic failure and died 9 days later. In contrast, the children
with AIDS
received several ganciclovir courses for different periods at the
lower dosage:
they generally improved during treatment but did not recover
completely, and
five children died with active CMV infections. Based on our
study,
CMV-associated liver disease can be efficiently treated with
ganciclovir both
in immunocompetent and immunodeficient children. However, a
single ganciclovir
course including a higher dosage and prolonged therapy appeared
to be more
effective than several courses with lower dosages.
5. J Leukoc Biol 1994 Aug;56(2):187-91
Analysis of human cytomegalovirus-infected peripheral blood
mononuclear cells
from infants with liver dysfunction by flow cytometry and the
polymerase chain
reaction.
Numazaki K, Asanuma H, Nagata N, Chiba S
Department of Pediatrics, School of Medicine, Sapporo Medical
University, Japan.
Perinatal human cytomegalovirus (HCMV) infection often involves
the
hepatobiliary tract, but infected individuals usually remain
asymptomatic. We
investigated the role of CD8+ lymphocytes in 13 infants with
liver dysfunction
associated with perinatal HCMV infection. In three patients more
than 40% of
CD8+ cells were positive for HCMV immediate early antigen (IEA)
and late antigen
(LA) by flow cytometry after selection of T lymphocytes
subpopulations. In the
other 10 infants, 20% to 30% of CD8+ cells were positive for HCMV
IEA and LA.
HCMV IE DNA was detected in CD8+ cells from one infant, in CD4+
cells from one
infant, and in both CD4+ and CD8+ cells from three infants. HCMV
infection of
CD8+ cells may play an important role in the process of perinatal
primary
infection.
6. Eur J Pediatr 1997 Jul;156(7):528-9
An immunocompetent infant with cow's milk allergy and
cytomegalovirus colitis.
Jonkhoff-Slok TW, Veenhoven RH, de Graeff-Meeder ER, Buller HA
Department of Paediatrics Spaarne Hospital, Haarlem, The
Netherlands.
A 5-week-old, severely ill, infant is described with diarrhoea
and rectal
bleeding, followed by vomiting and dehydration after introduction
of a cow's
milk formula. A diagnosis of cow's milk allergy was made because
of the
clinical presentation of an allergic enterocolitis, the rapid
improvement after
introduction of a hypo-allergenic formula and development of
colic directly
after rechallenge with cow's milk. Furthermore a highly specific
IgE for
alpha-lactalbumin strongly supported the diagnosis. Because of
recurrent rectal
bleeding a limited colonoscopy was performed at the age of 10
weeks.
Surprisingly a second diagnosis of histopathologically proven
cytomegalovirus
(CMV) colitis was made. Extensive immunological screening
revealed no signs of
immunodeficiency. The child thrived without any treatment for CMV
and developed
normally. This is the first description of an immunocompetent
infant with CMV
colitis. CONCLUSION: It cannot be excluded that the allergic
colitis
facilitated the CMV colitis, or vice versa CMV colitis triggered
cow's milk
protein induced entero-colitis. Further attention should be given
to children
with bloody diarrhoea to establish a possible relationship
between CMV
infection and cow's milk protein allergy.
7. J Virol 1988 Oct;62(10):3603-7
Cytomegalovirus infection of peripheral blood mononuclear cells:
effects on
interleukin-1 and -2 production and responsiveness.
Kapasi K, Rice GP
Cytomegalovirus suppresses the proliferative response of
peripheral blood
mononuclear cells to phytohemagglutinin. In these experiments, we
identified
which mononuclear cell subpopulation might be responsible for the
suppression.
We found that prior infection of either lymphocytes or monocytes
followed by
reconstitution with monocytes or lymphocytes, respectively, would
abrogate the
proliferative response in a subsequent culture with
phytohemagglutinin.
Infection of either cell type also reduced both the production of
interleukin-1
(IL-1) and IL-2 and the proliferative response to exogenously
supplied IL-1 or
IL-2. We did not find evidence for an IL-2 antagonist. These
experiments suggest
that cytomegalovirus causes a metabolic derangement in
lymphocytes and monocytes
and impairs their ability both to produce and to respond to
physiological
mediators of the immune response.
8. Roum Arch Microbiol Immunol 1997 Jul-Dec;56(3-4):165-78
Cytomegalovirus (CMV) in cervical secretion and breast milk. A
thirty years
perspective.
Diosi P
During the past 30 years prospective epidemiologic studies have
clearly
established that infants commonly acquire CMV infection in the
immediate
perinatal or early postnatal period. CMV reaches the offspring
with uterine
cervical secretions during the birth process and/or with maternal
milk during
the breast-feeding period, usually resulting in asymptomatic
infection in
full-term infants. In young women cervical shedding of CMV may
reflect a pelvic
inflammatory disease and involves the risk of sexual
transmission.
[comment: given the link between CMV and gastrointestinal
difficulties and atopic phenomena, as reviewed in Occena RO et al
1993p, we wonder how many infants receiving CMV via breast milk
are truly asymptomatic?]
9. J Autism Child Schizophr 1978 Mar;8(1):37-43
Autistic symptoms in a child with congenital cytomegalovirus
infection.
Stubbs EG
A case of intrauterine cytomegalovirus infection with onset of
autistic symptoms
apparently after 6 months of age is reported. Physicians who find
autistic
symptoms in very young children might include cytomegalovirus in
their
differential to document the presence or absence of a
correlation.
10. J Autism Dev Disord 1983 Sep;13(3):249-53
Autism in a child with congenital cytomegalovirus infection.
Markowitz PI
A case is reported of early infantile autism associated with a
congenital
cytomegalovirus infection. The diagnosis of autism is based on
the child's
f