>>> Posting number 22687, 
                              dated 6 Sep 1997 09:04:25

.....INTRODUCTION.....
Without debating the pros and cons of vaccinations, many studies report that febrile
convulsions occur in some kids as part of their response to vaccination (eg 7-9).
Usually, such febrile convulsions are said to have generated no neurologic sequelae,
tho' study design and duration make this conclusion other than necessarily valid.
Similarly, HHV-6 (human herpes virus #6) is realized to be a common source of
febrile convulsions in young children (eg, 4).
      Leaving aside the effects of vaccination-induced febrile seizures, not only
is HHV-6 "rarely diagnosed clinically" (ie, 'tis overlooked, which is very different
from "ruled out"), but it often includes rash and "inflamed tympanic membranes" as
well as seizures; and a recent review includes a most fascinating statement about
febrile convulsions:
    "Because there are long term sequelae of febrile convulsions,
     including hippocampal sclerosis..." (1)

In clear terms, the author seems to have said, febrile convulsions can damage
neurons in the hippocampi (plural of hippocampus, we have two, one on each side,
towards frontal region of temporal lobe). So what? 

1.    The hippocampus is involved with memory and has numerous inter- connections
with the nucleus basalis (a central source of cholinergic input to much of brain)
and with the amygdala. In fact, the recent works by Tunaanen and colleages has found
that deleterious neuronal activity in the hippocampal region can lead to amygdaloid
damage, including in a subarea wherein neurons have been identified as responsive
specifically to faces and eye-contact (primary cites in 6).
2.    Social behavior beyond the infant period is affected by neonatal hippocampal
lesions in primates (2).
3.    HHV-effects can range from "complete recovery without neurological deficit to
death." (3).
4.    Further deterioration of skills may also be derived as an after effect from
prior episodes of HHV-6 infection, as Kondo et al write: "recurrence of febrile
convulsions may be associated with reactivation of HHV-6." (5)

Conclusion: Vaccinations and HHV-6 induce febrile convulsions in some kids. Febrile
convulsions are associated with hippocampal sclerosis, whose effects would include
decline in cognitive skills and in social effectiveness.

<1>  Lyall EG.
Human herpesvirus 6: primary infection and the central nervous system.
     Pediatric Infectious Disease Journal.  15(8):693-6, 1996 Aug.

<2>  Beauregard M.  Malkova L.  Bachevalier J.
Stereotypies and loss of social affiliation after early hippocampectomy in primates.
     Neuroreport.  6(18):2521-6, 1995 Dec 15.
  The present study was aimed at determining whether early hippocampal damage alters
the development of normal social interactions. Results showed that, at 2 months of
age, animals with neonatal hippocampal lesions presented minor disturbances in
initiation of social interactions. These subtle changes in behavior were less
evident at 6 months, although at this age, the operated animals displayed more
withdrawals in response to an increase in aggressive responses from their unoperated
peers. Finally, in adulthood, the amount of time spent by the operated monkeys in
social contacts with their normal peers was markedly less than that in normal
dyads...

<3>  McCullers JA.  Lakeman FD.  Whitley RJ.
Human herpesvirus 6 is associated with focal encephalitis.
     Clinical Infectious Diseases.  21(3):571-6, 1995 Sep.
  Human herpesvirus 6 (HHV-6) is a cause of roseola infantum. Recent reports
associate HHV-6 with cases of encephalitis; however, conclusive etiologic data do
not exist. We evaluated clinical data and laboratory specimens obtained from
patients with focal encephalitis of unknown etiology. Cerebrospinal fluid (CSF)
specimens were tested by polymerase chain reaction for the presence of HHV-6 DNA.
Selected samples were analyzed by DNA sequencing. We detected HHV-6 DNA in the CSF
of nine of 138 patients. DNA sequencing revealed that group B strains of HHV-6 were
present in those specimens that were analyzed. No significant differences could be
demonstrated in clinical presentation, laboratory findings, or neurodiagnostic
imaging results between the nine patients with confirmed HHV-6 infection and the 129
patients without evidence of HHV-6 infection. Neurological outcome for the nine
HHV-6-infected patients varied from complete recovery without neurological deficit
to death. Further prospective study is warranted.

<4>  Barone SR.  Kaplan MH.  Krilov LR.
Human herpesvirus-6 infection in children with first febrile seizures.
     Journal of Pediatrics.  127(1):95-7, 1995 Jul.
  We evaluated febrile convulsions prospectively in 42 children to investigate the
association between acute human herpesvirus-6 (HHV-6) infection and first-time
febrile convulsions, using both virologic and serologic methods. Eight children had
primary HHV-6 infection documented by viral culture and an additional three by
acute- and convalescent-phase serologic studies. These findings indicate that acute
HHV-6 infection is a frequent cause of febrile convulsions in young children.

<5>  Kondo K.  Nagafuji H.  Hata A.  Tomomori C.  Yamanishi K.
Association of human herpesvirus 6 infection of the central nervous system
with recurrence of febrile convulsions.
     Journal of Infectious Diseases.  167(5):1197-200, 1993 May.
  To determine the relationship of human herpesvirus-6 (HHV-6) infection to febrile
convulsions, cerebrospinal fluid (CSF) from patients with a history of febrile
convulsion were tested by polymerase chain reaction (PCR) amplification for HHV-6
DNA. HHV-6 DNA was detected in 9 of 10 samples from patients with exanthem subitum
who showed neurologic symptoms. Also, 8 of 10 CSF samples from 8 patients who had
three or more febrile convulsions and 1 of 7 CSF samples from patients who had a
single febrile convulsion contained HHV-6 DNA. These data suggest that HHV-6 may
invade the brain during the acute phase of exanthem subitum and that recurrence of
febrile convulsions may be associated with reactivation of HHV-6.

6. Binstock T.  Hypothesis: Febrile seizures and the amygdala: a causal mechanism
in autism and related disorders.  Bit.listserv.autism (31 January 1997).

<7> Farrington Pet al
A new method for active surveillance of adverse events from
diphtheria/tetanus/pertussis and measles/mumps/rubella vaccines.
    Lancet.  345(8949):567-9, 1995 Mar 4.

<8>  Baraff LJ.  Manclark CR.  Cherry JD.  Christenson P.  Marcy SM.
Analyses of adverse reactions to diphtheria and tetanus toxoids and pertussis
vaccine by vaccine lot, endotoxin content, pertussis vaccine potency and percentage
of mouse weight gain.
     Pediatric Infectious Disease Journal.  8(8):502-7, 1989 Aug.

<9>  Pollock TM.  Miller E.  Mortimer JY.  Smith G.
Symptoms after primary immunisation with DTP and with DT vaccine.
     Lancet.  2(8395):146-9, 1984 Jul 21.

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      2 Vaccinations and/or HHV-6, autism & herpes
                              >>> Posting number 22694, 
                              dated 6 Sep 1997 10:27:11


In one or several of the cites in the prior post with same subject heading, the
statement is made that HHV-6 is seldom "looked for" in children and thus is seldom
diagnosed. Part of the reason is that the virus in only recently discovered, most
clinical-labs are not equipped to perform HHV-6 PCR, and the significance of the
virus has not been appreciated.
      The prior post contained cites supporting a rationale whereby HHV-6, via its
induction of febrile seizures (in some infants, toddlers, or even older children),
might lead to hippocampal sclerosis and, thereby, to effects seen later as impaired
cognitive and/or social function.
      In prior posts the topic of "stealth" has been applied to various viruses and
at least one article (J Aut Dev Dis) and a related web-site (search for ccid,
perhaps via altavista) have linked autism and a "stealth" virus.

Because HHV-6 and its link to febrile seizures have not been known for long, and
because febrile seizures have been known to induce neuronal sclerosis in areas
affecting cognitive and social function (3), the questions arise:
1)    How many cases within the range pointed towards via "PDD, PDD/NOS, and
autism-spectrum" might be due to prior and/or latently lingering HHV-6?
2)    Similarly, how many actual regressions or "disintegrative disorders" might be
caused by the re-activation of one or several of the stealth viruses?

We might keep in mind that in some kids with no outward symptoms (eg, rash), "...the
central nervous system may be the sole site of persistence." (1); and since PCR for
HHV-6 (or for HSV-1 or HSV-2) is not likely to have occurred in nearly all
autism-spectrum kids alive today, the answer to questions 1 & 2 is, *No one knows*.
      As PCR becomes more readily available, and as the internet enables parents to
connect with research labs capable of PCR, answers to questions 1 & 2 may be
obtainable in the near future.
      There is an important ramification: treatment may be available that could help
in some cases -- eg, soon after a febrile-seizure episode occurred (if proper lab
diagnostics were initiated), or *perhaps* subsequently in regard to a lingering,
latent infection.
      However, just how effective a given anti-viral pharmaceutical would be re:
latent CNS infections is a very complex issue. Clues are found in the Lyall essay
(3), wherein ganciclovir (a "kissing cousin" of acyclovir) is mentioned as possibly
effective against HHV-6. But the complexity is brought forth in other cites about
ganciclovir (eg, 4-10).
      Nonetheless, a number of recent findings suggest that various viruses have the
ability to induce damage in neuronal regions known to be affected in autism, ie,
regions known to subserve traits affected in autism. Thus the following questions
seem more pressingly legitimate:
  (i) How many cases within the autism/PDD spectrum have their roots in past viral
infections, some of which may remain within the CNS as latent infections awaiting
re-activation?
 (ii) How many such cases might avoid further deterioration if anti-viral
pharmaceuticals were properly used?
(iii) How many such near-future cases might be avoided if PCR diagnostics become
more widely appreciated and utilized?

REFERENCES

<1>   Caserta MT et al
Neuroinvasion and persistence of human herpesvirus 6 in children.
      Journal of Infectious Diseases.  170(6):1586-9, 1994 Dec.
  Human herpesvirus 6 (HHV-6) causes a febrile illness in children and has been
implicated as a cause of encephalitis and recurrent seizures. Paired samples of
cerebrospinal fluid (CSF) and peripheral blood mononuclear cells (PBMC) from 487
children were evaluated by nested polymerase chain reaction (PCR) for evidence of
current or past infection with HHV-6. PBMC were also cultured for isolation of
HHV-6. These data were correlated with the patients' clinical information. HHV-6 DNA
was detected in 72 (14.8%) of 487 CSF samples. HHV-6 persistence was documented in
142 children by PCR detection of HHV-6 DNA in PBMC or CSF (or both) in the absence
of primary HHV-6 infection; the central nervous system was the only site of HHV-6
DNA persistence in 28.9%. HHV-6 DNA can be detected in the CSF of children during
and after primary infection, and the central nervous system may be the sole site of
persistence.

<2>  Hall CB et al
Human herpesvirus-6 infection in children. A prospective study of
complications and reactivation.
     New England Journal of Medicine.  331(7):432-8, 1994 Aug 18.
  BACKGROUND. Infection with human herpesvirus-6 (HHV-6) is nearly universal in
infancy or early childhood. However, the course of this infection, its
complications, and its potential for persistence or reactivation remain unclear.
METHODS. We studied infants and children under the age of three years who presented
to our emergency department with acute illnesses. Infants and young children without
acute illness were studied as controls. HHV-6 infection was identified by
blood-mononuclear-cell culture, serologic testing, and the polymerase chain reaction
(PCR). RESULTS. No primary HHV-6 infection was found among 582 infants and young
children with acute nonfebrile illnesses or among 352 controls without acute
illness. Of 1653 infants and young children with acute febrile illnesses, 160 (9.7
percent) had primary HHV-6 infection, as documented by viremia and seroconversion.
They ranged in age from 2 weeks to 25 months; 23 percent were under the age of 6
months. HHV-6 infections accounted for 20 percent of 365 visits to the emergency
department for febrile illnesses among children 6 to 12 months old. Of the 160
infants and young children with acute HHV-6 infections, 21 (13 percent) were
hospitalized, and 21 had seizures. Often the seizures appeared late and were
prolonged or recurrent. HHV-6 infections accounted for one third of all febrile
seizures in children up to the age of two years. In follow-up studies over a period
of one to two years, the HHV-6 genome persisted in blood mononuclear cells after
primary infection in 37 of 56 children (66 percent). Reactivation, sometimes with
febrile illnesses, was suggested by subsequent increases in antibody titers in 16
percent (30 of 187) and by PCR in 6 percent (17 of 278). No recurrent viremia was
detected. Of 41 healthy newborns studied, 12 (29 percent) had the HHV-6 genome in
their blood mononuclear cells; nevertheless, 6 of these newborns subsequently had
primary HHV-6 infections. CONCLUSIONS. In infants and young children HHV-6 infection
is a major cause of visits to the emergency department, febrile seizures, and
hospitalizations. Perinatal transmission may occur, with possible asymptomatic,
transient, or persistent neonatal infection.

<3>  Lyall EG.
Human herpesvirus 6: primary infection and the central nervous system.
     Pediatric Infectious Disease Journal.  15(8):693-6, 1996 Aug.
<4>  Musch DC.  Martin DF.  Gordon JF.  Davis MD.  Kuppermann BD.
Treatment of cytomegalovirus retinitis with a sustained-release
ganciclovir implant. The Ganciclovir Implant Study Group.
     New England Journal of Medicine.  337(2):83-90, 1997 Jul 10.
<5>  Smith IL et al
High-level resistance of cytomegalovirus to ganciclovir is associated with
alterations in both the UL97 and DNA polymerase genes.
     Journal of Infectious Diseases.  176(1):69-77, 1997 Jul.
<6>   Mahieu LM.  Ieven M.  Van Hoeck KJ.  Parizel PM.  Van Acker KJ.
Diagnosis of cytomegalovirus meningoencephalitis by polymerase chain
reaction in an immunocompetent infant who recovered after treatment with
ganciclovir.
      Clinical Infectious Diseases.  24(3):520-1, 1997 Mar.
<7>  Whitley RJ et al
Ganciclovir treatment of symptomatic congenital cytomegalovirus infection:
results of a phase II study. National Institute of Allergy and Infectious
Diseases Collaborative Antiviral Study Group.
     Journal of Infectious Diseases.  175(5):1080-6, 1997 May.
<8>  Conti DJ.  Shen G.  Singh T.  Isenberg A.  Freed BM.
Ganciclovir prophylaxis of cytomegalovirus disease.
     Transplantation Proceedings.  29(1-2):804-6, 1997 Feb-Mar.
<9>  Reymen D et al
Antiviral activity of selected acyclic nucleoside analogues against human
herpesvirus 6.
     Antiviral Research.  28(4):343-57, 1995 Dec.
<10>  Burns WH.  Sandford GR.
Susceptibility of human herpesvirus 6 to antivirals in vitro.
      Journal of Infectious Diseases.  162(3):634-7, 1990 Sep.        eof


            1 MMR/HHV-6: general considerations
                              >>> Posting number 25001, 
                              dated 2 Oct 1997 14:37:47


Here are some thoughts about MMR and HHV-6. We must keep in mind that each child is
different and that the timing during which a child might have acquired HHV-6 will
differ from person to person. Therefore, the following comments should be taken as
a general sketch, a starting point in trying to understand each child's specific
case. We must also keep in mind that, in many individuals, there may be more than
one virus, bacteria, and/or fungus present; and this kind of inter-individual
variation is likely to be seen as differences in each child's specific traits and
medical history. So, here are some thoughts centered upon MMR and HHV-6.

1.    Measles and measles vaccinations induce immunospression. This is well known,
well documented; and a primary researcher in this is Diane E. Griffin of Johns
Hopkins. (Cites will be in subseqeunt post).
2.    HHV-6 is ubiquitous, many kids have it and handle it quite OK. However, HHV-6
is also known to induce high fever and/or seizures in a goodly number of kids. The
healthier a given child's immune system, the likelier that HHV-6 will not cause
problems to that child.
3.    At least hypothetically, the immunosuppression that accompanies measles
vaccination would allow HHV-6 to blossom more fully within the child. What might be
seen is roseola (aka exanthema subitum) and/or fevers and/or some mild or not so
mild febrile convulsions. (some HHV-6 cites will be posted separately too).
4.    HHV-6 is also known to be able to produce its own immunosuppression, and can
even find its way into bone marrow. In some children, the HHV-6 immunosuppression
would become additive with the immunosuppression already induced by the measles
component of the MMR vaccination.
5.    Giving MMR prior to the age of 12 months would seem to be a way to ensure a
prolonged Transient Hypogammaglobulinemia of Infancy (pTHI), thereby inducing
another kind of double immunosuppression -- that from the infant's normal THI plus
that from measles-vaccination immunosuppression.
6.    If a pregnant woman were to receive a measles vaccination, then her
measles-related immunosuppression would increase the likelihood that other viruses,
bacteria, and/or fungi would gain a foothold or (if present and normally
immunosuppressed) to blossom in ways affecting fetal development.
7.    The work of Tasnee Chonmaitree and colleagues has demonstrated that many cases
of recurrent otitis media (rOM) are viral in origin. In a study of 271 kids with
rOM, 10 percent were found to have cytomegalovirus and/or herpes simplex virus in
middle ear effusion (CMV, HSV, MEM). Her studies prove that, in some kids, heavy
duty viruses can be present at an early age, even if the only symptom is rOM.
8.    HHV-6, CMV, and Epstein-Barr virus (EBV) are known to be able to induce
immunosuppression. When Drs. Baker and Martin find CMV in peripheral blood, that is
a very important finding. Treating the CMV and reducing it or eliminating it can
only help the child -- even if he or she has other viruses in the CNS, viruses that
may not be detectable by peripheral measures or even via viral culture of CSF.
9.    If an infant has any of these viruses (eg, HHV-6, CMV, or EBV) in his or her
system when the MMR is given, then (due to the immunosuppressivity of the measles
component) that child would seem at risk for any of the three immunosuppressive
viruses to become more entrenched and active.
10.   HSV is a very special virus. It is present in some kids with recurrent otitis
media (rOM), yet may remain within the CNS with *no* exterior symptoms one the
otitis has subsided. Depending upon its route of entry (eg, oral/gastrointestinal,
nasal-cativy, scraped skin, etc), HSV will travel to various parts of the peripheral
and central nervous systems. Once there, if a child is immunocompetent, the virus
may remain latent and, while latent, may induce no neuronal death.
11.   If HSV is latently present in CNS neurons when the MMR is given, two effects
are likely: (i) the measles-induced immunosupression may allow some of the latent
HSV to become re-activated, and (ii) the MMR's induction of interferon gamma (1)
ought lead to MHC-I presentation of viral particles upon the surface of neurons,
which would then be killed by the person's own immune surveillance processes.
Importantly, HSV is capable of migrating to neural substrates that have been
identified in autism (eg, cerebellum and temporal lobe) and/or that participate in
autistic traits -- eg, neuronal regions subserving language, emotions, sensory
sensitivities, and direct eye-contact.

.....Closing Comments.....
Each child is very different; each child's medical history prior to, during, and
subsequent to the MMR is very different and ought be considered as the tapestry in
which the MMR and HHV-6 occurred.
      Several parental anecdotes have mentioned the temporal sequence MMR followed
by signs of HHV-6. This is an extremely important relationship, and possible causal
links were outlined in the first portion of this document. However, each parent
would be well served to look for additional clues prior to and subsequent to the
vaccination. Such introspection may generate additional clues instructive regarding
the child's specific pathogenesis into autism and, most importantly, may provide
clues towards designing the most effective treatments.
      In other words, the link "MMR and HHV-6" is important, but each child's
medical history may have some additional clues that can be considered --
eg, familial infections such as mononucleosis or herpes or?
eg, gastrointestinal problems in the child and/or in other members of the
    family or ?
eg, other?

These developments are very exciting and are occurring because of each person's
committment to ask questions and to share. From the pioneers such as Rimland, Baker,
Pangborn, Martin and others, to the parents and a few researchers, and a growing
number of parents-as-researchers, might we say,
             Progress is being made and shall continue!

1) Pabst HF et al. Kinetics of immunologic responses after primary MMR
vaccination. Vaccine.  15(1):10-4, 1997 Jan.
 "To study the kinetics of humoral as well as cellular immunity to measles and to
test for associated immunosuppression 124 12 month old children were studied twice,
before routine MMR and either 14, 22, 30, or 38 days after vaccination...
Interferon-gamma was the principal cytokine produced after primary measles
immunization..."

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            2 MMR/HHV-6: immune suppression by measles virus/vaccine
                                    >>> Posting number 25023, 
                                    dated 2 Oct 1997 20:15:14

Measles virus can induce immune suppression, by vaccinations and/or infection. The
first seven citations are by DE Griffin and colleagues. Cites 8 thru 10 are by other
groups researching immunosuppression caused by measles virus, whether the
"wild-type" or the type found in certain vaccines.

<1> Karp CL.  Wysocka M.  Wahl LM.  Ahearn JM.  Cuomo PJ.  Sherry B.
    Trinchieri G.  Griffin DE.
Mechanism of suppression of cell-mediated immunity by measles virus
     Science.  273(5272):228-31, 1996 Jul 12.
<2>  Hussey GD et al.
The effect of Edmonston-Zagreb and Schwarz measles vaccines on immune
response in infants.
     Journal of Infectious Diseases.  173(6):1320-6, 1996 Jun.
<3>  Auwaerter PG et al
Changes within T cell receptor V beta subsets in infants following measles
vaccination.
     Clinical Immunology & Immunopathology.  79(2):163-70, 1996 May.
<4>  Griffin DE.
Immune responses during measles virus infection.
     Current Topics in Microbiology & Immunology.  191:117-34, 1995.
<5>  Ward BJ.  Griffin DE.
Changes in cytokine production after measles virus vaccination:
predominant production of IL-4 suggests induction of a Th2 response.
     Clinical Immunology & Immunopathology.  67(2):171-7, 1993 May.
<6>  Wu VH.  McFarland H.  Mayo K.  Hanger L.  Griffin DE.  Dhib-Jalbut S.
Measles virus-specific cellular immunity in patients with vaccine failure.
      Journal of Clinical Microbiology.  31(1):118-22, 1993 Jan.
<7>  Griffin DE et al
In vitro studies of the role of monocytes in the immunosuppression
associated with natural measles virus infections.
     Clinical Immunology & Immunopathology.  45(3):375-83, 1987 Dec.

<8>  Schnorr JJ et al.
Induction of maturation of human blood dendritic cell precursors by
measles virus [vaccine & wild type] is associated with immunosuppression.
     Proc of the National Acad of Sciences USA  94(10):5326-31 1997.
  As well as inducing a protective immune response against reinfection, acute
measles is associated with a marked suppression of immune functions against
superinfecting agents and recall antigens, and this association is the major cause
of the current high morbidity and mortality rate associated with measles virus (MV)
infections. Dendritic cells (DCs) are antigen-presenting cells crucially involved
in the initiation of primary and secondary immune responses, so we set out to define
the interaction of MV with these cells. We found that both mature and precursor
human DCs generated from peripheral blood monocytic cells express the major MV
protein receptor CD46 and are highly susceptible to infection with both MV vaccine
(ED) and wild-type (WTF) strains, albeit with different kinetics. Except for the
down-regulation of CD46, the expression pattern of functionally important surface
antigens on mature DCs was not markedly altered after MV infection. However,
precursor DCs up-regulated HLA-DR, CD83, and CD86 within 24 h of WTF infection and
72 h after ED infection, indicating their functional maturation. In addition,
interleukin 12 synthesis was markedly enhanced after both ED and WTF infection in
DCs. On the other hand, MV-infected DCs strongly interfered with mitogen-dependent
proliferation of freshly isolated peripheral blood lymphocytes in vitro. These data
indicate that the differentiation of effector functions of DCs is not impaired but
rather is stimulated by MV infection. Yet, mature, activated DCs expressing MV
surface antigens do give a negative signal to inhibit lymphocyte proliferation and
thus contribute to MV-induced immunosuppression.

<9>  Aaby P.
Assumptions and contradictions in measles and measles immunization
research: is measles good for something?.
     Social Science & Medicine.  41(5):673-86, 1995 Sep.
  Measles infection, the major cause of childhood mortality among infections
preventable by immunization, has been considered to kill mainly young and
malnourished children. Assuming that mainly 'weak' children are saved by
immunizations, it has been speculated that the impact on survival of immunization
is likely to be limited because the malnourished children are more prone to die of
other infections. However, recent studies from developing countries have suggested
that host factors may not be the most important determinants of acute and long-term
mortality after measles infection. Instead, it was found that infection contracted
after exposure at home infection contracted from someone outside the home.
Furthermore, measles is particularly severe if contracted from someone of the
opposite sex. Hence transmission factors, in particularly intensity of exposure and
cross-sex transmission, may be more important determinants of measles mortality than
the determinants of measles mortality than the host factors usually emphasized.
Consistent with these observations and in contrast to assumptions about 'weak'
children dying, immunization is associated with a major reduction in mortality.
Since measles immunization is associated with a 30% reduction in mortality or more,
the impact is much larger than should be expected from the proportion of all deaths
attributed to measles. It has therefore been suggested that measles immunization may
prevent the persistent immunosuppression and delayed mortality assumed to be
associated with measles. However, several observations contradict the common
understanding that the function of measles immunization is only to prevent the acute
and long-term mortality associated with measles infection. Recently, the high-titre
measles immunization recommended by WHO was found to be associated with reduced
survival for female recipients compared with girls who have received the standard
low-dose measles vaccine, and this difference in survival was not due to suboptimal
protection against measles infection. Contrary to usual assumptions. against measles
infection. Contrary to usual assumptions, standard low-dose measles vaccine reduces
mortality even more when given before 9 months of age, the age currently recommended
by WHO. The beneficial impact of standard vaccine is apparently temporary, lasting
1 to 2 years, whereas it should increase with the age of the child. The beneficial
effect seems to be particularly strong for girls. The most likely interpretation of
these observations, is that standard low-dose measles vaccine has a non-specific
beneficial effect. Contrary to current assumptions, children who survive the acute
phase of measles infection may have a survival advantage compared with unimmunized,
uninfected children...

<10>  Smedman L et al.
Immunosuppression after measles vaccination.
     Acta Paediatrica.  83(2):164-8, 1994 Feb.
  The influence of conventional live attenuated measles vaccine on cellular immune
responsiveness was investigated in Sweden and Guinea-Bissau. Sixteen children in a
residential area in Bissau and 16 living in southern Stockholm were examined before
and 8-10 days after vaccination... These observations may be relevant to the
increased mortality found in children immunized with high-titre measles vaccines,
as compared to controls, in recent studies...

eofPOSTING HISTORY

>>> Posting number 22687, dated 6 Sep 1997 09:04:25
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      Vaccinations and/or HHV-6, autism & herpes

>>> Posting number 22694, dated 6 Sep 1997 10:27:11
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock
Subject:      2 Vaccinations and/or HHV-6, autism & herpes

>>> Posting number 25001, dated 2 Oct 1997 14:37:47
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      1 MMR/HHV-6: general considerations

>>> Posting number 25023, dated 2 Oct 1997 20:15:14
Sender:       SJU Autism and Developmental Disablities List
              
From:         Teresa Binstock 
Subject:      Re: 2 MMR/HHV-6: immune suppression by measles virus/vaccine