>From 1998
Teresa Binstock wrote:
> 
> The work of Diane E Griffin and colleagues of Johns Hopkins establishes
> that measles virus and measles-vaccinations impair cell-mediated immunity
> (CMI) and increase the likelihood of other viral infections (eg, 1-3).
>      These findings are supported by the work of Martinez et al (i) who
> admit and are trying to solve vaccination-induced, *long-term* impairment
> of CMI, and (ii) who mention herpes simplex virus (HSV) as an example of
> the kind of infection exacerbated by vaccination-induced, long-term
> impairments of CMI (4).
>      The work of Itzhaki and colleagues has identified HSV as an
> important component of Alzheimer's, especially in persons having the a
> certain allele of an apolipoprotein gene (5).
> 
> Conclusions:
> 1.  These data suggest that a person's risk of developing Alzheimer's is
> increased by having had vaccinations and the resulting long-term
> impairment of cell-mediated immunity.
> 2.  These data also suggest that, if vaccinated, an older person who has a
> latent infection with one of the herpes-class viruses would be likelier to
> (i) experience a significant re-activation of the virus, and/or (ii) be at
> increased risk for other viral infections -- due to vaccination-induced
> impairments of cell-mediated immunity.
> 
> Teresa
> 
> 1) Karp CL et al. Mechanism of suppression of cell-mediated immunity by
> measles virus.  Science.  273(5272):228-31, 1996 Jul 12.
>   The mechanisms underlying the profound suppression of cell-mediated
>   immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12),
>   derived principally from monocytes and macrophages, is critical for the
>   generation of CMI. Measles virus (MV) infection of primary human monocytes
>   specifically down-regulated IL-12 production.
> 
> <2> Hussey GD... Griffin DE.
> The effect of Edmonston-Zagreb and Schwarz measles vaccines on immune
> response in infants.
>           Journal of Infectious Diseases.  173(6):1320-6, 1996 Jun.
>   ...Eighty-eight children were immunized at 6 or 9 months of age with the
>   Edmonston-Zagreb (EZ) or Schwarz (SW6, SW9) strain of measles vaccine.
>   Children were studied before and 2 weeks and 3 months after immunization.
>   ...Mitogen-induced lymphoproliferation was decreased at 2 weeks
>   in the SW9 group and at 3 months in all groups and was negatively
>   correlated with measles antibody level at 3 months (r = -.387, P = .003).
>   CD8 T cells, soluble CD8, neopterin, and beta2-microglobulin were
>   increased at 2 weeks in the SW9 group, and soluble CD8 and
>   beta2-microglobulin remained elevated at 3 months. Therefore, measles
>   immunization resulted in suppression of lymphoproliferation, which was
>   most evident in infants with the highest antibody responses and most
>   immune activation.
> 
> 3) Auwaerter PG... Griffin DE.
> Changes within T cell receptor V beta subsets in infants following measles
> vaccination.
>           Clinical Immunology & Immunopathology.  79(2):163-70, 1996 May.
>   Measles produces immune suppression which contributes to an increased
>   susceptibility to other infections. Recently, high titered measles
>   vaccines have been linked to increased long-term mortality among some
>   female recipients....
> 
> [The following citation reiterates that vaccinations can impair
> cell-mediated immunity by shifting cytokines release into a Th2 pattern,
> thereby allowing intracellular pathogens (eg, many viruses) to be more
> successful. We note that the authors of this 1997 study are trying to
> devise a way around the general immune-impairing effect of conventional
> vaccinations.]
> 
> 4. Martinez X et al. DNA immunization circumvents deficient induction of T
> helper type 1 and cytotoxic T lymphocyte responses in neonates and during
> early life.     Proc of the National Academy of Sciences  94.8726-31 1997.
>   ab:  The relative deficiency of T helper type 1 (Th1) and cytotoxic T
>   lymphocyte (CTL) responses in early life is associated with an increased
>   susceptibility to infections by intracellular microorganisms. This is
>   likely to reflect a preferential polarization of immature CD4 T cells
>   toward a Th2 rather than a Th1 pattern upon immunization with conventional
>   vaccines...
> 
> 5) Itzhaki RF et al. Herpes simplex virus type 1 in brain and risk of
> Alzheimer's disease. Lancet 349(9047):241-4 1997.
>   BACKGROUND: The apolipoprotein E epsilon 4 (APOE-epsilon 4) allele is a
>   risk factor for Alzheimer's disease (AD), but it is neither essential nor
>   sufficient for development of the disease. Other factors-genetic or
>   environmental-must therefore have a role. By means of a PCR we have
>   detected herpes simplex virus type 1 (HSV1) in latent form in brains of
>   elderly people with and without AD. We have postulated that limited
>   reactivation of the virus causes more damage in AD patients than in
>   elderly people without AD because of a difference in the hosts. We now
>   report the APOE genotypes of AD patients and non-AD sufferers with and
>   without HSV1 in brain. METHODS: DNA was extracted from 84 samples of brain
>   from 46 AD patients (39 temporal lobe, 39 frontal lobe, three hippocampus)
>   and from 75 samples of brain from 44 non-AD elderly people (33 temporal
>   lobe, 36 frontal lobe, six hippocampus). PCR amplification was used to
>   detect HSV1 thymidine kinase gene and the host APOE gene. FINDINGS: By
>   multiple logistic regression, the APOE-epsilon 4 allele frequency was
>   significantly higher in the patients positive for HSV1 in brain than in
>   the HSV1-negative AD group, the HSV1-positive non-AD group, or the
>   HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%, respectively).
>   The odds ratio for APOE-epsilon 4 in the HSV1-positive AD group compared
>   with HSV1-negative non-AD group was 16.8 (95% CI 3.61-77.8) and in the
>   HSV1-negative AD group, 1.67 (0.21-13.4). We also compared APOE genotypes
>   of 40 people who had recurrent cold sores and 33 non-sufferers; the
>   APOE-epsilon 4 allele frequencies were 36% and 9%, respectively (p <
>   0.0001). INTERPRETATION: These findings suggest that the combination of
>   HSV1 in brain and carriage of an APOE-epsilon 4 allele is a strong risk
>   factor for AD, whereas either of these features alone does not increase
>   the risk of AD. The findings in people with cold sores support our
>   hypothesis that APOE-epsilon 4 and HSV1 together are damaging in the
>   nervous system.
>                                                                   eof
 
 

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