Measles Vaccination, Alzheimers and Herpes Simplex Virus--Teresa Binstock

Measles Vaccination, Alzheimers and Herpes Simplex Virus--Teresa Binstock

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.

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. 1996 Jul 12;273(5272):228-31. PMID: 8662504
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, Goddard EA, Hughes J, Ryon JJ, Kerran M, Carelse E, Strebel PM, Markowitz LE, Moodie J, Barron P, Latief Z, Sayed R, Beatty D, Griffin DE. The effect of Edmonston-Zagreb and Schwarz measles vaccines on immune response in infants. J Infect Dis. 1996 Jun;173(6):1320-6. PMID: 8648203
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, Hussey GD, Goddard EA, Hughes J, Ryon JJ, Strebel PM, Beatty D, Griffin DE. Changes within T cell receptor V beta subsets in infants following measles vaccination. Clin Immunol Immunopathol. 1996 May;79(2):163-70. PMID: 8620622 [PubMed - indexed for MEDLINE]
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, Lin WR, Wilcock GK, Faragher B. 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.