PMID: 

J Trace Elem Med Biol. 2019 Jan ;51:28-30. Epub 2018 Sep 18. PMID: 30466934

Abstract Title: 

Testing new hypotheses of neurological and immunological outcomes with aluminum-containing vaccines is warranted.

Abstract: 

[n/a]

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PMID: 

Ann Dermatol. 2013 Nov ;25(4):489-92. Epub 2013 Nov 30. PMID: 24371399

Abstract Title: 

New Onset Guttate Psoriasis Following Pandemic H1N1 Influenza Vaccination.

Abstract: 

Since the introduction of H1N1 influenza vaccine in the wake of the 2009 H1N1 pandemic, many serious and non-serious vaccine-related adverse events have been reported. The vaccination could induce pain, erythema, tenderness, and induration on injected areas. These symptoms usually disappear in a few days after the vaccination. In this case, we observed a 26-year-old woman with multiple erythematous scaly macules scattered on the extremities and trunk. She was injected with an inactivated split-virus influenza A/H1N1 vaccine without adjuvant (Greenflu-S®, Green Corp.) on her left deltoid area 10 days earlier. The first lesion appeared on the injection site three days after the vaccination, and the following lesions spread to the trunk and extremities after a few days. Histopathological examinations showed neutrophilic collections within the parakeratotic cornified layer, moderate acanthosis, diminished granular layer, elongation and edema of the dermal papillae, and dilated capillaries. The lesions were successfully treated with topical steroids and ultraviolet B phototherapy within three weeks, and there was no relapse for the following fourteen months. We assumed that pandemic vaccination was an important trigger for the onset of guttate psoriasis in this case.

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PMID: 

Vaccine. 2017 09 25 ;35(40):5314-5322. PMID: 28917295

Abstract Title: 

Association of spontaneous abortion with receipt of inactivated influenza vaccine containing H1N1pdm09 in 2010-11 and 2011-12.

Abstract: 

INTRODUCTION: Inactivated influenza vaccine is recommended in any stage of pregnancy, but evidence of safety in early pregnancy is limited, including for vaccines containing A/H1N1pdm2009 (pH1N1) antigen. We sought to determine if receipt of vaccine containing pH1N1 was associated with spontaneous abortion (SAB).METHODS: We conducted a case-control study over two influenza seasons (2010-11, 2011-12) in the Vaccine Safety Datalink. Cases had SAB and controls had live births or stillbirths and were matched on site, date of last menstrual period, and age. Of 919 potential cases identified using diagnosis codes, 485 were eligible and confirmed by medical record review. Exposure was defined as vaccination with inactivated influenza vaccine before the SAB date; the primary exposure window was the 1-28days before the SAB.RESULTS: The overall adjusted odds ratio (aOR) was 2.0 (95% CI, 1.1-3.6) for vaccine receipt in the 28-day exposure window; there was no association in other exposure windows. In season-specific analyses, the aOR in the 1-28days was 3.7 (95% CI 1.4-9.4) in 2010-11 and 1.4 (95% CI 0.6-3.3) in 2011-12. The association was modified by influenza vaccination in the prior season (post hoc analysis). Among women who received pH1N1-containing vaccine in the previous influenza season, the aOR in the 1-28days was 7.7 (95% CI 2.2-27.3); the aOR was 1.3 (95% CI 0.7-2.7) among women not vaccinated in the previous season. This effect modification was observed in each season.CONCLUSION: SAB was associated with influenza vaccination in the preceding 28days. The association was significant only among women vaccinated in the previous influenza season with pH1N1-containing vaccine. This study does not and cannot establish a causal relationship between repeated influenza vaccination and SAB, but further research is warranted.

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PMID: 

Ugeskr Laeger. 1992 Jul 13 ;154(29):2008-13. PMID: 1509566

Abstract Title: 

[Duration of immunity and occurrence of secondary vaccine failure following vaccination against measles, mumps and rubella].

Abstract: 

The present article illustrates the extent of secondary vaccine failure after vaccination for measles, mumps and rubella (MMR). Secondary vaccine failure means loss of the immunity induced by vaccination to such an extent that infection becomes possible. Serological investigations carried out with follow-up periods of up to 16 years after vaccination for measles, 21 years after vaccination for rubella and 12 years after vaccination for mumps reveal that loss of antibodies occurs with the elapse of time but that the clinical significance of this is probably very limited. Where all three types of vaccination are concerned, secondary vaccine failure has hitherto been very seldom. Infection with measles after secondary vaccine failure is generally described as running a milder course. In rare cases, rubella re-infection has resulted in infection in utero, so that a slight risk of congenital rubella cannot be entirely excluded after successful vaccination. No extensive systematic investigations of the effect of revaccination have been carried out and, similarly, the optimal interval between two or more vaccinations has not been illustrated in more detail in the literature. Subclinical infection is not uncommon after all three vaccines. Where measles is concerned, immunity may possibly be regarded as a continuum which, depending upon the antibody level, protects the individual from various degrees of clinical disease. If wild virus can be spread via individuals with subclinical infections, it is doubtful whether population immunity (herd immunity), which is necessary to eliminate the three diseases, can be attained in large populations.(ABSTRACT TRUNCATED AT 250 WORDS)

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PMID: 

SIAM J Appl Math. 2014;74(6):1810-1830. PMID: 25878365

Abstract Title: 

EPIDEMIOLOGICAL CONSEQUENCES OF IMPERFECT VACCINES FOR IMMUNIZING INFECTIONS.

Abstract: 

The control of some childhood diseases has proven to be difficult even in countries that maintain high vaccination coverage. This may be due to the use of imperfect vaccines and there has been much discussion on the different modes by which vaccines might fail. To understand the epidemiological implications of some of these different modes, we performed a systematic analysis of a model based on the standard SIR equations with a vaccinated component that permits vaccine failure in degree ("leakiness"), take ("all-or-nothingness") and duration (waning of vaccine-derived immunity). The model was first considered as a system of ordinary differential equations, then extended to a system of partial differential equations to accommodate age structure. We derived analytic expressions for the steady states of the system and the final age distributions in the case of homogenous contact rates. The stability of these equilibria are determined by a threshold parameter, a function of the vaccine failure parameters and the coverage. The value offor which= 1 yields the critical vaccination ratio, a measure of herd immunity. Using this concept we can compare vaccines that confer the same level of herd immunity to the population but may fail at the individual level in different ways. For any fixed>1, the leaky model results in the highest prevalence of infection, while the all-or-nothing and waning models have the same steady state prevalence. The actual composition of a vaccine cannot be determined on the basis of steady state levels alone, however the distinctions can be made by looking at transient dynamics (such as after the onset of vaccination), the mean age of infection, the age distributions at steady state of the infected class, and the effect of age-specific contact rates.

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PMID: 

J Neurovirol. 2011 Oct ;17(5):448-54. Epub 2011 Jul 27. PMID: 21792750

Abstract Title: 

Cytotoxicity of glioblastoma cells mediated ex vivo by varicella-zoster virus-specific T cells.

Abstract: 

Clinical or laboratory evidence of varicella-zoster virus (VZV) infection has been consistently associated with lower glioma risk in case-control studies, suggesting a protective effect of VZV against glioma. We formulated the following explanatory hypotheses: reactivated VZV preferentially infects and kills gliomas compared to normal parenchyma; and VZV-specific cytotoxic T lymphocytes (CTL) cross-react with gliomas. We established an ex vivo model of VZV infection, which showed that glioma cell lines and primary astrocytes were equally permissive to VZV infection and had similar 15% average decrease in viability upon infection. In co-cultures, the relative growth of glioma cells and astrocytes was not affected by the VZV infection. However, VZV stimulated, but not mock stimulated, peripheral blood mononuclear cells from VZV-seropositive individuals recognized and killed HLA class I-matched glioma cells (mean±SE decrease in viability of 26 ± 12%, p = 0.04), but not matched astrocytes. VZV infection of the glioma cells did not affect the T cell-mediated killing. Taken together, these data suggest that ex vivo VZV infection has similar direct effects on glioma cells and astrocytes. The protective effect of prior VZV infection against the incidence of glioma may be mediated by CTL that recognizes epitopes shared by VZV and glioma cells.

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PMID: 

MBio. 2014 Apr 22 ;5(2):e01074. Epub 2014 Apr 22. PMID: 24757216

Abstract Title: 

Global population structure and evolution of Bordetella pertussis and their relationship with vaccination.

Abstract: 

Bordetella pertussis causes pertussis, a respiratory disease that is most severe for infants. Vaccination was introduced in the 1950s, and in recent years, a resurgence of disease was observed worldwide, with significant mortality in infants. Possible causes for this include the switch from whole-cell vaccines (WCVs) to less effective acellular vaccines (ACVs), waning immunity, and pathogen adaptation. Pathogen adaptation is suggested by antigenic divergence between vaccine strains and circulating strains and by the emergence of strains with increased pertussis toxin production. We applied comparative genomics to a worldwide collection of 343 B. pertussis strains isolated between 1920 and 2010. The global phylogeny showed two deep branches; the largest of these contained 98% of all strains, and its expansion correlated temporally with the first descriptions of pertussis outbreaks in Europe in the 16th century. We found little evidence of recent geographical clustering of the strains within this lineage, suggesting rapid strain flow between countries. We observed that changes in genes encoding proteins implicated in protective immunity that are included in ACVs occurred after the introduction of WCVs but before the switch to ACVs. Furthermore, our analyses consistently suggested that virulence-associated genes and genes coding for surface-exposed proteins were involved in adaptation. However, many of the putative adaptive loci identified have a physiological role, and further studies of these loci may reveal less obvious ways in which B. pertussis and the host interact. This work provides insight into ways in which pathogens may adapt to vaccination and suggests ways to improve pertussis vaccines. IMPORTANCE Whooping cough is mainly caused by Bordetella pertussis, and current vaccines are targeted against this organism. Recently, there have been increasing outbreaks of whooping cough, even where vaccine coverage is high. Analysis of the genomes of 343 B. pertussis isolates from around the world over the last 100 years suggests that the organism has emerged within the last 500 years, consistent with historical records. We show that global transmission of new strains is very rapid and that the worldwide population of B. pertussis is evolving in response to vaccine introduction, potentially enabling vaccine escape.

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PMID: 

BMJ. 1999 Jan 16 ;318(7177):193. PMID: 9888928

Abstract Title: 

Public should be told that vaccines may have long term adverse effects.

Abstract: 

[n/a]

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PMID: 

Epidemiol Infect. 2000 Apr ;124(2):263-71. PMID: 10813152

Abstract Title: 

Secondary measles vaccine failures identified by measurement of IgG avidity: high occurrence among teenagers vaccinated at a young age.

Abstract: 

Failure to seroconvert (primary vaccine failure) is believed to be the principal reason (approx.>95%) why some vaccinees remain susceptible to measles and is often attributed to the persistence of maternal antibodies in children vaccinated at a young age. Avidity testing is able to separate primary from secondary vaccine failures (waning and/or incomplete immunity), but has not been utilized in measles epidemiology. Low-avidity (LA) and high-avidity (HA) virus-specific IgG antibodies indicate primary and secondary failure, respectively. Measles vaccine failures (n = 142; mean age 10.1 years, range 2-22 years) from an outbreak in 1988-9 in Finland were tested for measles-virus IgG avidity using a protein denaturating EIA. Severity of measles was recorded in 89 failures and 169 non-vaccinees (mean age 16.2 years, range 2-22 years). The patients with HA antibodies (n = 28) tended to have clinically mild measles and rapid IgG response. Among failures vaccinated at15 months of age with single doses of Schwarz-strain vaccine in the 1970s, 50 (95% CI 1-99), 36 (CI 16-56) and 25% (CI 8-42) had HA antibodies, respectively. When a single measles, mumps and rubella (MMR) vaccine had been given after 1982 at 15 months of age, only 7% (CI 0-14) showed HA antibodies. Omitting re-vaccinees and those vaccinated at

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PMID: 

PLoS One. 2009 ;4(5):e5538. Epub 2009 May 14. PMID: 19440239

Abstract Title: 

Vaccination against human influenza A/H3N2 virus prevents the induction of heterosubtypic immunity against lethal infection with avian influenza A/H5N1 virus.

Abstract: 

Annual vaccination against seasonal influenza viruses is recommended for certain individuals that have a high risk for complications resulting from infection with these viruses. Recently it was recommended in a number of countries including the USA to vaccinate all healthy children between 6 and 59 months of age as well. However, vaccination of immunologically naïve subjects against seasonal influenza may prevent the induction of heterosubtypic immunity against potentially pandemic strains of an alternative subtype, otherwise induced by infection with the seasonal strains. Here we show in a mouse model that the induction of protective heterosubtypic immunity by infection with a human A/H3N2 influenza virus is prevented by effective vaccination against the A/H3N2 strain. Consequently, vaccinated mice were no longer protected against a lethal infection with an avian A/H5N1 influenza virus. As a result H3N2-vaccinated mice continued to loose body weightafter A/H5N1 infection, had 100-fold higher lung virus titers on day 7 post infection and more severe histopathological changes than mice that were not protected by vaccination against A/H3N2 influenza. The lack of protection correlated with reduced virus-specific CD8+ T cell responses after A/H5N1virus challenge infection. These findings may have implications for the general recommendation to vaccinate all healthy children against seasonal influenza in the light of the current pandemic threat caused by highly pathogenic avian A/H5N1 influenza viruses.

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