Rubella Strains

Rubella

 

Global Measles and Rubella Laboratory Network, January 2004-June 2005

 

Seven genotypes and three additional provisional genotypes of rubella virus are recognized by WHO (Figure 2). These genotypes are classified into two clades (i.e., groups of similar genotypes), designated 1 and 2; clade 2 viruses have not been found circulating in the western hemisphere. Although knowledge concerning the geographic distribution of rubella genotypes has progressed substantially since 2003, the genotypes of rubella viruses present in many countries and regions remain unknown.

 

rubella2

 

 

Global strains of rubella virus

 

 

Based on analysis of the viral E1 gene, there are two genotypes of rubella virus: Genotype I is present in Europe, North America, and Asia; Genotype II is present in China, Israel and Korea and appears to co-exist with Genotype I viruses in these countries 14. While these genotypes differ by 7-11% at the nucleotide level, they differ by less than 3% at the amino acid level and are of the same serotype. Therefore, the biological significance of the evolution and maintenance of two genotypes is unclear. Following the widespread use of rubella vaccine in developed countries from the 1970s onward, a change in rubella strains occurred in which an

intercontinental genotype clade of Genotype I present in Europe, North America, and Japan replaced the geographic clades from each continent. There are still large areas of the world from which no rubella virus isolates have been analyzed (Africa, Australia, and most of mainland Asia) and thus there could be additional genotypes as well as unrecognized geographic clades of Genotypes I and II. It will be important to obtain a selection of rubella virus isolates from these regions before or concurrent with widespread introduction of rubella vaccination so that the pre-existing endemic virus genotypes can be identified…(Frey TK, Abernathy ES, Bosma TJ et al. Molecular analysis of rubella virus epidemiology across three continents, North America, Europe, and Asia, 1961-1997. Journal of Infectious Disease 1998;178:642-650).

 

EVOLUTION AND DISTRIBUTION OF RUBELLA VIRUS GENOTYPES

 

Rubella virus is a sole member of Rubivirus group of Togaviridae and its genotypes has been classified in 2004 at WHO meeting. They are genotype 1B, 1C, 1D, 1E, 1F , 2A and 2B as confirmed and 1a, 1g and 2c as provisional. They have unique chronological and geographical characteristics. Genotype 1a worldwide distributed in 1960s and 70s, however almost disappeared since 1980. Genotype 1B mainly has distributed in Europe and genotype 1C in North and South American continents. Genotype 1D has distributed mainly in Asia and genotype 1F is restricted in China. Genotype 1E looks to be derived from genotype 1D and recently becomes to be predominant circulating one worldwide since 1997. Genotype 1g looks to be derived from genotype 1B and distributes in Europe and Americas. Genotype 2A was restricted in China and 2B in Eurasia and Africa. Genotype 2c was found in Russia. Molecular epidemiological study of rubella virus genotype could reveal the transportation of rubella virus from a country to another country. It will greatly help to make a effective plan of rubella immunization program to eliminate and eradicate for a certain country.

Ancestor dating analysis resulted in 1942-46 for virus strains in genotype 1 and 1840 for those in genotype 2.

By these analysis shift of major prevailing genotype of rubella virus may happened in the history of this diseases, at least from genotype 2 to genotype 1 and genotype 1a to genotype 1E.

As rubella has no relating animal viruses as far as studied, this evolution and emergence is very curious to be known in the future.

 

 

Mapping of Genetic Determinants of Rubella Virus Associated with Growth in Joint Tissue

J Virol. 2000 January; 74(2): 796–804. PMCID: PMC111599

 

Rubella virus (RV), the etiologic agent of German measles, belongs to the family Togaviridae and is the only member of the genus Rubivirus. Natural infection in childhood causes a systemic illness characterized by a short-lived maculopapular rash and mild fever (50). The disease is generally benign, and infection is often asymptomatic. It is the teratogenic potential of rubella that brought the virus to the forefront of public health interests and provided the impetus for isolation of the virus and subsequent vaccine development (35, 49). The current vaccine strain RA27/3 has been very effective in reducing the incidence of congenital rubella syndrome in North America, where it is given to all children between 12 and 18 months of age. However like the wild-type strains and the earlier vaccine strain, HPV77/DE5, it is reported to be associated with acute and late-onset joint and neurological symptoms (20, 46, 47, 50).

The association of RV with acute, transient joint manifestations, after both natural infection and vaccination, has been recognized for many years (14, 23, 34, 46, 47). Rubella-associated arthritis (RAA) is usually short-lived, although a number of patients go on to develop chronic or recurrent pauci- or polyarticular symptoms which can persist for some time (7, 8, 22, 43, 45, 47). Studies to define the mechanism of pathogenesis of RAA have been limited by the fact that humans are the only natural host for RV and there is presently no animal model of infection. However, the frequency and intensity of clinical symptoms reported for wild-type (wt) and vaccine strains correlate directly with the ability of the infecting strain to propagate in organ cultures of human synovial tissue, suggesting that tropism for joint tissue is a measure of viral arthritogenicity (31). Although RV strains are genetically around 98% homologous, they display striking phenotypic variation in growth characteristics and plaque morphology as well as tropism for joint tissue (9, 31). The wt strains, such as Therien, which have the highest association with persistent joint symptoms (30%) (47), commonly replicate to titers of 106 to 107 PFU/ml in organ cultures of human joint tissue, comparable to the yields from the most permissive cell lines for RV. The vaccine strain RA27/3, which is associated with much lower levels of recurrent arthritis (4%) (47), is severely restricted in these cultures and does not attain titers greater than 103 PFU/ml. However RA27/3, like the wt Therien strain, was found to persist in joint culture for over 3 months (31). In contrast, no replication of the European vaccine strain, Cendehill, was detected in human joint tissue in this study. Cendehill strain is reported to have a very low association with acute arthritis and none with chronic joint manifestations (4). These results indicate a correlation between the arthrotropism of a specific RV strain and its ability to induce joint symptoms and lends support to the hypothesis that recurrent RAA is triggered by reactivation of virus which has established a persistent infection in the joint.

The Vaccines:

 

 

Soon after the rubella virus was first isolated in tissue culture in 1962, several live-attenuated vaccine strains were developed. HPV-77 (duck embryo), HPV-77 (dog kidney) and Cendehill (rabbit kidney) strains were originally licensed in the USA between 1969 and 1970. These vaccines were replaced in 1979 by RA 27/3 (human diploid fibroblast), which produces a strong immune response (similar to natural infection) of 95% or more. While rubella immunity induced by vaccination has been reported to persist for at least 16 years and probably to be lifelong, other recent data indicate that this immunity may wane after 8 years of age. [3] Rubella vaccine is usually offered in combination with measles (MR) or measles and mumps (MMR) vaccines. [1,5] This combination offers the same high levels of immunogenicity and safety as does its individual components. Most of the currently licensed vaccines are based on a live, attenuated strain of rubella virus known as RA 27/3. The vaccines are administered subcutaneously. To avoid interference with possible remaining maternal antibodies the vaccine is usually given at the age of 12-15 months. Attempts to develop killed virus vaccines or sub-component vaccines against rubella have not been successful…

 

MERUVAX* II

Wistar RA 27/3 strain of live attenuated rubella virus propagated in WI-38 human diploid lung fibroblasts.

(package insert)

 

BIAVAX® II (Rubella and Mumps Virus Vaccine Live) is a live virus vaccine for immunization against rubella (German measles) and mumps. BIAVAX II is a sterile lyophilized preparation of the Wistar RA 27/3 strain of live attenuated rubella virus grown in human diploid cell (WI-38) culture

PROQUAD -MMRV(Measles, Mumps, Rubella, Varicella)

Has been suspended.

 

ProQuad* is a combined attenuated live virus vaccine containing measles, mumps, rubella, and varicella viruses. ProQuad is a sterile lyophilized preparation of (1) the components of M-M-R*II (Measles, Mumps and Rubella Virus Vaccine Live): Measles Virus Vaccine Live, a more attenuated line of measles virus, derived from Enders’ attenuated Edmonston strain and propagated in chick embryo cell culture; Mumps Virus Vaccine Live, the Jeryl Lynn™ (B level) strain of mumps virus propagated in chick embryo

cell culture; Rubella Virus Vaccine Live, the Wistar RA 27/3 strain of live attenuated rubella virus propagated in WI-38 human diploid lung fibroblasts; and (2) Varicella Virus Vaccine Live (Oka/Merck), the Oka/Merck strain of varicella-zoster virus propagated in MRC-5 cells. The cells, virus pools, bovine serum, and human albumin used in manufacturing are all tested to provide assurance that the final product is free of potential adventitious agents.

ProQuad, when reconstituted as directed, is a sterile preparation for subcutaneous administration.

Each 0.5-mL dose contains not less than 3.00 log10 TCID50 (50% tissue culture infectious dose) of measles virus; 4.30 log10 TCID50 of mumps virus; 3.00 log10 TCID50 of rubella virus; and a minimum of 3.99 log10 PFU (plaque-forming units) of Oka/Merck varicella virus.

 

 

M-M-R® II (MEASLES, MUMPS, and RUBELLA VIRUS VACCINE LIVE)

 

Package insert

 Note:  “….contains attenuated live measles and mumps viruses propagated in chick embryo cell culture, plus “the Wistar RA 27/3 strain of live attenuated rubella virus propagated in WI-38 human diploid lung fibroblasts.”(1) Principal studies published in the American Journal of Diseases of Children and the American Journal of Epidemiology, reveal that the rubella strain was cultured from an aborted human fetus.(2,3) In addition, the growth medium for the three live viruses that are needed to produce the MMR vaccine is a buffered salt solution “supplemented with fetal bovine serum.”(4) Other ingredients include sucrose, phosphate, glutamate, recombinant human albumin, sorbitol, hydrolyzed gelatin stabilizer, and approximately 25 mcg of neomycin (an antibiotic).(5) The MMR vaccine does not contain a preservative. In fact, according to the FDA, MMR-II never contained thimerosal, a potentially dangerous chemical used in some vaccines.(6) However, trace amounts of mercury were detected in an earlier MMR formulation.”

 

Genomic sequence of the RA27/3 vaccine strain of rubella virus. 

Arch Virol. 1997; 142(6):1165-80. PMID: 9229006 [PubMed – indexed for MEDLINE]

 

The sequence of the genome of the RA27/3 vaccine strain of rubella virus (RUB) was determined. In the process, several discrepancies between the previously reported genomic sequences of two wild RUB strains (Therien and M33) were resolved. The genomes of all three strains contain 9762 nucleotides (nts), exclusive of the 3′ poly A tract. In all three strains, the genome contains (5′ to 3′), a 40 nt 5′ untranslated region (UTR), an open reading frame (ORF) of 6348 nts that encodes nonstructural proteins, a 123 nt UTR between the two genomic ORFs, a 3189 nt ORF that encodes the structural proteins, and a 62 nt 3′ UTR. The 5′ end of the subgenomic RNA was found to correspond to a uridine residue at nt 6436 of the genomic RNA. At the nucleotide level, the sequence of the three strains varied by 1.0 to 2.8%, while at the amino acid level, the sequence varied by 1.1 to 2.4% over both ORFs. The RA27/3 sequence will be of use in identification of the determinants of its attenuation, in vaccine production control and in development of second generation RUB vaccines based on recombinant DNA technology.

 

A comparative field evaluation of three live, attenuated rubella virus vaccines.

Am J Public Health. 1971 January; 61(1): 152–156.

 

*Before aborted fetal cell lines were used

 

rubella-strain

 

 

Countries using rubella vaccine, by WHO region, as of December 1999* (pg 69)

 

Rubella and congenital rubella syndrome: global update

 

rubella

 

 

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Monovalent vaccines for Measles, Mumps, Rubella

Merck Focusing on Combination Vaccine

Manufacturer Stops Sales of Monovalents for Measles, Mumps, Rubella

By David Mitchell
12/24/2008

Merck & Co. Inc. has stopped production and sales of its monovalent vaccines for measles, mumps and rubella. The manufacturer instead plans to focus on its combination vaccine, MMRII.

Merck spokeswoman Amy Rose said MMRII accounts for 98 percent of the company’s volume for measles, mumps and rubella vaccines, compared to just 2 percent from monovalent vaccines Attenuvax (measles), Mumpsvax (mumps) and Meruvax (rubella).

“The combination vaccine is what’s recommended, and it’s such a significant portion of the orders we see,” said Rose. “It’s in the best interest of public health to make more of that rather than dedicate manufacturing capacity to monovalents.”

Rose said Merck had not decided when, or if, it might make the monovalent vaccines available for sale in the future.

Doug Campos-Outcalt, M.D., M.P.A., who serves as the AAFP’s liaison to the CDC’s Advisory Committee on Immunization Practices and is a former member of the AAFP Commission on Clinical Policies and Research, said Merck’s decision was insignificant in terms of public health. He added, however, that some parents likely will be unhappy.

“The use of the single antigen is pretty limited,” he said. “There’s no harm if you need one in getting all three. There are some parents out there that want a delayed vaccine schedule. They want the vaccines spread out over a longer period of time and not so many at once. That’s a lot of hooey. Alternative schedules have never been proven to be superior.”

Rubella

Are Some Cases of Autism Actually Subclinical, Congenital Attenuated Rubella Syndrome?

                    www.nccn.net/~wwithin/autismrubella.pdf

 

  • F. Edward Yazbak, MD, FAAP, found a link between mothers’ rubella susceptibility in pregnancy and their having children with autism spectrum disorders. He described 60 previously vaccinated women who were considered “rubella susceptible” during their routine prenatal OB/GYN visits. All of these women were revaccinated in the post partum period due to their not having antibodies to rubella. Each of these women could be described as having failed to seroconvert to an previous vaccination or having rubella immunity that declined over time.

     

     

     

     

  • A few ideas and questions are warranted on WHY some females may unknowingly be serving as hosts to a persistent rubella infection and why the RA27/3 vaccine strain of rubella virus might be particularly well adapted to persist undetected in females.

     

     

     

     

  • Information provided by the FDA in Appendix A on the history of the development of rubella vaccines used in the US prompts many questions about the safety of RA27/3 strain of rubella vaccine and its use in females. Per the FDA, the rubella virus used in the vaccine originated from a fetus that was aborted in 1964. It was isolated in and recovered from fetal tissue. It was attenuated through 25 passages through human fetal cells, and it is grown in human fetal cells.

     

     

     

     

 

 

 

 

 

 

 

 

 

 

 

 

MMR Vaccine, Measles, Mumps, Rubella

Dr Richard Halvorsen answers the big questions about MMR, Vaccines and Diseases

Rubella and CRS

Rubella and Congenital Rubella Syndrome

 

     Rubella had a natural virulence cycle of every 6-9 years and was once a disease of school-aged child that was typically caught between the ages of 5-9 year old. 80% thus developed natural antibodies to Rubella and protected them into adulthood, while 15% remained susceptible to the disease. The goal of the Rubella vaccine program was to prevent fetal infection, or CRS, in women in the childbearing years who had not acquired natural immunity in childhood.  Unfortunately, the original goal has not been obtained. The exact opposite is occurring as young adult women in their childbearing years now have the highest rate of Rubella incidence. Is this a new phenomenon occurring in today’s generation? No. To spite the large Rubella vaccine program, since 1969 there has been a shift in incidence and a shift in age susceptibility.

 
 
 
 
 
 
 

 

              

“During the 1990s, the characteristics (ie, age distribution, sex, and race/ethnicity) of rubella cases changed significantly. In 1990, incidence was higher among children younger than 15 years than among persons aged 15 to 44 years… since the mid 1990s, incidence has increased among persons aged 15 to 44 years and decreased among children younger than 15 years. In 1990, children younger than 15 years accounted for 69% of cases. Since 1996, the highest percentage of cases occurred among persons aged 20 to 29 years, with a high in 1999 of 49%.  

  

     According to a 1980 Pediatrics study, the susceptibility rate of 6th graders was 15% in those vaccinated. (2) The susceptibility rate has remained the same rate as in the pre-vaccine era, even after the late 1970’s initiative to re-immunize all females during the child bearing years.

 

 

      

     Has the Rubella vaccine reduced Congenital Rubella Syndrome? You be the judge. Rubella was not a nationally notifiable disease until 1966. Rubella vaccine was licensed and recommended in 1969 for girls and boys in infancy and/or the preschool years, and then eventually recommended for adolescents. Since 1969, Rubella cases have declined, yet CRS cases increased after the introduction of the vaccine. In 1966, the pre-vaccine era, there were 11 cases of CRS. In 1969, after the introduction of the vaccine, there were 31 CRS cases. By 1970, there was an increase of 77 cases and in 1971, 68 cases. During the 1980’s, CRS cases declined once again but still remained higher than the pre-vaccination era. In 1992, there were 11 cases of CRS which is the same exact number of cases in 1966 before the Rubella vaccine was routinely used.  In 2000, there were 9 cases of CRS and in 2006, one case.

 

     As you can see, the Rubella vaccine has had little impact on reducing the number of CRS cases over the last 40 years since its introduction, yet it increased CRS cases in some years. There are even incidences were women had high levels of antibodies to Rubella before pregnancy, yet the babies had CRS. There are also some women who will never seroconvert (show positive antibodies) no matter how many times they are vaccinated.

      

     What has vaccination really accomplish if immunity wanes from infancy, if vaccinated young women are made more susceptible when they need immunity the most, and the increase in congenital rubella syndrome? Yet, natural immunity in early childhood can protect for a lifetime. Think about this statement made in 1964, before there was a Rubella vaccine implemented, by Dr. Hugh Paul in The Control Of Diseases:

     “The disease (rubella) cannot be prevented, and in view of its very mild character, and the possibility that it may have catastrophic effects if contracted by an expectant mother, it is questionable if it should be prevented in childhood and adolescence even if this were possible.  It has been suggested that female children should be deliberately exposed to infection in order to achieve a life-long immunity from the disease and possibly from malformation in the offspring in later life.  This idea is not an unreasonable one… Rubella does not kill, and even complications are uncommon.” 

 

      

 

 

 

 

 

 

 

MMR Vaccine

MMR vaccine is it safe or effective? You be the judge based on the medical literature that is available to you.

 

 The MMR vaccine consists of 3 live viruses for Measles, Mumps and Rubella. The MMR-V has live chicken pox added to the mix. It contains a weakened or partially inactivated, live measles virus which is grown in cell cultures of a chick embryo. A weakened live strain of mumps virus is grown in cell cultures of a chick embryo. A weakened Wistar RA 27/3 strain of live attenuated rubella virus which is grown in human diploid cell (W-38) culture originating from the tissues of a fetus aborted in 1964. There is no preservative such as Thimerosal(mercury). It contains the antibiotic neomycin, and Sorbitol and Hydrolyzed Gelatin as stabilizers. All three live viruses are available as single vaccines but doctors will most often tell you they are not available, or refuse to give them as separate vaccines.

 

 How it can shed to others:

 

Mumps vaccine virus genome is present in throat swabs obtained from uncomplicated healthy recipients. 
  
Seven children were followed for up to 42 days post-vaccination with live mumps vaccine and 37 throat swabs were obtained serially. Viral genomic RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) in the phosphoprotein (P) and hemagglutinin-neuraminidase (HN) regions. Virus isolation was also attempted. Genomic differentiation of detected mumps virus genome was performed by sequence analysis and/or restriction fragment length polymorphism (RFLP). No adverse reaction was observed in these children. Although mumps virus was not isolated from any of the samples, viral RNA was detected in four samples from three vaccine recipients, 18, 18 and 26, and 7 days after vaccination, respectively. Detected viral RNA was identified as the vaccine strain. Our data suggests that vaccine virus inoculated replicates in the parotid glands but the incidence of virus transmission from recipients to other susceptible subjects should be low. 

 

Detection of measles vaccine in the throat of a vaccinated child. 
   
Measles vaccine is widely used, most often in association with mumps and rubella vaccines. We report here the case of a child presenting with fever 8 days after vaccination with a measles-mumps-rubella vaccine. Measles virus was isolated in a throat swab taken 4 days after fever onset. This virus was then further genetically characterised as a vaccine-type virus. Fever occurring subsequent to measles vaccination is related to the replication of the live attenuated vaccine virus. In the case presented here, the vaccine virus was isolated in the throat, showing that subcutaneous injection of an attenuated measles strain can result in respiratory excretion of this virus. 
 

 Reactions to MMR Vaccine are Triphasic:

Any reactions that are 6 – 14 days are the measles component and usually show as temperature and rash, and sometimes seizures.
The second phase is between 11 and 32 days which is the mumps components. This can consist of temperature, seizures, and acquiring mumps.
The third phase can occur within the first 0 – 30 days, and is the rubella component. It can cause joint pain or arthritis. This most often occurs in adolescents and adults, and perhaps babies, but they wouldn’t be able to tell you.

 

  
 Delaying MMR until a child is older makes it ‘safer’? The reality is there is no ‘safe’ time to delay as reactions can occur at any time if the conditions are right. A 6 year old, or 12 year old child, or a young adult can have serious reactions or death associated with the vaccine. Parents can opt to have titer tests done first.
 

 

 

The CDC, AAP, FDA, NIH, etc., can say what they wish to the public and promote MMR and its safety, continue to put their heads in the sand, and talk out their rear ends, but let’s get real and look at some of the studies:


AAP Study: Relationship b/t MMR & Encephalitis w/ Perm. Brain Injury or Death.

  

 

The purpose of this study of claims submitted to the National Vaccine Injury Compensation Program is to determine whether or not there is evidence for a causal relationship between the first dose of a currently used attenuated measles vaccine, MR, MMR, mumps, or rubella vaccine and encephalopathy of undetermined cause with permanent brain injury or death that occurred within 15 days after administration.
A total of 403 [compensation] claims of encephalopathy and/or seizure disorder after measles, MR, MMR, mumps, or rubella vaccination were identified during this 23-year period [1970-1993]. Of these claims, 48 (25 males and 23 females) met the inclusion criteria and acquired an acute encephalopathy of undetermined cause 2 to 15 days after receiving measles vaccine, MR, or MMR. This acute encephalopathy was followed by permanent brain impairment or death. The patients ranged in age from 10 months to 49 months, with a median age of 15 months and a mean age of 17.5 months.
Results
A total of 48 children, ages 10 to 49 months, met the inclusion criteria after receiving measles vaccine, alone or in combination. Eight children died, and the remainder had mental regression and retardation, chronic seizures, motor and sensory deficits, and movement disorders. The onset of neurologic signs or symptoms occurred with a nonrandom, statistically significant distribution of cases on days 8 and 9. No cases were identified after the administration of monovalent mumps or rubella vaccine.
Conclusions
This clustering suggests that a causal relationship between measles vaccine and encephalopathy may exist as a rare complication of measles immunization
 
 
  Former science chief: ‘MMR fears coming true’

 He said he has seen a “steady accumulation of evidence” from scientists worldwide that the measles, mumps and rubella jab is causing brain damage in certain children.

But he added: “There are very powerful people in positions of great authority in Britain and elsewhere who have staked their reputations and careers on the safety of MMR and they are willing to do almost anything to protect themselves.”
 In the late Seventies, Dr Fletcher served as Chief Scientific Officer at the DoH and Medical Assessor to the Committee on Safety of Medicines, meaning he was responsible for deciding if new vaccines were safe.

He first expressed concerns about MMR in 2001, saying safety trials before the vaccine’s introduction in Britain were inadequate.
Now he says the theoretical fears he raised appear to be becoming reality.
He said the rising tide of autism cases and growing scientific understanding of autism-related bowel disease have convinced him the MMR vaccine may be to blame.
“Clinical and scientific data is steadily accumulating that the live measles virus in MMR can cause brain, gut and immune system damage in a subset of vulnerable children,” he said. “There’s no one conclusive piece of scientific evidence, no ‘smoking gun’, because there very rarely is when adverse drug reactions are first suspected. When vaccine damage in very young children is involved, it is harder to prove the links.
“But it is the steady accumulation of evidence, from a number of respected universities, teaching hospitals and laboratories around the world, that matters here. There’s far too much to ignore. Yet government health authorities are, it seems, more than happy to do so.”

 “Yet there has been a tenfold increase in autism and related forms of brain damage over the past 15 years, roughly coinciding with MMR’s introduction, and an extremely worrying increase in childhood inflammatory bowel diseases and immune disorders such as diabetes, and no one in authority will even admit it’s happening, let alone try to…

 

 

   Very informative presentation:

The Seat of the Soul The Origins of the Autism Epidemic

 

Sally Beck wrote an article on the study at Wake Forest University School of Medicine in North Carolina titled Scientists fear MMR link to autism”, which was similar to the one reported by Andrew Wakefield, MD, in 1998.


In the American study, 275 children with regressive autism and bowel disease
were evaluated. Of the 82 children completely tested, 70 proved positive for
the measles virus. Beck quoted Stephen Walker, MD, the team leader as
saying, “Of the handful of results we have in so far, all are vaccine strain
and none are wild measles. This research proves that in the gastrointestinal
tract of a number of children, who have been diagnosed with regressive
autism, there is evidence of measles virus.”

Very little was reported about the Wake Forest research in the American media. But with no surprise, immediately afterwards, this came out:

Reuters Health Information in New York published an account of a different study headlined No Evidence of Measles Virus in MMR-Vaccinated Autistic Children.” It said “contrary to the findings of some earlier studies, measles virus genetic material was not detected in the blood of MMR-vaccinated autistic children with development regression, according to a report in the Journal of Medical Virology for May.”

 

 

 
So here we have two studies that are contradictory. What are the differences between the two studies?
 
 
 
 In the U.S. study, measles virus genomic RNA was actually found in the gut of 70 affected children and the viral results of another 200 children with typical gut pathology are still pending.

In the U.K. study, the researchers “could not detect” measles virus genetic material in the blood of 15 MMR-vaccinated children with autism.

It is essential to also point out that the above-mentioned M.A. Afzal is not N.A. Afzal, a pediatric gastroenterologist attached to the Centre for Pediatric Gastroenterology at The Royal Free Hospital, London, U.K. It was at the Royal Free Hospital that Andrew Wakefield practiced gastroenterology for years and where he was the shining star before he dared to “rock the boat” and was forced to resign. It is also at the Royal Free and University College Medical School in London that Brent Taylor, one of Wakefield’s most vocal critics, is professor of community pediatrics. N.A. Afzal published his first study with the Royal Free team in December 2002.  He published two more studies in 2004 and one in 2005. The abstracts of all four studies did not contain any reference to autism and vaccines.

M.A. Afzal, on the other hand, is a member of the virology department at the National Institute for Biological Standards and Control (NIBSC). The Institute is a respected multi-disciplinary scientific establishment with national and international roles in the standardization and control of biological substances including viral and bacterial vaccines. Since 1976, the institute has been directly funded by the United Kingdom Health Departments.

But back to M.A. Afzal of the NIBSC, who according to Reuters was certain in 2006 that the measles virus material genuinely did not exist in the patients ‘ blood samples because he and his team did not find it. He must have been aware that a Japanese team from Tokyo University led by H. Kawashima had found the same “genetic material” in the blood of children with autism in 2000: “In order to characterize the strains that may be present, we have carried out the detection of measles genomic RNA in peripheral mononuclear cells (PBMC) in eight patients with Crohn’s disease, three patients with ulcerative colitis, and nine children with autistic enterocolitis…”

Kawashima discovered and reported that “the sequences obtained from the children with autism were consistent with being vaccine strains” and that the results were concordant with the exposure history of those children.

 

 

So how come Team Tokyo found vaccine-strain measles virus genomic RNA in peripheral mononuclear cells of vaccinated autistic children in 2000 and Team U.K. found nothing in 2006? The answer to that perplexing and rather sensitive question may be in a very interesting study that was published in the Journal of Medical Virology in May 2003, titled appropriately “Comparative evaluation of measles virus-specific RT-PCR methods through an international collaborative study” and authored by both Afzal and Kawashima, in addition to renowned experts A.D. Osterhaus, S.L. Cosby, L. Jin, J. Beeler and K. Takeuchi.

 

 

Measles infection and inflammatory bowel disease


Afzal and colleagues published “Absence of detectable measles virus genome sequence in inflammatory bowel disease tissues and peripheral blood lymphocytes” in the Journal of Medical Virology.  According to the authors, in spite of using a “highly sensitive measles-specific RT-PCR-nested PCR system,” they failed to detect the presence of measles virus in 93 colon biopsies and 31 peripheral blood lymphocyte preparations, examined and obtained from patients with IBD and non-inflammatory controls.

It seems from the above that M.A. Afzal was looking for evidence of viral presence in the colon (large intestine) and did not find any. Wakefield had better luck, a little later, when he looked for such evidence in the ileum. Afzal was certainly aware that the children tested by the Royal Free Team had ileal lymphonodular hyperplasia.

 
(Lancet. 1998.Feb 28; 351(9103): 646-7. PMID: 9500326) (J Med Virol. 2003 May; 70(1): 171-6. PMID: 12629660) (Absence of measles-virus genome in inflammatory bowel disease. Ital J Gastroenterol Hepatol. 1998 Aug; 30(4): 378-82. PMID: 9789132)  (Absence of detectable measles virus genome sequence in inflammatory bowel disease tissues and peripheral blood lymphocytes. J Med Virol. 1998 Jul; 55(3): 243-9.)
 
 
 
 

 

  Measles virus and Crohn’s disease

In April 1999, Wakefield, Montgomery and Pounder published “Crohn’s disease: the case for measles virus.”  They reported, “We and others have suggested that measles virus may be causally related to Crohn’s disease, and that the associated risk is an atypical pattern of exposure. The data for Crohn’s disease suggest that persistent infection may follow early low dose exposure and low zone immunological tolerance. The changing pattern of measles virus exposure this century would be consistent with a shift toward lower dose of infection. Such an exposure would also be consistent with persistence of the virus at very low copy number within discrete foci of granulomatous inflammation..”  Afzal, Minor, Armitage and Gosh published “Measles virus and Crohn’s disease” in June of the same year.  

(2000: MMR Wakefield AJ, Montgomery SM, Pounder RE. Crohn’s disease: the case for measles virus. Ital J Gastroenterol Hepatol. 1999 Apr; 31(3): 247-54. Review. PMID: 10379489.)  (Afzal MA, Minor PD, Armitage E, Ghosh S. Measles virus and Crohn’s disease. Gut. 1999 Jun; 44(6): 896-7. PMID: 10375297 Safety Review.)

Measles, mumps, rubella vaccine: through a glass, darkly,” Wakefield and Montgomery reviewed the safety testing of MMR vaccine or lack thereof.

(Potential viral pathogenic mechanism for new variant inflammatory bowel disease. Mol Pathol. 2002 Apr; 55(2): 84-90. PMID: 11950955)

In “Clinical safety issues of measles, mumps and rubella vaccines,” Afzal, Minor and Schild did not directly respond but essentially reviewed all the studies that had been done by the anti-Wakefield camp and had failed to identify the presence of measles virus genomic RNA in patients with IBD. In the available abstract, M.A. Afzal stated, “Based on the published data reviewed here, it can be concluded that there is no direct association between measles virus or measles vaccines and the development of Crohn’s disease, a conclusion which is supported by most epidemiological findings.” (Bull World Health Organ. 2000; 78(2): 199-204. Review. PMID: 10743285)

As to the safety of the MMR vaccine, the Cochrane MMR Review: “The design and reporting of safety outcomes in MMR vaccine studies, both pre- and post-marketing, are largely inadequate.”

 

April 2002

 

In “Potential viral pathogenic mechanism for new variant inflammatory bowel disease,” Uhlmann and associates, including Wakefield, published results of their meticulous research. It revealed that “75 of 91 patients with a histologically confirmed diagnosis of ileal lymphonodular hyperplasia and enterocolitis were positive for measles virus in their intestinal tissue compared with five of 70 control patients. Measles virus was identified within the follicular dendritic cells and some lymphocytes in foci of reactive follicular hyperplasia. The copy number of measles virus ranged from one to 300,00 copies/ng total RNA.” The authors concluded, “The data confirm an association between the presence of measles virus and gut pathology in children with developmental disorder.” 

 

(Dig Dis Sci. 2000. Apr; 45(4): 723-9.)

 

March 2008-

 

 

MMR: Vaccine can cause blood disorder

 There’s more bad news for advocates of the MMR (measles-mumps-rubella) vaccine with the discovery this week that it can cause a blood disorder.  Researchers have found that it may trigger immune thrombocytopenic purpura (ITP), an immune system malfunction that destroys the body’s own blood platelets. The effect seems to last for an average of seven days, during which time the child’s platelet count could fall.

The risk is relatively low, say researchers, and one case of ITP will be caused per 40,000 vaccinations.  The risk appears to last for up to 42 days after vaccination.
Researchers from Kaiser Permanente Colorado, Denver analyzed the health profiles of more than 1 million children who had been vaccinated.  Of these, 259 developed ITP, and they reckon the vaccine was responsible for 76 per cent of these cases.
(Source: Pediatrics, 2008; 121: e687-e692).

 
 

 

Persistence of Measles, Mumps, and Rubella Antibodies in an MMR-Vaccinated Cohort: A 20-Year Follow-up.

 

Conclusions.  A high rate of seropositivity was found 20 years after the first MMR dose, particularly for rubella and measles. Our results show that MMR vaccine–induced antibodies wane significantly after the second dose. According to epidemiological data, the protection induced by MMR vaccination in Finland seems to persist at least until early adulthood. However, the situation requires constant vigilance. (The Journal of Infectious Diseases 2008;197:950–956)

 

 MMR vaccine and Tylenol Use:

 Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: The results of a parent survey.


The present study was performed to determine whether acetaminophen (paracetamol) use after the measles-mumps-rubella vaccination could be associated with autistic disorder. This case-control study used the results of an online parental survey conducted from 16 July 2005 to 30 January 2006, consisting of 83 children with autistic disorder and 80 control children. Acetaminophen use after measles-mumps-rubella vaccination was significantly associated with autistic disorder when considering children 5 years of age or less (OR 6.11, 95% CI 1.42-26.3), after limiting cases to children with regression in development (OR 3.97, 95% CI 1.11-14.3), and when considering only children who had post-vaccination sequelae (OR 8.23, 95% CI 1.56-43.3), adjusting for age, gender, mother’s ethnicity, and the presence of illness concurrent with measles-mumps-rubella vaccination. Ibuprofen use after measles-mumps-rubella vaccination was not associated with autistic disorder. This preliminary study found that acetaminophen use after measles-mumps-rubella vaccination was associated with autistic disorder.
 We know that acetaminophen impairs the glutathione pathways, as well as hormone balance. The glutathione pathways are the same ones involved in naturally “chelating” out metals. Acetaminophen can also suppress the immune system and when given with Gardasil, results in a lower antibody development. Thus it can crash some aspects of the immune system. So, if autism results from a situation where if the immune system is suppressed and nutrition isn’t quite right, the body is not able to clear out heavy metals, and then anything can make that situation worse and contribute to the problem. This study does not mean that MMR is not implicated, but that Acetaminophen was part of an overall negative equation.

 

Proquad

 Children suffered higher rates of fever-related convulsions when they received the combination vaccine Proquad instead of two separate shots. The study (Nicola P. Klein, MD, PhD, a research scientist from Northern California Kaiser Permanente and co-director of the Kaiser Permanente Vaccine Study Center) which included children ages 12 months through 23 months, found the rate of seizures was twice as high in toddlers who got ProQuad, compared with those who got separate shots for MMR and Chicken Pox (Varicella vaccine).

ProQuad was licensed in 2005 but had suspended production because of manufacturing problems. There is five times more chickenpox antigen in the ProQuad shot than in the Varicella vaccine.

 

ACIP approves MMRV vaccine revision 2008

Possible increased risk for febrile seizures found among children aged 12 to 23 months after receipt of MMRV vaccine.

“MMRV vaccine has not been widely distributed in the United States since June 2007 and is not expected to be available again until 2009; however, some providers might still have some supply in stock,” she said. “As far as postvaccination safety monitoring, in October 2007 following FDA review of adverse event reports submitted to VAERS and Merck’s worldwide adverse experience system, MMRV vaccine labeling was updated to include convulsion and febrile seizures among adverse reactions postvaccination.”

Quick Picks:

 

According to The New England Journal of Medicine, 60 percent of all measles cases among American school children between 1985 and 1986 occurred in those who were vaccinated.

  The Journal of the American Medical Association published a study in 1986, which showed that among 235 cases of student measles reported in Dane County, Wisconsin; more than 96 percent had received a measles vaccine. A study reported in Morbidity and Mortality Weekly Report found that 58 percent of 1600 cases of measles in Quebec, Canada, in 1989 occurred in those who had already been vaccinated.  The World Health Organization has conceded that those administered the measles vaccine have a 14 times greater likelihood of contracting the disease than those who remain unvaccinated.

 

 Jamie Murphy “The vaccine can never duplicate the kind of immunity that we get from nature…When children get the measles after they’ve been vaccinated, they’re getting it from the vaccine and the virus (because there’s so much virus in the vaccine that stays in the body). When their resistance becomes lowered, that can become reactivated. Also, when a natural epidemic of measles occurs, as it does every three to four years in the United States, those children who have been vaccinated, because they did not get a true immunity from the vaccine, become susceptible to measles.”

 Vera Scheibner reports that “In April 1993, the Ministry of Health and Welfare in Japan decided to discontinue the use of measles, mumps, and rubella vaccine (Sawada et al., 1993). This decision was prompted by published reports of vaccinated children and their (unvaccinated) contacts contracting mumps from the MMR vaccine, and reports of one in 1044 vaccinees developing encephalitis.”

 

A study published in 1994 in the Archives of Internal Medicine evaluated all U.S. and Canadian articles reporting measles outbreaks in schools, and found that, on average, 77 percent of all measles cases in these outbreaks were occurring among vaccinated individuals. The authors concluded that “the apparent paradox is that as measles immunization rates rise to high levels in a population, measles becomes a disease of immunized persons.

 

 In 2007, a study performed at the National Institute of Communicable Diseases in South Africa reviewed the increase in mumps outbreaks in the UK and US. In the US, 56,000 cases were reported in 2004-2005. Many of these cases are occurring on college campuses. A mumps outbreak at a New York summer camp found that 96% of those infected had prior vaccination coverage. A similar outbreak in Nova Scotia among vaccinated adolescents and young adults has also been reviewed and it was found that the virus’ genotype was the same as that in the UK and US. These recent outbreaks have raised concerns among scientists about the effectiveness of the mumps vaccine in the MMR. According to the South African scientist, there may be a waning immunity towards mumps in the vaccinated population, which in time could make the vaccine ineffective. Belgian scientists came to the conclusion that the secondary mumps vaccination was a failure during a 2004 outbreak affecting 105 Belgian children from ages 3-12.

 Antibody levels 5 to 6 years after immunization with (the now discredited) high-potency EZ and high-potency Schwarz measles vaccine were insufficient in 40 percent and 50 percent of vaccinated children. The authors concluded, “Given the rapid decline in antibody titers over a 5- to 6-year period in an area where measles vaccine coverage was high, it seems likely that multiple-dose immunization schedules will be needed in the future to maintain protective antibody concentrations….”

 

As a consequence of the fact that antibody response to the vaccine virus is temporary, today we are facing cases of atypical measles occurring in infants under a year old, as well as in older children and in adults. Atypical measles is a severe disease that was first described in the early 70s in children, and later in adolescents and young adults exposed to the wild-type measles virus several years after being vaccinated with the killed or attenuated measles vaccine. The condition is characterized by atypical rash, high fever, cough, headache, and pneumonia. Further complications can include hepatitis, persistence of pulmonary lesions for several years, thrombocytopenia and other circulatory system problems, and cardiac involvement.

 

Another problem found with measles vaccination, documented in several studies, is that it produces immune suppression that contributes to an increased susceptibility to other infections.


The 60% of people who were vaccinated in 1970 have caused many of them to be susceptible to natural measles, because the shots were given too early. This is also why most analyses which profess to have a scientific element, go from the 1973 licensure.

Atypical measles explained by James Cherry: (PMID: 14765342. Page 505).