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2012 NAIAD Report on Status of Vaccine Research and Development


THE JORDAN REPORT, periodically reviews the progress in vaccine development and is published by NAIAD (USA). In recent years, there has been a growing, negative opinion towards vaccination. However, when one looks back 30 years one finds that life expentancy of the human being has been extended far more in the last century than in the several preceding thousands of years of human existence.

In 1981, the program of Accelerated Development of Vaccines was established by National Institute of Allergy and Infectious Diseases (NIAID) to build on the success of the past triumphs against important infectious diseases as diphtheria, measles, pertussis, poliomyelitis, tetanus, yellow fever, and others. In 1961, it was not unusual to see children crippled by polio. Today, that is rare. Clearly, vaccinations have contributed to a society which is healthier and preserves human life.  The new program was ably directed for 6 critical early years by William S. (Bill) Jordan (1917–2008). Hence, the periodical reviews are named after him. You may click here to read the 2012 review. It takes time to load, since it is large, and you may want to allow time for that.

Addressing Adverse Effect Concerns: Parents claim that their child showed the first signs of autism after a series of childhood vaccinations. While vaccine researchers do not find clinical support for this statement, they have removed mercury from their vaccines and also have preservative-free vaccines. The search for the causal factors for Autism Spectrum Disorder is ongoing.How is a decision maker to move forward facing such challenges?

Contents of the 2012 Jordan Report: 

Below is the Table of Contents covered in the 2012 Jordan Review. You may find a vaccine within your interests. To read more about each vaccine study, you will want to click here. Of particular interest to a worldwide audience might be Malaria, West Nile Virus, Chlamydia, Neglected tropical diseases like viral Dengue and a new emerging viral disease like Chikungunya.

Table of Contents
INTRODUCTION
Foreword by Anthony S. Fauci, M.D. ………………………………….. 3 Tribute by Carole A. Heilman, Ph.D. ………………………………….. 5
EXPERT ARTICLES
Vaccinomics and Personalized Vaccinology
Gregory A. Poland, M.D., Inna G. Ovsyannikova, Ph.D. and Robert M. Jacobson, M.D. …………………………………………………….11
Sex Differences in Immune Responses to Vaccines
Col. Renata J. M. Engler, M.D. and Mary M. Klote, M.D. ……. 19 Immunization and Pregnancy
Flor M. Munoz, M.D. ………………………………………………………… 27
Second-Generation Malaria Vaccines: A Definitive End
to Malaria-Related Deaths?
Vasee S. Moorthy, MRCP, Ph.D. ………………………………………….. 34
Structural Biology and Other Resolution-Enhancing Technologies in the Design of an Effective HIV–1 Vaccine Peter D. Kwong, Ph.D., John R. Mascola, M.D. and
Gary J. Nabel, M.D., Ph.D. ………………………………………………….. 40
New Methods for Analyzing Vaccine Responses
Mark M. Davis, Ph.D. and John D. Altman, Ph.D……………….. 46
Developing Vaccines for the Neglected Tropical Diseases
David J. Diemert, M.D., FRCP(C) and
Saman Moazami, B.A…………………………………………………………. 53
The Public Health Need for a Staphylococcus aureus Vaccine Scott K. Fridkin, M.D. and John A. Jernigan, M.D., M.S. …….. 66
Adjuvants—Past, Present, and Future
Nicholas I. Obiri, Ph.D. and
Nathalie Garçon, Pharm.D., Ph.D. ……………………………………….74
Progress, Promises, and Perceptions: The National Vaccine Plan—A Path Forward for the Coming Decade
Bruce G. Gellin, M.D., M.P.H. and Sarah R. Landry, M.A…… 85
VACCINE UPDATES
Dengue
M. Cristina Cassetti, Ph.D. …………………………………………………. 95
HIGHLIGHT BOX
Vaccine Against Chikungunya Virus in Development
Gary J. Nabel, M.D., Ph.D. and Ken Pekoc ……………………. 97
Severe Acute Respiratory Syndrome
Frederick J. Cassels, Ph.D. …………………………………………………… 98
HIGHLIGHT BOX
Vaccine Delivery Technologies
Martin H. Crumrine, Ph.D………………………………………….. 105 West Nile Virus
Patricia M. Repik, Ph.D…………………………………………………….. 106
HIGHLIGHT BOX
Henipaviruses (Nipah Virus and Hendra Virus)
M. Cristina Cassetti, Ph.D…………………………………………… 109
Group B Streptococcus
Xin-Xing Gu, M.D., Linda C. Lambert, Ph.D. and
Carol Baker, M.D………………………………………………………………..110
HIGHLIGHT BOX
CMV Vaccine Shows Promise
Walla Dempsey, Ph.D., M. Cristina Cassetti, Ph.D.
and Mason Booth………………………………………………………….114
HIV/AIDS
Rona L. Siskind, M.H.S……………………………………………………….115
HIGHLIGHT BOXES
Herpevac Trial for Women Concludes
Amanda Schleif, M.P.H……………………………………………….. 120
Chlamydia Vaccine Being Tested in
Nonhuman Primates
Harlan D. Caldwell, Ph.D. and Ken Pekoc …………………… 122
Promising HIV Vaccine Trial Results: RV144,
the Thai HIV Vaccine Trial
Rona L. Siskind, M.H.S. ………………………………………………. 126
1
Influenza
Linda C. Lambert, Ph.D. and Frederick J. Cassels, Ph.D. …… 127
HIGHLIGHT BOX
NIAID Centers of Excellence for Influenza Research
and Surveillance
Sarah E. Miers, J.D………………………………………………………. 132
Malaria
Peter D. Crompton, M.D., M.P.H. and Steven R. Rosenthal, M.D., M.P.H. …………………………………………………………………….. 133
HIGHLIGHT BOX
The International Centers of Excellence for Malaria Research
Malla R. Rao, Dr.P.H., M.Eng. …………………………………….. 134
Respiratory Syncytial Virus
Sonnie Kim, M.S. ………………………………………………………………. 139
HIGHLIGHT BOX
Impact of Regulatory Science on Influenza
Vaccine Development
David S. Cho, Ph.D., M.P.H…………………………………………. 139
Tuberculosis
Christine F. Sizemore, Ph.D. ……………………………………………… 144
HIGHLIGHT BOX
Hepatitis C Virus: Prospects for Vaccine Development
Sarah E. Miers, J.D. and Rajen Koshy, Ph.D. ……………….. 147 Rotavirus
Diana S. Berard ………………………………………………………………… 149 APPENDIXES
Appendix A: Status of Vaccine Research and
Development, 2012……………………………………………………………. 153
Appendix B: NIAID-Supported HIV Vaccine Candidates in Preclinical Development…………………………………………………… 179
Appendix C: Ongoing Clinical Trials of HIV Vaccine Candidates in HIV-Uninfected Adults……………………………… 180

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A documentary about the stories after Gardasil vaccination


Think East Productions, creator brothers Ryan Richardson and David Richardson have business experience and have worked on Hewlett-Packard and Disney film projects. Now, they turn their attention to the vaccine Gardasil. Click here and here for more information on release dates. Below, the documentary film is described by the brothers themselves:

One More Girl is a documentary about the stories of anguish and travesty, futures destroyed, and families reduced to financial ruin by medical costs brought on by a vaccine, Gardasil. The vaccine is designed to prevent Human Papillomavirus (HPV).

Pre-production is in process right now and we are raising funds so that we can begin production this summer with a tentative 2012 release date.

We are two brothers that were motivated to make this documentary when our sister had experienced several serious side-effects after her first injection of the Gardasil vaccine. Her adverse reaction demanded further investigation which led to the startling discovery that thousands of young girls were having serious reactions to the vaccine, including death. At last count, there have been 89 confirmed deaths as a result of Gardasil.

These girls’ reactions to the vaccine range from muscle pain, weakness, seizures, strokes, autoimmune problems, paralysis, tremors, heart issues, and the list goes on and on. Furthermore, it is estimated that only 1-10% of vaccine related side-effects are reported.

Treating these girls is a challenge. Doctors don‘t know how to treat them and are reluctant to do so without establishing the cause of their symptoms.

Haunted by the tragic stories of thousands of girls injured by Gardasil, we began in-depth research to verify a correlation between the vaccine and the girls’ medical conditions. We wanted to know more about the HPV that causes cervical cancer, the vaccine created to prevent it, and Merck Pharmaceutical Company, which developed the HPV vaccine Gardasil.

The Gardasil Girls’ stories are backdropped with research and data from global activists, attorneys, medical experts and journalists. Dr. Dianne M. Harper, the leading researcher that worked for 20 years developing the Gardasil vaccine states that, ”There is not enough evidence gathered on the side-effects to know that safety is not an issue” and “giving it to 11 year old girls is a great big public health experiment.” Dr. Harper speaks out even though her words could be detrimental to Merck. She claims, ”That she wants to be able to sleep with herself when she goes to bed at night.”

As filmmakers, we decided that the best way to bring this topic to the forefront was to make a documentary giving the “Gardasil Girls“ a voice. We intend to educate the public on HPV, hear from the experts about the medical history and marketing campaigns, and the impact of Gardasil on young girls’ lives.

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Could the vaccine Gardasil cause neurological side reaactions?

Know your G proteins: relevant for allergy, aspergers, ASD

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Norovirus, reactive arthritis and should a child with diarrhea be vaccinated?


Below is a wonderful, detailed, thorough excerpt from the Centers of Disease Control about the Norovirus. When infected, the symptoms include diarrhea, vomiting and cramping.  In some individuals, perhaps with a genetic predisposition, a reactive arthritis appears following a norovirus attack. As a result of the infection by the norovirus the body’s immune system continues to attack “self” cells believing they are enemy “norovirus” cells. Read the detailed original description of the Norovirus here. Cruise ships, nursing homes, college dorms are places were a norovirus infection spreads quickly where people live in enclosed conditions.

A cruise ship with a reported norovirus infection during a year when there were several diarrhea epidemics on cruise ships. Photo inlay of Norovirus. Photo ABC news

My question was that should a child with diarrhea or gastroenteritis be allowed to be vaccinated say perhaps with MMR vaccine or should this child wait until the child is fully recovered? How long should this gap be? The MMR vaccine contains components of three viruses to prevent three diseases. The vaccine aims to train the child’s immune system to recognize the foreign material and train in advance to prepare against an infection. Is the child with gasteroenteritis or diarrhea compromised in any way prior to being vaccinated? I could not find any scientific study published to answer this question. Is there any study on how many children had an infection upto one month prior to any immunization? How did they fare after that?

The second question which follows is which is more dangerous – losing a child to measles given a 1 in 1000 chance or having a child live a dependent life forever with Autism Spectrum Disorder with a 1 in 100 chance? I wonder which is more of a public burden. Should it be safer to ask a family with a norovirus infection to give a far lengthier gap prior to vaccinating a child? Except for an Italian court ruling a connection between a child with autism and a MMR vaccine (following a gastroenteritis infection), all official scientific studies have ruled out a connection between the MMR vaccine and autism. Yet, most parents continue to insist that their child was a normal baby who was able to communicate prior to the MMR vaccine. Could the norovirus provide one more clue to this puzzle?

Quote:

Biology and Epidemiology

The Virus

Noroviruses are a group of nonenveloped, single-stranded RNA viruses classified into the genus Norovirus (previously referred to as Norwalk-like viruses [NLVs] or small round-structured viruses [SRSVs]) of the family Caliciviridae. Other genera within the Caliciviridae family include Sapovirus (previously referred to as Sapporo-like viruses [SLVs]), which also cause acute gastroenteritis (AGE) in persons, as well as Lagovirus, Vesivirus, and Nebovirus, which are not pathogenic for humans (11). Noroviruses can be divided into at least five genogroups, designated GI–GV, based on amino acid identity in the major structural protein (VP1) (12). The strains that infect humans (referred to collectively as “human noroviruses”) are found in GI, GII, and GIV, whereas the strains infecting cows and mice are found in GIII and GV, respectively (Figure 1). Although interspecies transmission of noroviruses has not been documented, strains that infect pigs are found in GII (13), and a GIV norovirus was discovered recently as a cause of diarrhea in dogs (14), suggesting the potential for zoonotic transmission. On the basis of >85% sequence similarity in the complete VP1 genome, noroviruses can be classified further into genotypes, with at least eight genotypes belonging to GI and 21 genotypes belonging to GII (12,13; CDC, unpublished data, 2011). Since 2001, GII.4 viruses have been associated with the majority of viral gastroenteritis outbreaks worldwide (15). Recent studies have demonstrated that these viruses evolve over time through serial changes in the VP1 sequence, which allow evasion of immunity in the human population (15,16).

Clinical Features

Noroviruses cause acute gastroenteritis in persons of all ages. The illness typically begins after an incubation period of 12–48 hours and is characterized by acute onset, nonbloody diarrhea, vomiting, nausea, and abdominal cramps. Some persons might experience only vomiting or diarrhea. Low-grade fever and body aches also might be associated with infection, and thus the term “stomach flu” often is used to describe the illness, although there is no biologic association with influenza. Although symptoms might be severe, they typically resolve without treatment after 1–3 days in otherwise healthy persons. However, more prolonged courses of illness lasting 4–6 days can occur, particularly among young children, elderly persons, and hospitalized patients (17,18). Approximately 10% of persons with norovirus gastroenteritis seek medical attention, which might include hospitalization and treatment for dehydration with oral or intravenous fluid therapy (7,19,20). Norovirus-associated deaths have been reported among elderly persons and in the context of outbreaks in long-term–care facilities (21,22). Necrotizing enterocolitis in neonates, chronic diarrhea in immunosuppressed patients, and postinfectious irritable bowel syndrome also have been reported in association with norovirus infection (23–25); however, more data from analytic studies are needed to confirm a causal link with these conditions.

Norovirus is shed primarily in the stool but also can be found in the vomitus of infected persons, although it is unclear if detection of virus alone indicates a risk for transmission. The virus can be detected in stool for an average of 4 weeks following infection, although peak viral shedding occurs 2–5 days after infection, with a viral load of approximately 100 billion viral copies per gram of feces (26). However, given the lack of a cell culture system or small animal model for human norovirus, whether these viruses represent infectious virus is unknown, and therefore the time after illness at which an infected person is no longer contagious also is unknown. Furthermore, up to 30% of norovirus infections are asymptomatic, and asymptomatic persons can shed virus, albeit at lower titers than symptomatic persons (26–28). The role of asymptomatic infection in transmission and outbreaks of norovirus remains unclear.

Immunity

Protective immunity to norovirus is complex and incompletely understood. In human challenge studies, infected volunteers were susceptible to reinfection with the same strain as well as to infection with heterologous strains (29–32). In addition, those with preexisting antibodies were not protected from infection unless repeated exposure to the same strain occurred within a short period. Two of these studies demonstrated that homologous antibody protection might last anywhere from 8 weeks to 6 months (30,31). However, the infectious dose of virus given to volunteers in these challenge studies was several-fold greater than the dose of virus capable of causing human illness, and thus immunity to a lower natural challenge dose might be greater and more cross-protective.

Because preexisting antibodies among challenged volunteers did not necessarily convey immunity, and some persons seemed to remain uninfected despite significant exposure, both innate host factors and acquired immunity have been hypothesized to contribute to the susceptibility to infection (31). Histo-blood group antigens (HBGAs), including H type, ABO blood group, and Lewis antigens have been proposed as candidate receptors for norovirus. Expression of HBGAs is associated with strain-specific susceptibility to norovirus infection (17,33–38). Resistance to norovirus infections has been associated with mutations in the 1,2-fucosyltransferase (FUT2) gene leading to a lack of expression of HBGAs on the surface of intestinal cells (33–35,39). Thus, persons who have the normal FUT2 gene and who express these antigens are termed “secretors” whereas mutations in the FUT2 gene leading to the absence of HBGA expression result in “nonsecretor” persons who are less susceptible to infection. However, secretor status does not completely explain the differences seen among infected and uninfected persons for all strains of norovirus. Thus, additional mechanisms of immunity are likely involved, and this remains an ongoing field of research. In addition, evidence suggests that new GII.4 variants evolve to escape the build-up of acquired immunity and innate resistance in the human population (16,40).

Transmission

Norovirus is extremely contagious, with an estimated infectious dose as low as 18 viral particles (41), suggesting that approximately 5 billion infectious doses might be contained in each gram of feces during peak shedding. Humans are the only known reservoir for human norovirus infections, and transmission occurs by three general routes: person-to-person, foodborne, and waterborne. Person-to-person transmission might occur directly through the fecal-oral route, by ingestion of aerosolized vomitus, or by indirect exposure via fomites or contaminated environmental surfaces. Foodborne transmission typically occurs by contamination from infected food handlers during preparation and service but might also occur further upstream in the food distribution system through contamination with human waste, which has been demonstrated most notably by outbreaks involving raspberries and oysters as vehicles (42–46). A recent outbreak involving consumption of delicatessen meat also demonstrated the potential for norovirus contamination during processing (47). Finally, recreational and drinking water can serve as vehicles of norovirus transmission and result in large community outbreaks (48,49). These outbreaks often involve well water that becomes contaminated from septic tank leakage or sewage (50) or from breakdowns in chlorination of municipal systems (51).

Sporadic Disease

As diagnostic methods have improved and become more widely available, the role of noroviruses as the leading cause of sporadic gastroenteritis in all age groups has become clear. Approximately 21 million illnesses caused by norovirus are estimated to occur each year in the United States, approximately one quarter of which can be attributed to foodborne transmission (52). A recent systematic review of 31 community, outpatient, and hospital-based studies in both developed and developing countries estimated that noroviruses accounted for 10%–15% of severe gastroenteritis cases in children aged <5 years and for 9%–15% of mild and moderate diarrhea cases among persons of all ages (53). Although laboratory-based data on endemic norovirus disease in the United States are sparse, recent studies suggest that norovirus is the leading cause of acute gastroenteritis in the community and among persons seeking care in outpatient clinics or emergency departments across all age groups (54,55; CDC, unpublished data, 2011).

Serosurveys have demonstrated that norovirus infections are prevalent throughout the world, with initial exposure typically occurring early in life (5). In population-based studies from Australia, England, Hong Kong, and the Netherlands, norovirus infection has accounted for 9%–24% of gastroenteritis cases (19,20,56–58). In these studies, infection was more frequent in certain age groups (e.g., children aged <5 years and adults aged >65 years). In studies that have used sensitive molecular assays, a relatively high prevalence of norovirus-positive samples in asymptomatic persons has been detected, ranging from 5% in the Netherlands to 16% in England (20,56). This background rate of asymptomatic infection, coupled with innate resistance attributable to secretor status and acquired immunity, helps explain why attack rates rarely exceed 50% in outbreaks.

Outbreaks

Noroviruses are the predominant cause of gastroenteritis outbreaks worldwide. Data from the United States and European countries have demonstrated that norovirus is responsible for approximately 50% of all reported gastroenteritis outbreaks (range: 36%–59%) (5). Outbreaks occur throughout the year although there is a seasonal pattern of increased activity during the winter months. In addition, periodic increases in norovirus outbreaks tend to occur in association with the emergence of new GII.4 strains that evade population immunity (Table) (40,59). These emergent GII.4 strains rapidly replace existing strains predominating in circulation and can sometimes cause seasons with unusually high norovirus activity, as in 2002–2003 and 2006–2007. Because the virus can be transmitted by food, water, and contaminated environmental surfaces as well as directly from person to person, and because there is no long lasting immunity to norovirus, outbreaks can occur in a variety of institutional settings (e.g., nursing homes, hospitals, and schools) and affect people of all ages. Whereas prior national estimates of outbreak attribution by mode of transmission were likely biased toward foodborne disease (60,61), more recent data from individual states indicate that the majority of norovirus outbreaks primarily involve person-to-person transmission (62,63). Multiple routes of transmission can occur within an outbreak; for example, point-source outbreaks from a food exposure often result in secondary person-to-person spread within an institution or community. Of the 660 norovirus outbreaks laboratory confirmed by CDC during 1994–2006 that indicated the setting, 234 (35.4%) were from long-term–care facilities (e.g., nursing homes); 205 (31.1%) were from restaurants, parties, and events; 135 (20.5%) were from vacation settings (including cruise ships); and 86 (13.0%) were from schools and communities (59). Although GII.4 variants predominate overall, the role of GI and other GII genotypes appears to be greater in settings that involve foodborne or waterborne transmission (Figure 2).

Long-Term Care and Other Health-Care Facilities

Health-care facilities including nursing homes and hospitals are the most commonly reported settings of norovirus outbreaks in the United States and other industrialized countries (59,60,63–65). Virus can be introduced from the community into health-care facilities by staff, visitors, and patients who might either be incubating or infected with norovirus upon admission or by contaminated food products. Outbreaks in these settings can be prolonged, sometimes lasting months (66). Illness can be more severe in hospitalized patients than for otherwise healthy persons (18), and associated deaths have been reported (21,22). Strict control measures (including isolation or cohorting of symptomatic patients, exclusion of affected staff, and restricting new admissions into affected units) are disruptive and costly but might be required to curtail outbreaks (9,67,68).

Restaurants and Catered Events

Norovirus is now recognized as the leading cause of foodborne disease outbreaks in the United States. Norovirus accounted for 822 (35%) of the 2,367 foodborne disease outbreaks reported to CDC during 2006–2007 (Figure 3) and half of the 1,641 foodborne disease outbreaks with a confirmed or suspected etiology (69,70). Food can become contaminated with norovirus at any point during production, processing, distribution, and preparation. Thus, a variety of products have been implicated in outbreak investigations; foods eaten raw (e.g., leafy vegetables, fruits, and shellfish) are identified most commonly (69,70). Handling of ready-to-eat foods by infected food employees is commonly identified as a contributing factor in outbreaks of foodborne norovirus associated with food-service establishments (71,72). Norovirus outbreaks also have resulted from fecal contamination of certain food products at the source. For example, oysters harvested from fecally contaminated growing waters and raspberries irrigated with sewage-contaminated water have been implicated in outbreaks (44,73). Because gross sewage contamination will contain a collection of viruses circulating in the community, multiple norovirus genotypes often are detected in such outbreaks. Contamination with norovirus also can occur during processing, as demonstrated by a recent outbreak involving delicatessen meat (47). Only a small dose of virus is needed to cause infection, and thus infected food handlers can contaminate large quantities of product. For example, approximately 500 cases of gastroenteritis were reported during a 2006 outbreak caused by a foodhandler who vomited at work (74). Drinking water or ice also might become contaminated with norovirus and result in outbreaks in food-service settings. Secondary person-to-person transmission is common following point-source food or water exposures.

Schools and Other Institutional Settings

Norovirus outbreaks occur in a range of other institutional settings including schools, child care centers, colleges, prisons, and military encampments. Outbreaks of gastroenteritis in child care centers also are caused by other pathogens, including rotavirus, sapovirus, and astrovirus, as a result of a lack of immunity to these viruses in young populations (75). Outbreaks have been reported recently from multiple universities in different states and have led to campus closures (76). An intervention study in elementary schools demonstrated that improved hand hygiene and surface disinfection can lead to lower rates of absenteeism caused by nonspecific gastroenteritis and reduced surface contamination with norovirus (77). Norovirus was also the most common cause of gastroenteritis in U.S. marines during Operation Iraqi Freedom (78) and a common cause of outbreaks among deployed British troops (79).

Cruise Ships and Other Transportation Settings

Passengers and crew aboard cruise ships are affected frequently by norovirus outbreaks (80). Virus generally is introduced on board by passengers or crew infected before embarkation but might also result from food items contaminated before loading or persistently contaminated environmental surfaces from previous cruises. Virus also might be acquired when ships dock in countries where sanitation might be inadequate, either through contaminated food or water or passengers becoming infected while docked. Repeated outbreaks can occur in subsequent sailings as a result of environmental persistence or infected crew, particularly if control measures have not been implemented consistently and thoroughly. Genotyping of outbreak strains from repeated outbreaks has demonstrated that this can occur through the introduction of new virus or recrudescence of virus from one sailing to the next (81,82). CDC’s Vessel Sanitation Program assists the cruise ship industry in preventing and controling the introduction and transmission of gastrointestinal illness by inspecting cruise ships, monitoring gastrointestinal illnesses, and responding to outbreaks (http://www.cdc.gov/nceh/vsp). Outbreaks also have been reported in association with bus tours and air travel, in which environmental contamination and proximity to ill passengers facilitated norovirus transmission (83,84).

Unquote
Read the entire original article here by Centers of Disease Control of the United States.

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Could the vaccine Gardasil cause neurological symptoms as an adverse reaction?


The Lyme Disease vaccine was removed from the market after patients complained about severe arthritis and neurological symptoms after receiving the vaccine.  Is Gardasil not getting enough public anger yet. Nobody died from the Lyme vaccine and the public got attention. Is the Connecticut public simply more intellectual than the rest of America? Or is the rest of America extremely accepting of medical harm, injected by their trusted family Pediatrician in all good faith?

A registered nurse commenting on an article on PANS on Mailonline.com certainly has observed neurological adverse reactions following the Gardasil vaccine. Most of the other comments implicated gardasil.

A mother commented on my article on “LeRoy high school…Tourettes…” that her daughter has been chronically ill since she took her third gardasil shot in 2009. Most of the other comments implicated a vaccine, either gardasil or a swine flu vaccine.

An organization dedicated to gardasil’s adverse reaction lists the names of our young girls with their own or their mother’s version of the history of the development of their symptoms. One common theme in these stories is ‘brain fog’ and stomach pain so severe that doctors recommend operations which parents indicate were unwarranted. If you care and have noticed that adverse reaction reporting is not being done in a scientific manner, or surprised why doctors do not understand the vaccine are dangerous when improperly designed by non-dedicated scientists, then:

write to the people who have provided their emails and leave them messages of support and then use your own voice to be active to protect your own community from negligence.

Henrietta Lacks died from cervical cancer and donated unknowingly her cancer cells to research. She died at the age of thirty and was often infected with STDs by a philandering husband. Her HeLa cells have given so much help to our society. Cancer research progressed with HeLa cells at a fast pace because HeLa cells multiplied faster than any known and available cancer cells in culture. Before HeLa it was difficult to grow a cancer cell in culture.

The Gardasil vaccine’s goal is to prevent the early death from cervical cancer. The aim is commendable. However, the vaccine researchers may have simply taken the virus strains and decided to use standard procedures to create a bottled product.

They would have done well to have heeded the reaction to the Lyme Disease vaccine which was developed by non-dedicated Yale scientists. They had the literature which would have advised against developing a vaccine to OspA protein and could have gone with the OspB bacterial protein. But instead they rushed in their eagerness to fame and licensed the rights to big Pharma, whose regulators did not do their job and apply their expertise to check the literature and earnestly began marketing the drug. Fortunately, the public in Connecticut, where Lyme disease was originally recognised and a vaccine developed, rose against the vaccine in a large group and took the matter to the attention of the Attorney General. The Lyme vaccine was having side effects of rheumatoid arthritis and neurological issues and the vaccine had to be removed from the market. Read the articles published in 2002 by washington medical writer Lauren Neergaard and Dr Andrea Gateo’s comment on the side bar of the article by Lymeinfo.net an advocacy group urging caution with a new vaccine.
Glaxo Smith Kline, the marketer of this vaccine Limerix was miffed.

Is there a pattern emerging here?
1)It is obvious that Gardasil (or swine flu vaccine) alone is not the cause of neurological adverse reactions, otherwise all who receive the vaccine would have similar symptoms.
2) Also, a genetic basis has been ruled out because all who show adverse symptoms appear so far to lack an obvious common genetic profile.
3) Yet, when an online community of concerned parents are observing serious neurological issues following some vaccinations, then their collective observations can no longer be ignored.

What should a community do? As a responsible community, we must begin to ask:
What are the common factors when a cluster of people present with the same symptoms? Please, keep in mind that although logically a number of factors together cause a signal cascade presenting the said neurological symptoms, current scientific methodology allows for testing of only single factors at a time.

Our community should begin to demand large scale multi-factorial cause-effect studies. Trust me, we have the computer tools and the scientists capable of interpreting the results. For example, the New York Department of Health has collected data on some symptoms which have more than 80,000 students. Yet, they lack qualified or even unqualified personnel to simply add more columns with data points asking “Did you get a vaccine x,y or z when you had the common cold or strep throat infection?” They lack scientists to summarize the data collected and interpret it. They have a hiring freeze at a critical time when mass vaccinations are being enforced nationally and internationally.

What can you do? Are you a responsible adult who cares to ensure that we do not harm our children, adolescents and young adults? Then add your voice and begin to question. Just begin. The questions will form.

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Tracking the seasonal flu, The History of the Flu Vaccine and The Flu Vaccine of 2011


The seasonal flu of 2011 arrived with the first confirmed case in Arkansas (Read more). The vaccination of the public swung into action with the seasonal flu vaccine components of 2011, which were exactly the same as the vaccine components of 2010, and described in my previous article, entitled, “Should I get the flu vaccine this year?”. The 2011 – 2012 flu season is going to be an ordinary one, unlike the one in 2009 and the far deadlier one in 2018, all of them caused by the same deadly swine flu H1N1 strain of the flu virus. First reported death from swine flu in 2009 was a 23 month old boy in Texas (Read more). The vaccination of the public swung into action in 2009. Why was 2018 the deadliest flu season in America with over 40 million estimated to be killed world-wide, far more than by the war?  Why was the 2009 flu season pandemic by the same flu virus strain  far less deadlier? The answer is the flu vaccine, the story of which I will tell you here.

A Flu Virus

The Story of The Flu Vaccine:
This year quite different from other years in the story of the Flu Vaccine and that is because Prof. Edwin Kilbourne passed away very quietly in 2011. He had devoted his entire life to the study of the flu virus and played a leadership role in the history of the development of the flu vaccine. I could tell you about Dr Kilbourne but to tell you why he is important, I would need to tell you about the 2018 flu pandemic.

Many have wondered why the Flu pandemic of 1918 is not mentioned as a turning point in American lifestyles in the History books. The fall of 2018 began just like another fall in the middle of a chaos of a country in the midst of the a world war. Stealthier than any human enemy, arrived a tiny microbe, the flu virus strain H1N1 on a crisp New England fall day in a Boston sea port. It must have arrived with some sailors. The September of 1918, the Boston Port was busy with war shipments of machinery. The war efforts allowed the virus to spread and diffuse. It was named the “Spanish Flu” or the “La Grippe”.

The flu pandemic of 1918 devastated many towns and military cantonments by acting very strangely. It wiped out America’s young and healthy, particularly those aged 20-35 years of age. There was no cure. The ill were advised to rest lying down, get fresh air, and to take plenty of fluids. The healthy were advised to avoid crowded, public places. Many wore masks to protect themselves or to prevent infecting others.

The Contagious First Wave of the 1918 Flu Pandemic
The best recorded first case was in Fort Riley, USA. On March 11, 1918, Private Albert Gitchell, a cook at Fort Riley, came down with a cold that required isolation. Within 5 weeks, 1,127 soldiers came down with the same symptoms and 46 of them died. Soldiers trained at Fort Riley before being deployed for the war effort in Europe and unintentionally spread the flu to Europe. When the flu began to ravage the people of Spain, the Spaniards publicly announced the disease. Spain was not in World War 1 and was not censoring its news and the world first heard of the deadly flu from Spain. Hence, the name, the “Spanish Flu”. By July 1918, the “Spanish Flu” had visited Russia, India, China and Africa and appeared to be dying out. Nobody guessed that this was only the first wave of the deadly flu pandemic about to be unleashed upon an unsuspecting world of humans by a microscopic, indestructible microbe.

The Contagious and Deadly Second Wave of the 1918 Flu Pandemic
Towards the end of August, a more deadly flu struck three world cities simultaneously. Boston, USA; Brest, France; and Freeport, Sierra Leone. The overwhelmed hospitals asked for volunteers to take care of their sick, who had to be housed in tents because of their sheer numbers.

Nurses care for the sick in tents

Some died within two days of first symptoms which included coughing violently, bleeding from their ears or turning blue in color and of course, extreme fatigue, fever and headache. The Spanish flu in its second wave struck suddenly and severely, killing some within several hours or a few days, while sparing others. Not surprisingly, panic ensued. Public events were canceled. Schools and theaters closed. Masks were required by many communities. Popular homemade remedies of the past did nothing to prevent or cure this disease. The dead piled up and mass graves had to deal with the bodies. There were not enough people to dig individual graves.

The Third Wave of the 1918 Pandemic
On November 11, 1918, an Armistice brought an end to World War 1. The hugging and kissing of the returning soldiers, some carrying the flu virus helped to create yet another epidemic wave, spreading a weaker version of the “Spanish Flu”. This wave was largely ignored because people had to concentrate on rebuilding their lives, while the pandemic lingered alongside and slowly petered away. Some say the flu lingered until next year but nothing as deadly as the early fall of 1918.

Preventing Another Deadly Pandemic
In an effort to prevent another deadly pandemic in the future, the USA government allocated 1 million dollars to learn more about the “Spanish Flu”. Among many recruited towards the laboratory war against the “Spanish Flu” was a young and eager Dr Edwin Kilbourne, a medical school graduate who was well-trained in virology laboratory research.

Dr Edwin D Kilbourne and Dr D E Rogers testing the Asian Flu virus

It was particularly hard for the Alaskan Indians for whom the death rate was elevated beyond that of the non-Indians. In one Inuit village in Alaska 72 of its 80 residents  died within 5 days in November 1918. Years later in 1997, a researcher dug up remains in the permafrost to isolate the flu virus and reconstructed the fatal strain H1N1. The Spanish Flu had traveled from Boston to Alaska in 2 months, killing many in it’s path.

In 1918 children would skip to the rhyme (Source: Crawford)
I had a little bird, Its name was Enza. I opened the window, And in-flu-enza.

The “Spanish Flu” of 1918 killed over 40 million people worldwide that flu season, while the World War 1 claimed about 16 million. Archives of photos here describe how the public and the government reacted to a situation of panic in the midst of a world war. These archives will help guide future leaders when faced with a similar crisis in the future. The Flu virus mutates over the years and has a habit of returning every few decades to cause epidemics or pandemics, that kill many. A cryptic, well-researched PBS movie (click here to watch) entitled, “1918 Spanish Influenza”, follows the story of the 1918 flu virus pandemic.

Native American death rate from the flu

on
swine flu death rates elevated for alaska natives and american indians

http://www.washingtonpost.com/wp-dyn/content/article/2009/12/10/AR2009121003937.html

The “Spanish flu” of 1918-19 devastated Inuit villages in Alaska. In one, Brevig Mission, 72 out of 80 residents died over five days in November 1918. A researcher extracted tissue samples in 1997 from a body buried there in a mass grave in the permafrost, allowing scientists to reconstruct that fatal strain of influenza.

CDC brochure advising that antibiotics will not work against the flu

http://www.cdc.gov/getsmart/campaign-materials/print-materials/Brochure-NativeAmerican.html

Arkansas has confirmed the first case of seasonal flu for 2011 in America   http://nwahomepage.com/fulltext-news/?nxd_id=276457

First reported death from swine flu in 2009 was a 23 month old boy in Texas    http://www.chron.com/news/health/article/Swine-flu-s-spread-pushes-Texas-to-cut-high-1744879.php

Tracking swine flu worldwide   http://www.nytimes.com/interactive/2009/04/27/us/20090427-flu-update-graphic.html

The United States Department of Health and Human Services  – a one stop to flu   http://1918.pandemicflu.gov/

The flu season that should be in history books    http://virus.stanford.edu/uda/   http://virus.stanford.edu/uda/

In 1918 children would skip to the rhyme (Crawford)  (source  http://virus.stanford.edu/uda/  )     I had a little bird,Its name was Enza.I opened the window,And in-flu-enza.     It first arrived in Boston in September of 1918 through the port busy with war shipments of machinery and supplies. The war also enabled the virus to spread and diffuse.  

Watch the PBS movie on the 1918 Spanish Influenza  http://www.pbs.org/wgbh/americanexperience/films/influenza/

Watch an archive of photos of the 1918 flu that killed an estimated excess of 40 million people worldwide while the world war 1 during the same time claimed an estimated 16 million lives  http://www.archives.gov/exhibits/influenza-epidemic/

For the federal government answers to frequent questions go to   http://www.flu.gov/general/

For a brief history of the Flu vaccine in The Times in 2008   http://www.time.com/time/nation/article/0,8599,1864920,00.html

The CBS documentary by Norman Gorin on the 1976 flu vaccine that caused 4000 people to claim damages, two thirds of them neurological   http://www.dailymotion.com/video/x9nnh6_swine-flu-1976-propaganda_news#rel-page-1

Natural questions followed on how to deal with the 2009 flu pandemic heeding the lessons of the 1976 mass flu vaccination  http://www.time.com/time/health/article/0,8599,1894129,00.html

Looking back it is not difficult to see why the 1976 flu vaccination decisions were taken.  http://www.haverford.edu/biology/edwards/disease/viral_essays/warnervirus.htm  but with the knowledge now, that the 1976 vaccine had the trigger that could make 8.3 per million people with most likely no prior illness sick from GBS versus 0.7 per million people with most likely a prior illness sick from GBS. Rationale for future vaccination programs.

Dr Edwin Kilbourne was the virologist who convinced the US Public Health Service to mass vaccinate. His was a stellar career, devoted to outwitting the Flu Virus. 1920 – 2011.  http://www.virology.ws/2011/02/25/edwin-d-kilbourne-md-1920-2011/    The New York Times only featured a miniscule portion of his career and his role in the 1976 flu vaccine fiasco and ignored his tremendous contribution to the modern flu vaccine.

Palese and Garcia-Sastra continue the search for a diagnostic, preventive and curative agent for all strains of Influenza. http://www.freepatentsonline.com/y2011/0027270.html  and http://en.wikipedia.org/wiki/Peter_Palese  and the team at Mt Sinai

Towards a broadly protective flu vaccine  http://www.jci.org/articles/view/37232  The team at St Judes Medical center  with the goal to define the role of cross reactive lymphocytes. Webster’s article on flu history with photo of little girls skip roping to the poem above  http://people.scs.carleton.ca/~soma/biosec/readings/influenza/influenza.html   Also has great related internet sources.

Egg free vaccine – my earlier article

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Flu vaccination and egg allergy


I worked in a flu lab for a year and was part of the team trying to understand the genetic nature of the flu virus. How did it change it’s genetic makeup so quickly each year so that we needed to update our flu vaccination annually? Little did I expect to have to deal with questions on what to do about egg allergy. You see, until recently, all flu vaccines were prepared in eggs. Now, there are some brands available that are not made in eggs. Should a child or adult with egg allergy try to brave the flu season naturally or should they protect themselves by taking a vaccine, until recently only made in eggs?

A flu virus

The Flu photo (from CDC archives http://www.cdc.gov/h1n1flu/images.htm) which shows the external H and N proteins that change to require new vaccine every year and the internal, coiled RNA genetic material.

If you have never had the flu, chances are you may never get the flu. You may want to get expert advice on whether you need any protection at all. If you or your child has gotten the flu in the past, chances are that you and/or your child will get the flu again, and it may be best to get advice from an allergist on the safest vaccination options if egg allergy is an issue. There is an excellent article in the British Medical Journal in 2009 by Lajeunesse and colleagues on egg allergy and flu vaccines. You may also want to see my article on “Should I get the flu vaccine this year?” for the 2011-2012 flu season.

Egg free vaccines have recently been researched and produced using a new technique in a mammalian cell line instead of eggs. Surface antigen, split virion, subunit, split flu, and inactivated flu vaccines are grown in hens’ eggs and do contain residual egg proteins. During the 2008 flu season, some but not all flu vaccines reported maximum egg protein content above 1.2 ug/ml with levels up to 2ug/ml. The proposed safety egg content is less than 1.2ug/ml (0.6ug per dose). Some vaccines often have much less residual egg protein, although still grown in egg cultures, such as virosomal vaccines, which are highly purified.

The youngest and the oldest are most at risk from succumbing to the flu. Certain elderly are recommended a much higher dose of flu vaccine to be effectively protected. It is important to note that egg-free mammalian culture based flu vaccines are now available or under clinical trials and should be given preferentially under expert advise to individuals allergic to egg. If an egg-free vaccine is unavailable, then check the maximum egg content of the vaccine and ensure that it is below 1.2ug/ml. The vaccination should be done in a center experienced in management of anaphylaxis if the doctor advises so. A single dose protocol is effective for individuals with less severe allergy. A 2 dose split protocol is recommended for asthma prone or anaphylaxis prone individuals.

In USA, flu vaccines developed in egg-free manufacture protocols are unavailable. So, if you are allergic to eggs, do visit an allergist. They have a protocol with which they could administer the vaccine. The steps include pricking your arm with egg extracts to elicit an allergy response from which they determine the pros and cons of giving you the vaccine. In Europe, Flugen is under clinical trial and showing promise. Celvapran (Baxter) a pandemic vaccine for A/H1N1 and Optiflu (Novartis) a seasonal flu vaccine have good safety records for egg allergy. You may also read “Next generation of flu vaccines coming of age: Cell – based technology may replace egg – based flu vaccines“, by Teddi Dineley Johnson

It is predicted that the H1N1 will return in 2010 fall around the same time as it did in 2009. The spring flu may have been displaced by the fall flu. If so, then it may be a race against time to vaccinate our kids safely and effectively before the fall H1N1 flu season descends upon us. Take advise, be cautious, and make a wise decision. If you had the H1N1 flu last year, then you may have a level of natural immunity to this year’s H1N1 flu virus. You may not need a vaccine for this flu variety, however, a vaccine would give you a quicker defense response on exposure (booster). This flu season the vaccine includes protection against additional A and B flu varieties called a trivalent protection. This vaccine gives you protection hopefully until next September, unless new flu strains develop before that. There is a race to produce a ‘life time’ flu vaccine targeting proteins of the flu virus that do not usually change every year. Then, one vaccine would give us life time protection. Until then, we have to consider the flu vaccine annually to protect us against the crafty new flu virus strain. I have full confidence in our global flu scientists and believe they can outwit the wily flu virus.

As for eating naturally to prevent the flu, there are oranges, providing vitamin C, there is garlic reputed to keep a family save through many recipes and always ginger, against inflammation. Gargling with salt daily in flu season is very helpful.

This article has been cited by ALLVoices, which covers health news and other news in San Francisco.

 

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