ChickenPox/Shingles Strains

Identification of Five Major and Two Minor Genotypes of Varicella-Zoster Virus Strains: a Practical Two-Amplicon Approach Used To Genotype Clinical Isolates in Australia and New Zealand


Whole genome phylogenetic analysis in this study resolved a total of five major genotypes among the 22 varicella-zoster virus (VZV) strains or isolates for which complete genomic sequences are available.


Acquiring one strain can result in immunity to all strains of the virus. In some cases, however, complete immunity is not attained and an individual can become re-infected.

Shingles, or herpes zoster, this is a later reactivation of latent virus. It can occur any time after the initial infection. Usually, it occurs years later, and is activated by stress or an unbalanced immune system.

Varicella Zoster Virus

VZV is a member of the herpes virus group or (alpha) herpes virus 3, and it is a DNA virus. VZV can persist as a latent infection in dorsal root or extra medullary cranial ganglia.


Toward Universal Varicella-Zoster Virus (VZV) Genotyping: Diversity of VZV Strains from France and Spain


…wild-type varicella-zoster virus (VZV) strains to seven genotypes: A1, A2, J1, B1, B2, C, and C1. VZV isolates identified as E (ORF22 method) had the genetic signature of genotype C VZV strains, M1 strains were A1, and M2 were A2. No J strains were detected, but parental Oka and vaccine Oka (genotype J) corresponded to genotype J1. M4 isolates (B) share the SNP array observed for M1 and E viruses, and probably represent recombinants between African-Asian (M1) and European (E) viruses. The two genotyping methods, using entirely different genomic targets, produced identical clusters for the strains examined, suggesting robust phylogenetic linkages among VZV strains circulating in Europe.


pOka is the parental Oka strain from which varicella vaccine was derived. Sequence positions are based on the published genomic sequence for the Dumas strain. Green cells indicate European genotype (E) markers; yellow cells are Japanese genotype (J) markers, rose cells are markers unique to various M genotype variants, and uncolored cells reflect markers that are consistent across genotypes. ND, not determined.

The Immunological Basis for Immunization Series    Module 10: Varicella

VZV is a member of the herpesvirus family. It has 71 genes, all of which are expressed in lytic infection and seven of which are expressed in latent infection (5). Only neurons support latent infection. There is one serotype, but several genotypes are known, with small differences in their DNAs, classified as European, Japanese, and Mosaic (6). Recently, 3% of VZV strains circulating in the United States of America have been identified as Japanese type (7).

VZV was successfully attenuated by Takahashi and colleagues in 1974, by serial passage of a clinical isolate from an otherwise healthy boy with chickenpox (13).

Attenuation was achieved by passage 11 times at 34ºC in human embryonic lung fibroblasts (HELF), 12 passages at 37ºC in guinea-pig fibroblasts, and 5 to 6 passages in MRC -5 human fibroblasts at 37ºC. Infected cell suspensions were sonicated to obtain cell-free VZV.Standard safety-testing after injection into small mammals was also performed, and did not identify any adventitious agents.

Varicella vaccines contain a mixture of Oka and parental strains (14-16). Sequencing of the Dumas strain of wild-type VZV, and the Oka strain, has shown that there are 42 differing bases, over one third of which are in gene 62.Three fixed mutations have been identified in Oka strains present in skin rashes of vaccinees, all located in gene 62 (15,17,18). Although the genetic basis for attenuation is still unknown, it is possible to differentiate Oka from wild-type VZV by PCR in clinical specimens (8).

Monovalent varicella vaccine is produced in the United States (VarivaxTM; Merck & Co., Inc.), the Kingdom of Belgium (VarilrixTM; GlaxoSmithKline), and Japan (OKAVAX™; Biken, distributed by Aventis Pasteur). These vaccines vary slightly in passage number in human diploid cells, antibiotics for sterility, stabilizers and minor constituents. Each preparation guarantees 1350 plaque forming units (PFU) per 0.5 ml at expiration; doses at release vary from 3 000 to 17 000 PFU.

Combination vaccines for measles-mumps-rubella-varicella (MMRV) are produced by Merck (ProQuadTM)and GSK (Priorix-TetraTM). MMRV vaccines are licensed for children 12 months to 12 years old. They contain the same measlesmumps-rubella (MMR) components as MMR vaccine, but have a higher concentration of Oka varicella vaccine (~ 10 000 PFU at expiration) than monovalent varicella vaccines.

A formulation of the Oka strain containing~ 17 000 PFU (ZostavaxTM), is used for prevention of zoster when administered to healthy adults above the age of 60 years.

VARIVAX® Varicella Virus Vaccine Live


VARIVAX* [Varicella Virus Vaccine Live] is a preparation of the Oka/Merck strain of live, attenuated varicella virus. The virus was initially obtained from a child with natural varicella, then introduced into human embryonic lung cell cultures, adapted to and propagated in embryonic guinea pig cell cultures and finally propagated in human diploid cell cultures (WI-38). Further passage of the virus for varicella vaccine was performed at Merck Research Laboratories (MRL) in human diploid cell cultures (MRC-5) that were free of adventitious agents. This live, attenuated varicella vaccine is a lyophilized preparation containing sucrose, phosphate, glutamate, and processed gelatin as stabilizers.


ZOSTAVAX® Zoster Vaccine Live


ZOSTAVAX is a lyophilized preparation of live, attenuated varicella-zoster virus (Oka/Merck) to be reconstituted with sterile diluent to give a single dose suspension with a minimum of 19,400 PFU (plaque forming units) when stored at room temperature for up to 30 minutes.


ProQuad® Measles, Mumps, Rubella and Varicella Virus Vaccine Live

(no longer available until further notice)


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.

Bringing Chickenpox to the Boil

Bringing Chickenpox to the Boil

by Hilary Butler

Avid readers of dramatic novels from yesteryear will recall stories from the days when fevered patients were watched over by family, and the oldies in the group just “knew” that a proper fever would “break” with a sweat. When that happened, they knew that the prognosis would be good. Of course, such sentiments today would be greeted with alarm, or scepticism, by those who consider illness should never be endured.

Isn’t that why acetaminophen (in all their different brand names) is reached for, at the first sign of a fever?

In 2001, a headline

1 made me look twice. “Sweat has the power to fight off disease.” We were told that sweat contains a versatile antibiotic that may be on the front line against disease-causing bacteria and that: “The researchers said dermcidin probably plays a key role in the innate immune responses of the skin”.  A news roundup from the British Medical Journal told us2 that dermcidin killed escherichia coli, enterococcus faecalis, staphylococcus aureus and Candida albicans. It was active at high salt concentrations and the acidity range of human sweat. In concentrations of 1–10 μg/ml, it killed all of the staph aureus colonies in only four hours. Unsurprisingly, the scientists didn’t know how dermcidin worked.

Up until the late 1990s the skin was simply thought to be a “barrier” with no active participation in the immune system. The original 2001 paper

3 said that during some inflammatory skin disorders and wound healing, skin cells functioning within a salty sweat with a pH of 4–6.8, produced many effective pharmacologically active substances, such as immunoglobulin A, interleukin 1, 6 and 8, tumour necrosis factor, transforming growth factor β receptor, epidermal growth factor, and a prolactin-inducible protein.

As time has gone on, other researchers have taken a closer look at skin, and have found that the neutrophil,

4 which is the professional phagocyte of fundamental importance for defence against micro-organisms, provides instant help, not only in microbial infection,5 but to the growth factors when the skin is broken and there is a risk of infection. Another article6 says that mast cells, macrophages and skin cells produce antimicrobial peptides. These are called cathelicidin, which disrupts bacterial cell walls, modifies the host cells inflammation, and provides additional immune defence. At the heart of this all, is our friendly neutrophil:

“These studies clearly illuminate the importance of neutrophil recruitment in cutaneous defense against bacterial infection. … Recent advances in understanding of innate immune defense systems have suggested that these ancient evolutionary immune mechanisms may be important to human disease yet previously underappreciated.” (Underlining mine)

The article looked at whether just skin and mast cells were involved, or whether neutrophils were also important. Using mice, they found that mice with few neutrophils developed much worse tissue death (necrosis) and had 3,000 times the amount of bacteria on the skin than mice with active neutrophils. The skin cells worked hard and could produce some cathelicidin on their own, but didn’t have the killing power of the skin cells plus neutrophils. The article’s conclusion said that life-threatening necrotizing skin and soft-tissue infections can develop in patients with depressed neutrophils, but that numerous examples exist of patients with increased frequency of skin infections who have no

“demonstrable defect 7 in leukocyte recruitment or function.”

Properly fed, healthy children, whose parents know what to do, and what not to do, will rarely get any complications to chickenpox. As was the case for our children, well-managed chickenpox should not even lead to any scarring. So let’s ask some questions here, with chickenpox in mind. What is the function of fever?

Here’s a really simple statement11 from twenty years ago: “… elevated body temperature enhances the infl ammatory response and function of the immune system at the same time that it reduces the replication of microbes and tumor cells.”





Not so simple is this sentence.


“Fever also appears to be a prominent component of cytokine therapy and attends the use of several biologic response modifiers.”

Fever switches on the chemical messengers and processes which call on the body immune system to respond and “modify” or deal with the infection.

If fever is a key to an immune-system process, without a fever, how effective is the body going to be in fi ghting viruses, or bacteria? With viruses like chickenpox, which are known to have an affinity with


group A streptococcus,

which can infect the pox rash and so have access to the body, what do we want the immune system to do? It’s pretty obvious isn’t it?




to allow the body temperature to rise to the level it needs so that all the on-switches can be thrown.




the body to send out all those little chemical messengers which get the antiviral side of things going.



want the messengers to call the neutrophils to join the skin cells in producing cathelicidin, and to work with the whole array of anti-viral and antibacterial components12 in “sweat” to stop group A streptococcus

in its tracks.

As a 1991 article13 says: “… temperature elevation … enhances the processes involved in initial antigen recognition and support for immunological specifi c response to challenge.

We want the body to recognize the virus, ring the bell and sound the red alert (fever) to fight, don’t we? Why, then, turn the fever off with acetaminophen products? Doesn’t that defy logic?

Another article14 of that era said: “There is considerable in-vitro evidence that a variety of human immunological defences function better at febrile temperatures than at normal ones … Studies have clearly shown that fever helps laboratory animals to survive an infection whereas antipyresis15 increases mortality.”

A 1998 article16 said: “The elevation of body temperature by a few degrees may improve the efficiency of macrophages in killing invading bacteria, whereas it impairs the replication of many microorganisms, giving the immune system an adaptive advantage. There is a simultaneous switch from the burning of glucose, an excellent substrate for bacterial growth, to metabolism based on proteolysis and lipolysis. The host organism is anorectic (doesn’t want to eat) minimizing the availability of glucose, and somnolent, reducing the demand by muscles for energy substrate. During the febrile response, the liver produced proteins known as acute phase reactants … the net effect … is to give the host organism an adaptive advantage over the invader.” (Underlining mine.)

Treating fevers is dicing with more severe infection, and a greater likelihood of death, because fever is a key immune response to get the immune system working properly.

You mess with fever, and you mess with lots of things. It stands to reason. Do you need to know what the medical profession does not yet know about fever in its totality, to see that?


Back to chickenpox. Tucked away in a small co


rner of the New Zealand Herald in 2001 was a warning:17 “GPs warned over chickenpox drug.” Doctors were warned about treating chickenpox with ibuprofen to reduce fever because of a higher rate of necrotizing fasciitis18. There was no mention of paracetamol in the warning, yet, since both perform the same function, there is reason to argue that paracetamol might do the same as ibuprofen. In USA, the link between the use of non-steroidal anti-infl ammatories and chickenpox reached the ears of doctors,19,20

but not, it seems, the public.

There was a flurry of articles suggesting it was dangerous to use anti-febrile drugs with chickenpox; there was also an article by a group of doctors, who in defiance of all logic and known immunological impacts of drugs used to reduce fever, decided that there was no association. They



decreed that when parents used drugs to “treat high fever and severe illness”, drug use was merely the identifying factor of who was at high risk for secondary bacterial infection! That interesting little word “coincidental” again.

… I see the increase in these infections as evidence of a total lack of common sense about how to prevent complications. I see the association between nonsteroidal anti-febrile drugs and GAS as a predictable outcome of the loss of home nursing skills and handed-down generational wisdom. I see the increase in secondary bacterial infections as something which can stem from parental lack of understanding that messing around with fever, and using symptom-suppressing/immune-suppressing drugs can restrict the ability of the immune system to fi ght the virus. It also reduces the ability of the leucocyte system of neutrophils, macrophages and phagocytes to fight bacterial toxins from secondary bacterial infections.

As pointed out in Chapter 70, if you don’t have enough vitamin C in your system, then the neutrophils won’t be recognized by the macrophages, and you might be in big trouble, because if that happens, the result could be toxic shock/sepsis taking hold very quickly. Even if you have enough vitamin C, if the amount of GAS toxin is such that the glucose transporters (which are part of the vitamin C shuttle service which takes ascorbate from A to B) are blocked, that can result in a GAS infection which threatens to run out of control. The quickest way to restore the immune function in a case of sepsis is by giving vitamin C intravenously. The body can fight sepsis by itself, but it’s a bit more of a lottery as to whether it will succeed if it doesn’t have the tools to do the job.

BOOK: From One Prick to Another


Chicken Pox cases in older children

Officials: Update chicken pox vaccine

Health officials are stumped as to why an outbreak of chickenpox has sickened more than 40 students at Spruce Creek High School — but they are taking steps to contain it, urging all parents to update their children’s vaccines.

The outbreak has affected just 1.5 percent of the school’s 2,700 students, but it’s been serious enough to warrant the Volusia County Health Department’s involvement as it’s become more serious since the first case was reported in September.

After 30 cases were reported this month, a third automated call went out to the homes of all Spruce Creek High School students Thursday night warning families to keep at home children who are showing signs of the illness that causes blistering and fever.

Today, parents will receive a letter detailing steps to take to ensure children are fully vaccinated.

The puzzling part for officials is that the chickenpox vaccine has been required for entering Volusia County schools since 1995 — about the time today’s high school students started school. Dr. Sanford Zelnick, the Health Department’s medical director, said he believes it’s a result of how the varicella virus that causes chickenpox is evolving.

“It’s hard to postulate why this cluster began,” Zelnick said, pointing out that the Centers for Disease Control began recommending in 2007 that children receive a booster chickenpox vaccine after their initial one. “What I can tell you is that other communities in the United States have noticed this gradual shift of varicella (chickenpox) moving into later childhood.”

The disease kills about 100 people a year, Zelnick said, but most of the time it just puts someone out of commission for four to seven days, causing a rash and a fever.

According to the Centers for Disease Control, one dose of the vaccine is about 80 to 85 percent effective. Following the CDC recommendation of a second dose in 2007, the Volusia County school district required the second dose for entrance into pre-kindergarten through sixth grade starting this year, said Nancy Wait, school spokeswoman.

Pediatrician Andrea Thorpe, who practices in Daytona Beach, said she recently had an 11-year-old patient who came down with chickenpox in spite of receiving his vaccination in 2001.

“He had a 104 fever, itching all over, covered (with the rash) from head to toe,” she said. “When you’re older and you get it, you get it bad. It’s miserable.”


See Trading Places

Herpes Zoster with Skin Lesions and Meningitis Caused by 2 Different Genotypes of the Oka Varicella-Zoster Virus Vaccine

Herpes Zoster with Skin Lesions and Meningitis Caused by 2 Different Genotypes of the Oka Varicella-Zoster Virus Vaccine


A previously healthy boy who had received varicella vaccine developed herpes zoster with meningitis. The vaccine strain recovered from scabs of 3 skin lesions had the wild-type allele at position 108111, a vaccine marker never previously associated with vaccine-associated adverse events. The vaccine strain from cerebrospinal fluid also contained mutations never previously observed at vaccine-associated single nucleotide polymorphisms that would alter amino acid sequences in ORF54 and ORF59. The presence of distinct strains in skin lesions and cerebrospinal fluid indicate that >1 variant strain may reactivate to cause herpes zoster.

The Journal of Infectious Diseases 2008;198:1444–1447

Chickenpox Vaccination Leads To More Shingles

New study UK: Chickepox Vaccine Leads to More Shingles

New modelling research presented at the Health Protection Agency’s annual conference in Warwick confirms that vaccination against chickenpox would significantly decrease the burden of this disease but would lead to more shingles among the elderly.

Researchers also found that vaccinating the elderly against shingles would only partially, but not completely, offset this increase.

Post-vaccination research from countries that routinely immunise their children against chickenpox, including the US, has found an increase in cases of shingles among non-vaccinated age groups.

The Health Protection Agency researchers modelled the impact of vaccinating children against chickenpox (with a two dose schedule) and the elderly (60+) against shingles.

Building on previous modelling data the team incorporated virological, epidemiological and recent data on age-specific contact patterns to see whether a vaccine for the young would impact on the number of shingles in the elderly.

The modelling suggested that a two dose schedule at the levels of coverage likely to be achieved in the UK would lead to an increase of at least 20% of shingles in the medium term (approximately 15-20 years). This increase could be partially, but not completely, offset by introduction of a vaccination against shingles among those aged 60+.

Albert Jan van Hoek, who performed the research for the Health Protection Agency, said; “Our models suggest that vaccination would reduce the burden of chickenpox in the young. However, it will lead to an increase in shingles in the medium term in adults because they will not get that ‘boosting’ effect from being in contact with cases of chickenpox.

“We also looked at whether vaccinating adults against shingles would be of benefit to counteract this. The research showed that a potential increase in shingles could be partly offset by vaccinating the elderly. The success of this, however, depends on uncertain vaccine efficacy parameters, particularly the duration of protection from the zoster virus.

“There are still uncertainties in the research and a lot more work needs to be done examining whether vaccination will be a benefit to all of the population. Also further work needs to be done on the cost effectiveness of any potential chickenpox vaccine before any policy conclusions can be reached.”

Chickenpox Parties

Tell me again what’s so wrong about chickenpox parties? 

Well if you read this…apparently plenty. But I still don’t agree.

Before a vaccine was recommended for all children, it was considered a  beneficial and benign disease. After the vaccine was recommended for all children, it was suddenly a serious and deathly disease. Funny how that works!

I had Chickenpox as a child. I was 6 years old and had it at the same time as my 3 siblings. I remember my Mom was thrilled we all had it at once to ‘get it over with.’

Two of my older children had chickenpox before a vaccine was ever recommended. They were exposed through a school-age child I was babysitting. I too was thrilled! They would have chickenpox before the start of school and be done with it. Several of my neighbors, along with other daycare children, came over to expose their children-we had a pox party!

Now I won’t say chickenpox is exactly fun. The kids had a pretty good case and were cranky, whiny, sickly, itchy and they looked like hell…everything you would expect them to be when they don’t ‘feel good’. But it wasn’t horrible either. My daughter would say it was but only because she’s a girl, and had them in private places, and well let’s face it, that’s not a place you want to have a constant itch:( The first 3-4 days were the hardest and then it got better from there.  For me, I got natural boosting, and more importantly them, a week of sickness sure outweighed a vaccine any day. We simply didn’t have to worry about it any was done and over with, unlike the vaccine. Unfortunately, I still have two younger school-age kids who haven’t gotten it…yet. Now that school is back in session, and other children are out getting their vaccine that sheds( for 6 weeks) to others, I’m confident it’ll knock on our doorstep soon!


By the way-We did the usual treatments minus today’s repetitive Tylenol use which is given for everything that ails you. Speaking of which, the only children who had more severe problems getting over it that were exposed when my children were, were given Tylenol repeatedly and other drugs. Their Mother was a nurse to boot.

Chicken Pox/Shingles/The Vaccines

Chickenpox is caused by the Varicella-Zoster virus. It is spread either by droplet infection or contact with the spots of a person with chicken pox. The incubation period is 2 – 3 weeks. During this time the virus replicates in the lymph nodes, liver, spleen, and a second viraemia occurs just before the rash appears. The infectious period starts one day before the rash appears and continues until the pox spots scab over.

Before the rash appears, the person may have a slight temperature, no appetite, feel tired, and have photophobia. The rash typically appears on the body and then spreads to the arms, legs, face and scalp. The rash can occur in the mouth. In girls, the rash can occur in the vagina area and cause discomfort. The rash is pimple-like at first, but turns into blisters. After a few days, they scab over. The scabs will then fall off, and should leave little or no scarring.

Complications which are rare could be:

Pneumonia – usual cause in adults is Staphylococcus Aureas

Bacterial super infection and encephalitis (rare in children)

Reye’s syndrome, mainly associated with the use of aspirin to control fever and pain

 Otitis media

 More Severe Rare Complications:

 Osteomyelitis, necrotising fasciitis, toxic shock syndrome, Guillain-Barré Syndrome, carditis, uveitis, myocarditis, bullous varicella, septic arthritis, deep tissue abscess, Group A beta-haemolytic streptococcus, nephritis, orchitis, thrombocytopenia, fulminant hepatitis, acute cerebellar ataxia, chorioretinitis, ocular defects, cutaneous scars, hypoplastic limbs, micrognathia, encephalomyelitis, cortical atrophy, and pneumonitis.




After you have had chickenpox, the virus can lay dormant for decades until the immune system is suppressed, and then the virus can re-appear. It can reappear as chicken-pox again or as shingles. Shingles appears as large blisters, like welts, on one side of the body. They can appear on the stomach, back, chest, or even on one side of the face. Shingles can be accompanied by photophobia (sensitivity to light), tiredness, and severe itchiness or sting-like pain. 


 Chickenpox Vaccine-Varicella

The vaccine was originally developed for immune compromised leukemic children. The live varicella zoster vaccine for chicken pox had difficulty getting FDA approval for many years because of its high failure rate which was often as high as 20 percent. The varicella vaccine was licensed by the FDA in 1995, and Universal Varicella Vaccination Program was implemented shortly thereafter.  The CDC recommended that all healthy, susceptible children aged 12 months to 12 years receive a single dose. The CDC then funded a Varicella Active Surveillance Project (VASP) to monitor trends in the disease. The three different areas were: Antelope Valley (California), West Philadelphia (Pennsylvania), and Travis County (Texas). By 1999, each VASP reporting incidence of varicella had shown dramatic decline in their studied communities. Currently, nearly all states have mandated varicella vaccination for school entry.


Varivax (chickenpox) Package Insert

Proquad (chickenpox, measles, mumps, rubella) Package Insert 

Zostavax (Shingles) Package Insert



“…VARIVAX is a preparation of the Oka/Merck strain of live, attenuated varicella virus. The virus was initially obtained from a child with natural varicella, then introduced into human embryonic lung cell cultures adapted to and propagated in embryonic guinea pig cell cultures, and finally propagated in human diploid cell cultures (WI 38). Further passage of the virus for varicella vaccine was performed at Merck Research Laboratories in human diploid cell cultures (MRC-5) that were free of adventitious agents…”


“…Each 0.5 ml dose contains the following: a minimum of 1350 PFU (plaque forming units) of Oka/Merck varicella virus when reconstituted; approximately 25 mg of sucrose; 12.5 mg hydrolysed gelatine; 3.2 mg sodium chloride; 0.5 mg monosodium L-glutamate; 0.45 mg of sodium phosphate dibasic; 0.08 mg of potassium phosphate monobasic; 0.08 mg of potassium chloride; residual components of MRC-5 cells including DNA and protein; and trace quantities of sodium phosphate monobasic; EDTA; neomycin, and fetal bovine serum. The product contains no preservative…”

 Translation:   The culture medium is human embryonic lung cells, from an aborted fetus, embryonic guinea pig cell cultures, WI 38 which is a different cell line from another aborted fetus, and another aborted fetus labeled MRC-5.


 “…The nearly 2 m g of unmodified mammalian DNA in each dose of Varivax exceeds that present in any other approved childhood vaccine…” Other vaccines also contain unmodified DNA, but chickenpox contains more than the others.


A medical study was done to see if any of the 293 people vaccinated with Varivax developed anti-DNA antibodies from residual fetal tissue/DNA in the vaccine. The study stated that there were no significant changes in anti-DNA antibody, or the frequency of elevated anti-DNA titers. However, if these people have had other vaccines, which already contain human DNA, and they already have anti-DNA antibodies, exactly what does the ‘significance’ mean?   Another possibility considered was that the human DNA present in Varivax might integrate into and transform the vaccinated person’s cells. A Human Rights Committee on karyolitic controls of human substrates proposed limits for chromosomal abnormalities in human diploid cell lines used to manufacture biologic products. These guidelines have become:


“…generally accepted upper limits for chromosomal abnormalities. A clonal 7; 12 chromosomal translocation in the MRC-5 cells used to produce some lots of Varivax exceeded these limits for structural abnormalities. To evaluate the theoretical concerns raised by this observation Merck undertook a comprehensive assessment of MRC-5 (aborted fetal) cells to document that they were not tumorigenic. MRC-5 cells from the cell banks used to produce vaccine did not produce tumors when injected into nude mice, reached senescence normally, and did not exhibit a malignant phenotype. Cells bearing the 7; 12 translocation did not proliferate preferentially during the lifetime of the cell line in comparison with MRC-5 cells lacking the translocation. No human disease associated with abnormalities involving a 7; 12 translocation has been reported. Outside experts concurred with the FDA’s assessment that the risk of MRC-5 DNA’s inducing a malignant transformation in vaccinees under the condition of vaccination was exceedingly low…” (J Pediatrics 1995; 127:518-25)



This information will simply ‘prove’ to doctors that the vaccine is safe, but far from reassuring or proven. Varivax contains 2 mg of WI 38 and MRC-5 which are two aborted fetuses. The chromosomal abnormalities in this cell line exceed the currently accepted upper limits. Merck assumed a comprehensive assessment to document that they were not oncogenic. Also stated:


“…Detectable infectious agents were not present in the material used to produce Varivax, nor were they introduced during the manufacturing process…”


The key word is “detectable”. You can only find what you have a test to identify and what you are looking for. Fetal bovine serum, including batches previously passed by the FDA and WHO, has been documented to be contaminated with several different viruses in the past.  New viruses every year come out, and new tests have to be made to test for them. There is no guarantee that these vaccines do not contain something that is unable to be detected, but advanced testing might show it in the future. So the answer for manufacturers is to protect themselves with the word ‘detectable’. This way they can only be held liable in the future for those things which were able to be identified at the date of manufacture.



Testing and Safety of Varivax Vaccine:


“Pregnancy: the possible effects of the vaccine on fetal development are unknown at this time. However, natural varicella is known to sometimes cause fetal harm… the duration of protection is unknown … vaccination should be deferred for at least 5 months following blood or plasma transfusions, immune globulin or varicella zoster immune globulin … vaccine recipients should avoid use of salicylates for 6 weeks after vaccination as Reye’s syndrome has been reported following the use of salicylates during natural varicella infection … Varivax should be deferred in patients with a family history of congenital or hereditary immunodeficiency until the patient’s own immune system has been evaluated … post- marketing experience suggests that transmission of vaccine virus may occur rarely between healthy vaccinees who develop a varicella- like rash and healthy susceptible contacts…” (Merck, Sharpe &Dohme, 1999)


Varivax has not been evaluated for its carcinogenic or mutagenic potential or its potential to impair fertility. It is not known whether varicella vaccine virus is secreted in human milk. No clinical data are available on safety or efficacy of Varivax in children less than one year of age, and administration to infants under 12 months of age is not recommended.


Multiple trials and post licensing studies and testing of vaccinees in the U.S. were conducted in communities where natural, or wild type, varicella incidence was still high. Estimates of the vaccine effectiveness, and the duration of immunity were overestimated and distorted because of the immunologic boosting alluded to by Merck. When natural varicella remains high in the community, it boosts immunity in vaccinees that received a single dose and there were no adverse effects on the closely related herpes-zoster epidemiology. (Seward et al.2004) 

For more in depth information: Medical Veritas   


In 2007, the CDC published an article in the New England Journal of Medicine that stated Merck’s VARIVAX vaccine has a high failure rate and mass vaccination of children has caused the disease to occur in older age groups. Now the CDC states children between 4 and 6 years old need a booster dose and a third booster may be needed for teenagers.

In 2000, the FDA reported that during the first three years of the vaccine’s use, 1 in 33,000 doses was followed by shock, convulsions, encephalitis, thrombocytopenia or death. Roughly 82 percent of the adverse event reports to VAERS occurred in those who only received the chicken pox vaccine. This led to the addition of 17 adverse events to the Merck product label which  include secondary bacterial infections or cellulitis; secondary transmission, transverse myelitis; GBS, and herpes zoster. In 2000, VAERS received reports of brain inflammation, convulsions, vaccine strain chicken pox, shingles, regressive autism and other serious health problems following injection of Varivax, or in combination with MMR, DTaP, influenza, pneumococcal and/or other vaccines.
Even if chickenpox was nearly eradicated by vaccination, the higher number of shingles cases could continue in the US for up to 50 years.



In 2006, the FDA approved Merck’s shingles vaccine, ZOSTAVAX, for adults 60 years and older who have had chickenpox previously. The ACIP soon afterwards recommended it for all adults over 60 regardless of whether they had chickenpox previously or not. ZOSTAVAX is similar to Merck’s Varivax but is 14 times more potent.

“The principal reason that chicken pox vaccines in Japan maintained high levels of immunity 20 years following vaccination was that only 1 in 5 Japanese children were voluntarily vaccinated. Those vaccinated received immunologic boosting from contact with children with natural chickenpox. But the mandatory vaccination program in the U.S. will nearly eradicate this natural boosting mechanism and leave our population vulnerable to shingles.”





Vaccines provide temporary, qualitatively inferior immunity compared to immunity achieved after natural recovery from disease. And just as mass antibiotic use has put pressure on organisms to evolve into antibiotic resistant forms, mass vaccine use can put pressure on organisms to mutate into vaccine resistant forms.

The Shingles Vaccine

 With the increasing use of Varicella vaccine, HZ incidence among adults increased 90%, from 2.77/1000 to 5.25/1000 in the period 1998 to 2003. (Yih et al. 2005).


 The Varicella Active Surveillance Project conducting active surveillance of HZ in the Antelope Valley region of California since 2000 found that Zoster cases among adults aged 20 years and older increased 18% from 237 cases in 2000 to 279 in 2001 with increases in nearly every 10-year age group from 20–29 through 60–69.  Young adults from the pre-vaccine era, experienced the greatest percentage increase in cases.


 Vaccination of adults has seldom been successful and adults tend to experience a higher rate of adverse effects versus children. Varicella vaccination is considered safe but there are no prescreening tests to determine whether an adverse reaction is likely to occur (Poser 2003). The medical literature contains a number of adverse reactions following varicella vaccination.


 The Oxman et al. 2005 study looked at adverse effects in one-sixth of the subjects during 42 days following vaccination. Kaufman states:


“Extrapolating the results to 19,273 subjects in the whole treatment group, this group had 132 more cases (0.7%) of one or more serious adverse events and 4,677 more cases (24%) of one or more adverse events than the placebo group.”


There is evidence already that Zostavax can induce autoimmunity or worsen a pre-existing autoimmune disorder and raise the risk of heart disease conditions.


 An FDA review of the Zostavax clinical data concluded that the vaccine was effective at reducing shingles pain but did not significantly reduce shingles related hospitalizations or death. In the Shingles Prevention Study, which enrolled 38,546 patients, the vaccine reduced the rate of shingles in persons 60 or older by half, and reduced the rate of postherpetic neuralgia by 66.5%. Those results were reported in the New England Journal of Medicine. The 5 and ½ year-trial randomized 19,270 patients to the active vaccine. The vaccine reduced the burden of illness due to herpes zoster by 61%, reduced the rate of postherpetic neuralgia by 66.5%, and reduced the rate of herpes zoster by 51.3%.
An Adverse Events Monitoring Study (AEMS) was conducted to look at safety. In this smaller study, serious adverse events for all age groups were noted in 1.9% of Zostavax patients, versus 1.3% of patients receiving placebo in the 42 days following vaccination. In the entire study population, the rates of overall cardiovascular events (0.4%) including coronary artery disease related conditions (0.2%) were similar in those vaccinated with Zostavax or placebo. In the AEMS substudy, during the first 42 days after vaccination, the rate of overall cardiovascular events was higher after 0.6% after Zostavax versus 0.4% after placebo. The rate of coronary artery disease-related conditions was slightly higher in Zostavax arm (0.3% versus 0.2%).


The U.S. Universal Varicella Vaccination Program and its cost-benefit analysis is no longer valid because most communities with widespread varicella vaccine coverage are still getting chicken pox. A single dose was touted as providing lifelong immunity when it does not. There is an immunologically-mediated link between varicella incidence and HZ incidence and the vaccine is not safe. See Vaers reports.


 Primary Vaccine Failure after 1 Dose of Varicella Vaccine in Healthy Children
The Journal of Infectious Diseases 2008; 197:944–949

Universal immunization of young children with 1 dose of varicella vaccine was recommended in the United States in 1995, and it has significantly decreased the incidence of chickenpox. Outbreaks of varicella, however, are reported among vaccinated children. Although vaccine effectiveness has usually been 85%, rates as low as 44% have been observed. Whether this is from primary or secondary vaccine failure—or both—is unclear. We tested serum samples from 148 healthy children immunized against varicella in New York, Tennessee, and California to determine their seroconversion rates, before and after 1 dose of Merck/Oka varicella vaccine. The median age at vaccination was 12.5 months; postvaccination serum samples were obtained on average 4 months later. Serum was tested for antibodies against varicella-zoster virus (VZV) by use of the previously validated sensitive and specific fluorescent antibody to membrane antigen (FAMA) assay. Of 148 healthy child vaccinees, 113 (76%) seroconverted, and 24% had no detectable VZV FAMA antibodies. Our data contrast with reported seroconversion rates of 86%–96% by other VZV antibody tests and suggest that many cases of varicella in immunized children are due to primary vaccine failure. A second dose of varicella vaccine is expected to increase seroconversion rates and vaccine effectiveness.


Second Dose of Varicella Vaccine for Children: Are We Giving It Too Late?

The Journal of Infectious Diseases 2008; 197:944–949

A large case-control study indicated that the vaccine’s overall effectiveness up to 8 years after immunization was 87% [7]. Thus, although the vaccination program certainly was effective, “breakthrough” varicella (varicella in persons who had previously received varicella vaccine) occurred with some frequency. Since most breakthrough disease is mild, why does this matter? In the first place, children with breakthrough disease are able to transmit the virus to others, which has resulted in numerous disruptive outbreaks of varicella in day-care centers and in schools despite high rates of immunization at many of these sites [89]. Moreover, approximately one-third of children with breakthrough varicella have moderate or severe disease, and there has been at least one death in an immunized child. In addition, those who have had breakthrough varicella may be at higher risk of subsequently developing zoster than are immunized persons.

In June 2006, the Advisory Committee on Immunization Practices recommended that a second dose of varicella vaccine be administered routinely to children [24]. Although the vaccine can be given as soon as 3 months after the first dose, it is recommended that it be administered between 4 and 6 years of age. This is largely because a combined measles-mumps-rubella-varicella (MMR-V) vaccine was approved in October, 2005 [25, 26]. As a result, both the first and second doses of varicella vaccine are easily given at the same time as MMR vaccine via this combined vaccine at 12–15 months and 4–6 years of age, respectively. This allows the second dose of the vaccine to be administered without requiring an additional injection in the already crowded schedule for childhood immunizations. However, if the substantial number of cases of breakthrough varicella is due to primary, rather than secondary, vaccine failure, this timing for the second dose risks leaving a substantial number of children susceptible for several years until they receive the second dose and may diminish its impact on the epidemiology of the disease.

To further complicate matters, the amount of varicella virus in monovalent varicella vaccine and in MMR-V vaccine differs substantially, because varicella vaccine is less immunogenic when combined with MMR vaccine in the same preparation. Monovalent varicella vaccine contains a minimum of 1350 pfu per dose, whereas MMR-V vaccine contains a minimum of 9700 pfu of varicella vaccine per dose (according to the package insert labeling) [27]. The few data available have indicated that, after 2 doses of monovalent vaccine, titers of antibody to VZV, as measured by gpELISA, increase by a factor of 12 but that, after 2 doses of MMR-V vaccine, titers may increase up to 40-fold [16, 28, 29]. However, immunogenicity of MMR-V vaccine has not been assessed using the clinically validated FAMA assay. Moreover, because of problems with production at Merck [30], MMR-V vaccine is either not available at this time or is in short supply, and most children are receiving monovalent vaccine. There is uncertainty about if and when MMR-V vaccine will again become available.





Chicken Pox/Shingles Treatment

  •  Vitamins A and C are the vitamin treatment of choice. Chickenpox can require large doses, but Shingles requires much larger doses. Selenium and Zinc are also beneficial.
  • Avoid sugar and undiluted fruit juices.



  •  Mint tea made with lemon balm or other mints may be beneficial: hyssop, oregano, peppermint, rosemary, sage, self-heal, spearmint or thyme. These are antiviral, anti-herpetic compounds. If there are spots in the throat, you can add licorice root. You could mix it with pear juice which is rich in antiviral caffeic acid.
  • Keep the skin clean and cool with frequent baths using 1 cup baking soda or 5 drops lavender essential oil in the bath water. Rubbing the juice from the fresh stems of aloe vera can also help the itching. Cider vinegar neat, used as compresses, changes the skin PH and when held against the pox spots can kill surface virus particularly where the blister is broken. No pox virus can survive a ph of 3.
  • An oil mix, for adults, is bergamot, chamomile, eucalyptus, geranium, lavender, lemon and tea tree oil… as above, or dilute them by adding 5 drops each to a couple of tablespoons of vegetable oil and apply them directly to rash if painful.
  • Epsom salts baths with oat straw/oatmeal-one cup per bath in a bag, hung under the hot water tap, and then float it, for children who are tense and itchy.
  • Echinacea and goldenseal combination helps prevent bacterial infections of the sores. So can Calendula (1 tsp tincture – 4 tsp water)
  • For severe, Lysine (an essential amino acid) inhibits replication of both chickenpox and shingles. Use 2,000 mg a day as a supplement (or smaller doses in children). Lysine works by blocking the virus’s ability to absorb arginine.
  • For pain in both children and adults, often the person is vitamin B deficient. For shingles in older adults, if nerve pain is severe B12 injections along with some of the others orally can relieve the pain, and shorten the course of illness.
  • If a bacterial infection looks like its setting in, a capsule of Transfer Factor may help. Breast milk, if available, may do the same.
  • Shingles is triggered by stress, and stress pulls out huge amounts of B-vitamins from the body. People with shingles need B supplementation.
  • For both chickenpox and shingles in adults, Hydrogen Peroxide gel, every 2 – 3 hours helps dry and heal blisters.
  • Alpha Lipoic acid is another some doctors prescribe for shingles in adults. It’s an antioxidant, and helps keep the scarring of both chickenpox and shingles to a minimum. It may affect blood sugar levels, so use with care with diabetics.
  • Pharmaceutical treatment for shingles is dependent upon symptom alleviation using drugs like prednisone and acyclovir.


CHICKEN POX: Why Do Children Die?


Age of Autism-Proquad Series:

Part 1    Part 2      Part 3      Part 4   Part 5     Part 6     Part 7