Chickenpox Vaccine May Increase Shingles Risk
- Following recovery from varicella zoster (chickenpox) virus infection, the virus lies dormant and occasionally reactivates as herpes zoster (shingles) later in life.
- When the live virus chickenpox vaccine was licensed in 1995, it was known that an increase in the incidence of shingles was likely if the vaccine was mandated and children obtained artificial vaccine immunity rather than natural immunity.
- The predicted increase in shingles incidence has been verified, and future research may more fully explain if and why natural “exogenous boosting” prevents reactivation of the chickenpox virus as shingles.
When the vaccine was licensed 20 years ago, there were about 50 to 100 deaths related to chickenpox complications reported in the U.S. every year, mostly among the immune compromised, with roughly half being children and half being adults.1 In this post-vaccination era, public health officials present chickenpox as a very serious disease with frequent complications, albeit one that they say has been almost eliminated and rendered harmless thanks to a successful mass vaccination program.
Rarely talked about is the fact that the protective effects of vaccine acquired artificial immunity do not last as long as naturally acquired immunity following recovery from the natural disease. After the CDC recommendation in 1995 that all children get one dose of chickenpox vaccine at between 12 and 15 months old failed to prevent varicella zoster virus from circulating, the CDC added a booster dose of the vaccine in 2007 for children four to six years old.2
Chickenpox in adulthood is associated with a much higher rate of pneumonia and other complications, such as brain inflammation, than when it is experienced as a mild disease by young children. Because the varicella zoster virus lies dormant in the body following recovery from chickenpox, there is another drawback to widespread vaccination: It may lead to an increase in the incidence of herpes zoster (shingles), a painful condition that occurs when the latent chickenpox virus becomes reactivated in later life.
Increase in Shingles Predicted from the BeginningBefore and after the licensing of the chickenpox vaccine, many researchers and consumer advocates predicted that reducing the childhood incidence of varicella zoster infections by vaccinating every child could have the unwelcome result of increasing the incidence and severity of herpes zoster infection (shingles).3
The concern was so widespread that many countries opted out of child mass vaccination campaigns to prevent chickenpox. The rationale behind the hesitation lies with the phenomenon known as “exogenous boosting,” meaning that exposure to children with active varicella zoster infection leads to a passive (asymptomatic) natural boosting of an individual’s chickenpox immunity and protects against later reactivation of the virus as herpes zoster (shingles).4
Numerous studies published within the first decade following introduction of the chickenpox vaccine have borne out the validity of the hypothesis, many of them outlined in a book by medical journalist Neil Z. Miller, Critical Vaccine Studies (New Atlantean Press, Santa Fe, NM, 2016). One study from 2002 looked at data from 244 patients and 485 controls and reported that re-exposure to varicella-zoster virus via contact with children offered as much as a 20 per cent reduction in risk for herpes zoster (shingles). These researchers warned that,
“Reduction of childhood varicella by vaccination might lead to increased incidence of adult zoster.”5Also in 2002, other researchers reported that exposure to the chickenpox virus experienced by adults living with children prior to the introduction of the vaccine was “highly protective against zoster (Incidence ratio=0.75, 95% CI, 0.63–0.89),” and they too predicted that “mass varicella vaccination [would be] expected to cause a major epidemic of herpes-zoster, affecting more than 50% of those aged 10–44 years at the introduction of vaccination.”6
A study was published in 2005 reporting that,
“Some studies suggest that re-exposure to [chickenpox] after primary infection may decrease the risk of herpes zoster through immunologic boosting. If this is the case, widespread use of varicella vaccine could, by reducing circulating [chickenpox], increase the incidence of herpes zoster over the first few decades of universal childhood vaccination.”7In 2013, a review of the U.S. varicella vaccine program was published in the medical journal, Vaccine, which revealed that having fewer opportunities for exposure to people infected with varicella zoster, who are shedding the wild-strain chickenpox virus has, in fact, significantly increased the risk for reactivation of the virus that causes shingles. The review’s authors said that this increase in morbidity “has disproportionately offset cost savings associated with reductions in varicella disease.” Their conclusion:
“Universal varicella vaccination has failed to provide long-term protection from VZV [shingles] disease.8Another examination of the evidence was published in 2013 and provided additional confirmation of the validity of the exogenous boosting hypothesis in a meticulous review of 40 studies that used a variety of study designs including mathematical models and observational, epidemiological, prospective longitudinal, and other types of designs.9 The researchers concluded that, while exogenous boosting does take place, further study is needed, with more well-defined parameters, to better clarify the true impact of immunologic boosting provided by exposure to chickenpox.
Predictions are Coming True, With Some SurprisesMost researchers agree that the incidence of shingles has increased dramatically over the years since the chickenpox vaccine was introduced, but disagree with each about the role played by the vaccine. Some allege that rates of shingles were beginning to increase before wide-scale vaccination. Admitting that an alternative explanation has yet to be determined, the strategy of public health officials in preventing shingles continues to focus on strongly encouraging every adult to get the live virus herpes zoster (shingles) vaccine.10
Although disagreements remain, the evidence is mounting that the increased incidence of shingles is directly related to the introduction of the chickenpox vaccine. No differences were seen in the first five years of the chickenpox vaccination campaign, but by 2001 the rate was clearly rising and by 2004, the rates of shingles were “significantly higher thanany of the rates calculated during the years prior to 2002,” and more than offset the decreased hospitalizations and hospital charges associated with the decline in chickenpox.11
A case report published in 2014 described a nine-year old boy, who developed shingles after receiving chickenpox vaccine. This highlights the potential for the development of vaccine strain varicella zoster infection that leads to shingles. Authors stated:
“The medical community should be aware that vaccination can lead to the occurrence of shingles in the same way that natural infection with wild-type varicella-zoster virus can.”12They added, “Vaccinated patients with subsequent zoster should be considered contagious.”
Not only does a recent research model predict that “implementing a varicella vaccination program for children would almost double the number of shingles cases 31 years later,” at least temporarily, it suggests that the increase will occur primarily in much younger people than is usual with shingles,13 which has traditionally been found mainly in older adults.14 The new research model also suggests that, while re-exposure to chickenpox it was originally believed to provide close to 20 years of protection against shingles, immunologic and virologic data indicate that the immunity boost may be much shorter, closer to two years.