March 20, 2008 by generic
Filed under: Vaccine/Disease Analysis
Look back to the time of the earliest humans and you’ll find chickenpox. Anywhere you go on the planet, you find human beings who carry and share the virus. No remote village or tribe on Earth has ever been discovered to be free of this virus. Quite an achievement! For the virus…
Scientists have studied small, isolated populations, trying to understand how the virus survives; it has a unique survival strategy we call “shingles”.
There are some viruses that need a large pool of humans for successful survival. Once everyone has had the disease, the virus will actually “die out” as a result of herd immunity. This is one reason why big cities have always been joyous playing grounds for disease. A never-ending supply of new bodies keeps flowing in, ready to catch whatever is currently going around. Put that same virus in a tiny and unchanging population on a remote island and the new bodies will quickly run out. Once everyone has been infected and become immune, the virus has nowhere to go and disease transmission is stopped. End of the road for that bug.
No end to chickenpox, though. It has an amazing method of ensuring that the next generation of humans will be infected. Here is an example of how it works: Amongst the isolated crofters of the Shetland Islands off the coast of Scotland in the early 1900′s, where the families lived far away from one another, the kids caught chickenpox, not from other children who caught it from other children, but from an adult with shingles. (1)
Most people on this planet had chickenpox as children, but not everyone comes down with shingles. Before the vaccine it was mainly an affliction of old age. Those who died before age 50 missed out, and even those who lived to be quite elderly had no more than a 50% chance of having shingles.
About half of the nearly 1 million Shingles cases in the United States each year occur in people aged 60 years and older. 1 out of 2 people living to age 85 will have Shingles.
Of these 1,000,000 cases, 40% to 50% occur in people 60 years of age and older.
Aside from folks who live a long time, who else is likely to succumb to shingles?
Let’s review some studies:
Pediatricians come down with shingles at one-half to one-eighth of the usual rate. (2) People with kids get less shingles. (3) If regular exposure to children with chickenpox prevents shingles, and varicella infection is found in every population on earth, then lack of exposure to children with chickenpox can logically be inferred to indirectly cause shingles. The mechanism is demonstrated here (4):
Resistance to reinfection with varicella-zoster virus (VZV) was evaluated in immune adults who had household exposure to varicella. Sixty-four percent of 25 adults exposed to varicella had a fourfold or greater rise in IgG antibody to VZV or had a high initial IgG antibody titer to VZV that declined by fourfold. IgM antibody was detected in only 12% of 25 VZV-immune subjects. Seventy percent of 23 subjects exposed to varicella had IgA antibody to VZV compared with 13% of 23 subjects with antibody to VZV who had no recent exposure (P less than 0.001, chi 2 test). Enhanced cellular immunity was documented by an increase in lymphocyte transformation to VZV antigen from a mean +/- SE index of 7.8 +/- 1.30 to 15.3 +/- 2.56 (P = 0.01, paired t-test). The increase in immunity to VZV in many immune subjects exposed to VZV suggests the occurrence of subclinical reinfection.
and here (5):
Whether reexposure of varicella-immune persons to varicella-zoster virus would protect against or predispose to development of zoster was analyzed. The rate of zoster in 511 leukemic recipients of varicella vaccine who had 1 or > 1 dose of varicella vaccine and in those who did or did not have a household exposure to varicella was determined. A Kaplan-Meier life-table analysis revealed that the incidence of zoster was lower in those given > 1 dose of vaccine (P < .05). A Cox proportional hazards analysis showed that both household exposure to varicella and receipt of > 1 dose of vaccine were highly protective (P < .01) against zoster. Thus, the risk of zoster is decreased by reexposure to varicella-zoster virus, either by vaccination or by close exposure to varicella.
So, someone had chickenpox as a child. They encounter a child with chickenpox. Their immunity to the virus is boosted. Later, when this same person’s immune system goes down a bit, from age or any other cause, and the virus attempts to come crawling out of latency and re-emerge as shingles, the virus fails. No shingles. There is another factor, described here (6):
Periodic episodes of subclinical reactivation of VZV from the ganglia occur through an individual’s lifetime, serving as immune boosters that increase the cell-mediated immune response to VZV… elderly adults have similar episodes of transient asymptomatic VZV viremia…. host factors are more important in determining whether the individual with a latent infection develops symptomatic VZV reactivation as HZ.
Host factors include overall health and immune function. We can hope that elderly people in vigorous health may be able to continue to avoid shingles even in the absence of circulating chickenpox, but the future is uncertain. Before the vaccine for chickenpox, 50% of the small group who lived 85 years or longer did so without experiencing zoster. This good fortune may or may not continue.
For a lot of us, however, lack of exposure to chickenpox, means waning immunity and the likelihood that the lurking chickenpox virus will reemerge as shingles. All adults over age (60) are recommended to receive Zostavax, a souped up version of the chickenpox vaccine, because the manufacturers hope it will mimic previous community exposure to chickenpox and put a stop to the growing incidence of shingles among adolescents, adults and older people.
Some questions spring to mind…
What has mass vaccination against chickenpox in children really done to shingles in adults? Is the emerging trend of dealing with shingles at an ever earlier age, a good tradeoff? Is a lifetime of vaccines to prevent this the true path to optimum health? The Brits are currently trying to decide this question–whether to add or not to add the varicella vaccine to their schedule. (7)
The group discussed published data from the USA. These studies indicate that mass childhood vaccination has reduced the incidence of varicella. The data are also consistent with modelling studies that have predicted an increase in zoster as a result of reduced virus prevalence and hence decreased opportunities for boosting of immunity to zoster by natural infection. In two studies where varicella rates were shown to decrease, there was also a significant increase in zoster post varicella vaccination.
The group noted, however, that the available USA data are not sufficiently robust to be able to estimate the full impact of vaccination.
This isn’t the end of the thrill ride we’re on with the chickenpox vaccine. No, the vaccine can actually cause shingles! (8)
Results. All of 57 vaccinees with breakthrough varicella, clinically diagnosed on the basis of a generalized maculopapular or vesicular rash, had wild-type VZV infection based on analysis of viral DNA. The Oka vaccine strain of VZV was not identified in any of these cases. In contrast, in 32 patients with zosteriform rashes, the vaccine strain was identified in 22 samples, and the wild-type strain was identified in 10 samples. Conclusions. Wild-type virus was identified in all generalized rashes occurring after the immediate 6-week postvaccination period. When reactivation of vaccine strain occurred, it presented as typical zoster.
Chickenpox vaccination can and does result in shingles outbreaks. And if anyone in the world has shingles they can infect another person with chickenpox. The shingles–chickenpox–shingles cycle guarantees that we will have to vaccinate everyone against chickenpox forever and ever or chickenpox will return. That sums up the benefits of the chickenpox vaccine and leaves us wondering, what unforeseen consequences might Zostavax (the shingles vaccine) have hidden under its belt?
The varicella virus has adapted over millions of years to re-emerge as shingles (herpes zoster) in elderly adults. Adding the vaccine into the equation seems to push shingles into younger age groups. Will we have repeated shingles throughout life? Will that mean repeated Zostavax boosters down through the years? One scientist thinks so and recommends this (6):
…the more effective the varicella vaccine is in reducing varicella, the more imperative is the need for an effective zoster vaccine as a means of boosting VZV-specific cell immunity responses…
…therefore health officials need to devise a cost-effective universal varicella vaccination program in coordination with a zoster booster vaccine intervention strategy that exceeds the level of natural boosting that occurred when wild-type varicella circulated in the community.
Hurrah! Two vaccines. Twice the cost. Twice the risk for adverse reactions. More than twice the risk because we will all need boosters. Start at one year of age with a chickenpox vaccine, boost it at school age, boost again at adolescence (not yet in the schedule, but I wouldn’t be surprised if it was added) and then start giving the zoster boosters to adults. The age of the zoster booster will have to go lower and lower of course, as shingles pops out in younger and younger age groups.
Do we have any say in the matter?
Is this listed on the “Vaccine Information Statement” we’re given to make sure we’re “informed vaccine consumers”?
(1) Varicella Zoster Virus: Out of Africa and into the Research Laboratory.
(2) Incidence of herpes zoster in pediatricians and history of reexposure to varicella-zoster virus in patients with herpes zoster.
(3) Exposure to varicella boosts immunity to herpes-zoster: Implications for mass vaccination against chickenpox.
(4) Immunologic evidence of reinfection with varicella-zoster virus.
(5) The protective effect of immunologic boosting against zoster: An analysis in leukemic children who were vaccinated against chickenpox.
(6) Herpes Zoster Ophthalmicus Natural History, Risk Factors, Clinical Presentation, and Morbidity Ophthalmology, Thomas J. Liesegang, Volume 115, Number 2, Supplement, February 2008.
(7) Joint Committee on Vaccination and Immunisation: Minutes of the Varicella / Herpes Zoster sub-group – 4 December 2007
(8) Viral strain identification in varicella vaccinees with disseminated rashes.