In the November issue of my Insiders’ Cures newsletter, I pointed out some disturbing findings about the chickenpox vaccine. Of 31 patients transplanted during 2012 in our center, 6 (19.3%) experienced varicella zoster virus (VZV) reactivation. Nine cases of zoster were observed among children who had acquired varicella during the first year of life, but there was no case of zoster in those who had acquired varicella after 1 year of age. Also known clinically as varicella-zoster virus (VZV), chicken pox is a relatively mild form of herpes virus that typically manifests itself during the early childhood years. Goldman’s findings have corroborated other independent researchers who estimate that if chickenpox were to be nearly eradicated by vaccination, the higher number of shingles cases could continue in the U.S. There are about 10,000 Juang in total. back in 1995, could damage this natural immune cycle.
Pharmacological effects 1, Ribavirin can be subject to phosphorylation in red blood cells to generate ribavirin monophosphate, diphosphate and triphosphate, wherein the ribavirin monophosphate is the strong inhibitor of the inosine monophosphate dehydrogenase which can inhibit cellular guanylate synthesis, decrease the tri-phosphorylation of the intracellular guanylate triphosphate, and blocking the synthesis of viral nucleic acid. They then develop into thin-walled blisters that are filled with clear fluid which collapse on puncture. These are known as asymptomatic cases. Triple concurrent infection caused 05% complications but no death was reported. But what this bloated bureaucracy is failing to disclose publicly is the fact that the sudden uptick in shingles cases is directly associated with the advent of the chicken pox vaccine. People who were vaccinated for chicken pox as children beginning in the 1990s are now eclipsing into adulthood. An article in this Issue describes the problem in urban Zimbabwe.
For decades it was thought shingles increased with age as older individuals’ immune systems declined. (After all, this happens with other forms of herpes viruses, which may lie dormant for years until the immune system is unable to keep them in check). Prospects for prevention worldwide and in the UK are problematic. However, his symptoms were worsening even on medication, so orbital cellulitis was suspected and he was referred to our clinic. The factors promoting sporadic and recurrent AHC epidemics are unknown but likely include unrestricted travel,5,31 antigenic/genetic divergence of AHC viruses,32–34 subclinical infection,35,36 and the absence or waning of population immunity.3,37–39 An additional confounding factor is the low frequency of seroconversion (15%–60%) reported in many AHC epidemics, suggesting that the ocular infection may not provide protection.3,37–41 The weak systemic immune response to AHC is likely due to the highly localized nature of the infection to the eye (mucosal epithelium) and rapid viral reduction, but hyporesponsiveness or local antibody production exclusively has not been ruled out.42,43 Para doxically, it has been reported that high pre-epidemic serum antibody titers provide sex-specific protection against EV70 AHC.44 Generally, subclinical infection is monitored between epidemics by detection of AHC virus and/or seropositive individuals, while the population’s relative susceptibility to an AHC epidemic is predicated upon the absence of, or decline in, serum antibody to the AHC viruses.3,32,33,37–41,44–46 The persistence of antibody to AHC viruses in tear postinfection is unknown. Goldman’s findings were, indeed, correct.