
By Lauren Adams, PhD student
In November, the Joint Committee for Vaccination and Immunisation (JCVI) announced that two doses of varicella vaccination are now recommended for all infants aged 12 and 18 months. The live attenuated varicella vaccine was developed in the 1970s and was consequently introduced to the standard immunisation programme including the United States in 1995. So, why has England only just made the recommendation? Why now? What has changed?
Varicella Zoster Virus (VZV) is a herpes virus that causes two distinct diseases, varicella (chickenpox) and herpes zoster (shingles). Chickenpox is the result of primary infection with VZV. Generally, clinical illness is mild but increases with severity with age. Adolescents and adults have a 10-20-fold higher rate of complications than infants. Severe complications can include bacterial infections of the skin and soft tissue, infections of the lungs (pneumonia) or swelling of the brain (encephalitis, cerebellar ataxia).
Following chickenpox the virus remains dormant in the body. Reactivation of the virus later in life is known as shingles. Reactivation only occurs in 15-25% of individuals and over 70% are in adults. However, shingles is associated with high rates of disease, severe complications (including long term pain, skin infections and muscle weakness) and a significant risk of fatality.
Although the extent is uncertain, it is known that shingles contributes to the force of infection of chickenpox. Furthermore, it has been theorised that exposure to varicella can temporarily boost a person’s immunity and prevent reactivation of the virus, in a process known as exogenous boosting. Therefore, the removal of naturally occurring chickenpox may cause an increase in shingles incidence. So it is essential to consider the dynamics of both diseases when planning a varicella vaccination programme.
Previous research used to inform on this topic has used a broad range of exogenous boosting duration. Consequently, the majority of the results showed a large increase in shingles incidence following vaccination. The increase in shingles outweighed the decrease in varicella and the programme was not likely to be cost effective.
Since this issue was last considered by the JCVI, universal shingles vaccination for those aged 70-80 has been introduced in the UK and new evidence on the quality of life lost as a consequence of varicella has been published. Additionally, after 20 years of varicella vaccination in the US the centre for disease control (CDC) has reported that varicella vaccination does not cause an increase in shingles incidence.
New modelling research has concluded that the protection from exogenous boosting is likely to last a maximum of 5 years, though this is significantly less than previous estimates. This was applied to a model of varicella vaccination in England with new estimates of quality of life loss due to chickenpox. It was found that the increase in costs and quality of life lost due to the increase in shingles cases was less then the costs and quality of life loss saved by the reduction in chickenpox cases. Therefore, the vaccination programme is cost effective.
This research has highlighted the importance of using data driven models, and the models use methods that show the most likely trajectory of a disease following an intervention. I believe further work needs to be conducted to ensure this happens in the future.