Vaccine efficacy

When a study is carried out using the most favorable, ideal or perfectly controlled conditions,[1] such as those in a clinical trial, the term vaccine efficacy is used.

It is best measured using double-blind, randomized, clinical controlled trials, such that it is studied under "best case scenarios.

[5][4] Because a clinical trial is based on people who are taking the vaccine and those who are not, there is a risk for disease, and optimal treatment is needed for those who become infected.

[4][failed verification] The major disadvantages of vaccine efficacy trials are the complexity and expense of performing them, especially for relatively uncommon infectious outcomes of diseases for which the sample size required is driven up to achieve clinically useful statistical power.

[4] Vaccine effectiveness estimates obtained from observational studies are usually subject to selection bias.

While conventional efficacy/effectiveness data typically shows the ability to prevent a symptomatic infection, this expanded approach could include prevention of outcomes categorized to include symptom class, viral damage minor/serious, hospital admission, ICU admission, death, various viral shedding levels, etc.

A potential solution is to give curative treatment before vaccination in areas where malaria is present.

[11] The effect of parasites on vaccine response has also been observed in individuals infected by helminths in areas that have a high burden of infectious diseases.

[13] Other biological factors such as smoking, age, sex, and nutrition also affect vaccine responses.

In the case of hepatitis B vaccine, for example, increasing age, being male, having a body mass index > 25, and smoking can result in lower seroprotection rates.

However, during research, it is possible that an intervention actually increases the risk of participants, for example, in the STEP and Phambili studies, which were both intended to test an experimental HIV vaccine .

Influenza activity was prolonged but of low intensity; type A (H3N2) was the virus that was generally spreading around the population, which was very like the vaccine itself.

[24] With serologic end points included, efficacy was demonstrated for the inactivated vaccine in a year with low influenza attack rates.

However, they are less effective in reducing cases of influenza-like illness and have a modest impact on working days lost.