Contribution of Vaccination to Human Health

Vaccination is an immensely successful public health intervention that has considerably reduced the burden of infectious disease in the world today. Coupled with other public health programs, ranging from insect suppression and clean water, it is likely that billions of lives have been saved. The success of these programs is due to the fact that the most successful vaccines are characterized by their ease of production, simple administration, and longevity of protection. In addition, vaccines are being administered to large number of at-risk individuals across the globe—the World Health Organization reports that ∼85% of the world's children receive vaccines that protect them against a variety of diseases, including polio, tuberculosis, measles, diphtheria, tetanus, and pertussis. Moreover, a major strength of vaccination programs is that protection can extend to unvaccinated individuals through herd immunity. Vaccination programs have also led to the eradication of smallpox and may soon eradicate polio, both much feared infectious diseases.

It is with this background that Mokhort and colleagues have analyzed the contribution of vaccination to the reduction of infectious mortality in Ukraine. In the current issue of Viral Immunology, the authors present an epidemiological analysis of annual indicators, such as cumulative incidence, mortality rate, and case fatality rate for infections preventable by vaccines compared with infections not preventable by vaccines. Their data indicate that between 1944 and 2015, the mortality reduction rate for vaccine preventable diseases was very impressive, ranging from 41-fold for tetanus to 1,061-fold for measles. However, the incidence reduction rate was significantly lower, most likely due to the contribution of a number of external factors unrelated to vaccines, such as improved public health services. The authors also report that the vaccination contribution to the reduction in infectious mortality was more significant for the pediatric population. These data are an important contribution to our understanding of the benefits and limitations of vaccine programs at the population level.

Although vaccines have led to the control of many infectious diseases, it has proven to be difficult to produce effective vaccines against many others. Examples include norovirus (NoV), the human immunodeficiency virus, and even the influenza virus (for which current vaccines have limited efficacy). In the case of NoV, Malm et al. note that GII.4 variants of the virus have been responsible for the majority of outbreaks over the past 20 years, but that since 2014, the GII.17 genotype has emerged as the dominant variant. As GII.17 is a recently evolved NoV strain, there is a lack of immunogenicity data. Therefore, the authors have analyzed healthy adult volunteers with a natural NoV exposure history for GII.17-specific seroresponses. Their data revealed low levels of pre-existing cross-reactive antibodies to GII.17, indicating the presence of a large pool of susceptible individuals. These data suggest that GII.17 and other newly emerging NoV genotypes should be considered as an antigenic component for future vaccine formulations.

The current issue of Viral Immunology also focuses on the innate immune response to viral infections. Tumala and colleagues have used a mouse model of paramyxoviral infection to study dendritic cells migrating from the lungs to the draining lymph nodes. They show that these dendritic cells in neonates exhibit a significant delay in the expression of various activation markers compared with adult mice. In addition, prostaglandin D2 was present at significantly higher levels in neonatal bronchoalveolar lavage fluid than in adults and that blocking prostaglandin D2 function with an antagonist restored dendritic cell activation in neonates. These findings suggest that there may be opportunities for therapeutic intervention in neonatal paramyxoviral infections.

Three additional innate immunity articles are included in this issue. Choudhary and colleagues have investigated susceptibility to severe influenza virus infection. Their data suggest that polymorphisms of the interleukin-10 and tumor necrosis factor alpha (TNFα) genes may be associated with disease severity. Liu et al. note that micro-RNAs have been reported to play crucial roles in various biological processes, including viral infections, but that little is known about their role in innate immune responses. In this study, they show that one particular micro-RNA (miR-26b) could inhibit vesicular stomatitis virus replication through the upregulation of type-I interferons and interferon-stimulated genes. Su et al. report on a longitudinal study of the relationship between systemic lupus erythematosus activity and the levels of various intracellular proteins that are associated with innate immune responses. They report that lupus disease activity was inversely associated with the levels of innate immunity.

Finally, one article in this issue of Viral Immunology focuses on the regulation of adaptive immune responses. B7-H3 is an immune checkpoint molecule that has been shown to be upregulated during hepatitis B virus (HBV) infection. Gao et al. have systematically investigated the expression of B7-H3 relative to the ratio of T lymphocyte subsets and clinical parameters at different stages in the course of the disease. Their data indicate that B7-H3 might contribute to the progression of HBV infection by triggering inhibitory signals in effector T cells. Furthermore, the authors note that the association of B7-H3 with the progression of HBV infection could be utilized as a potential clinical indicator of disease progression and also serve as a potential target for therapeutic strategies against HBV infection.

I thank the authors for their excellent contributions to the Journal and all of the scientists who generously contribute their expertise as reviewers to ensure the high quality of articles published.