Viral Immunology in 2011

A s we move into 2011, it is apparent that scientific research into the host response to viral infections continues to increase dramatically. Since Viral Immunology is the only journal that exclusively focuses on this important area of biomedical research, its role in disseminating the latest breakthroughs becomes more and more important. In the coming year, we want to continue the journal's growth by embracing the latest research in the rapidly expanding areas of veterinary immunology, clinical immunology, diagnostics, and biodefense. We also want to encourage more submissions from a broader geographic area to enhance the global nature of the journal. To achieve these goals, we plan to strengthen our scientific expertise in these areas of emerging research by expanding our Editorial Board. As these changes take effect, the journal will emerge even stronger in its position as the leading resource on host responses to viral infections.

The current issue features papers on both innate and adaptive immune responses. On the innate immunity front, Crowley and colleagues have examined the host response to chicken anemia virus (CAV). CAV infection results in anemia, lymphoid depletion, and immunosuppression, and has a significant economic impact on the chicken and egg industry. However, little is known about the early host response to infection. Using a microarray approach Crowley and associates identified immune response genes, such as cytokine/cytokine receptor genes and antiviral genes, that are differentially regulated during infection and point to pathways involved in the host response. Iannello and colleagues address immune responses to a virus of significant clinical importance, herpes simplex virus type 1 (HSV-1). HSV-1 usually infects humans early in childhood and persists for life in dorsal root ganglia. The virus reactivates under certain conditions, causing disease such as painful blisters or “cold sores” on the lips. The authors show that HSV-1 promotes the expression of FasL on the surface of infected cells, thereby inducing the death of interacting human CD4⁺ T cells, CD8⁺ T cells, and natural killer cells. The study highlights an important immune evasion mechanism that is utilized by the virus to avoid eradication by the host immune response.

Several articles discuss the adaptive immune responses to viral infections. Carotenuto and colleagues have analyzed the impact of chronic hepatitis B virus (HBV) infection on CD8⁺ T-lymphocyte subpopulations. Chronic hepatitis B patients exhibited higher percentages of naïve CD8⁺ T lymphocytes relative to healthy patients and patients recovering from acute hepatitis B. The authors speculate that differentiated CD8⁺ T lymphocytes may be removed from the circulation, thereby limiting the control of HBV replication. Dendritic cells (DCs) play a pivotal role in regulating both the immune response and pathology associated with viral infections, such as the human immunodeficiency virus 1 (HIV-1). In this regard, Zhao and colleagues have analyzed monocytes, myeloid DCs and their precursors, and plasmacytoid DCs in HIV-1-infected patients. Their data suggest that the route of HIV-1 infection in patients dramatically impacts the levels of blood DC subpopulations, thereby contributing to dysregulated immune responses and the pathogenesis of HIV-1. The regulation of adaptive immune responses is also mediated in part by regulatory T cells (Tregs). Li and colleagues demonstrate that the frequency of Tregs in AIDS patients was significantly higher than in long-term non-progressors, HIV-exposed seronegative persons, and healthy control patients. These data suggest that Tregs may play a role in disease progression. Another virus that is associated with immunopathology is influenza virus. Xu and colleagues outline a new vaccine approach that is designed to elicit strong immunity to both the current circulating strain of virus and to new heterosubtypic strains of viruses. Their analysis of a DNA vaccine that encodes both nucleoprotein and hemagglutinin proteins from a highly pathogenic H5N1 virus demonstrates that this approach may be very effective.

Finally, I would like to personally thank all of the reviewers who have helped make Viral Immunology such an important journal for the field. Their efforts on behalf of the journal are essential for its success and are very much appreciated by me, the staff at Mary Ann Liebert Publishing, and Viral Immunology's many readers. Thank you.