A link between Ljungan virus and type 1 diabetes?

T his issue of Viral Immunology features a number of articles that cover a variety of topics ranging from anti-viral immune responses to immunopathology. In this regard, a particularly interesting article investigates the possible linkage between infection with Ljungan virus (LV, a virus isolated from bank voles) and type 1 diabetes (T1D). Previous studies had implicated LV in the etiology of T1D, but it was unclear whether LV might contribute to islet autoimmunity, progression to clinical onset, or both. Nilsson et al. have now addressed this question in a cohort of patients aged 0–18 years that had been newly diagnosed with T1D. The authors show that anti-LV antibodies (LVAb) were common among the young T1D patients and that LVAb levels were higher in the younger age groups. In addition, LVAb correlated with known islet autoantibodies and HLA-DQ8. These data further support the concept that prior exposure to LV may be associated with T1D.

Another interesting report describes the murine response to intravaginal herpes simplex virus type 2 (HSV-2) infection which causes genital tissue damage and a subsequently fatal encephalopathy. Cherpes and colleagues compared gene expression in vaginal tissue from infected and uninfected mice and identified 156 genes that exhibited altered expression during the first few days of infection. These genes were predominantly linked to interferon (IFN)-mediated host immunity. Interestingly, intravaginal administration of a Toll-like receptor 3 agonist prior to infection reduced the incidence of genital pathology and encephalopathy. The authors conclude that that the antiviral response to infection occurs too late to prevent viral lytic replication and dissemination, but that prior induction of an antiviral state protects against primary intravaginal infection while permitting the development of HSV-specific protective immunity.

Four other viruses are reported on in this issue of Viral Immunology. First, van den Berg and colleagues investigated the relationship between recurrent exposure to hepatitis C virus (HCV) and the development of an HCV-specific T-cell response. The data suggest that both ongoing risk behavior and presence of HCV-RNA affect the HCV-specific T-cell response in terms of both magnitude and specificity. The authors suggest that these findings may have implications for vaccine development. Second, a paper by Yin et al. investigates the hypothesis that some anti-Dengue virus antibodies cross-react with some of the host's own proteins, with implications for the dengue hemorrhagic fever pathogenesis. Consistent with this idea, the authors identify several host proteins that may be involved in dengue pathogenesis. Third, Hejr et al. evaluated the association between Th17-related cytokine gene polymorphisms and hepatitis B virus (HBV) infection in kidney transplant patients who may experience acute rejection. The data indicate a higher frequency of the IL-17, IL-21, and IL-23R allele polymorphisms in HBV infected kidney transplant patients who experienced acute rejection. And fourth, Hu et al. show that both overexpression of HLA-G and infection with human papilloma virus are positively associated with Kazakh esophageal squamous cell carcinomas.

Finally, one paper in this issue of Viral Immunology diverges from normal virus infections to the topic of prion disease development and progression. Cho et al. have examined lymphocyte proliferation and innate immune function in scrapie-infected mice. The authors demonstrate altered innate immunity during infection and further show that lymphocyte proliferation and innate immune function deteriorate with disease progression. These data are among the first to address the role of innate immunity in scrapie-infected animals.

Taken together, this issue of Viral Immunology offers a smorgasbord of viruses, immune responses, and immunopathological consequences. I would like to thank the authors for their exciting contributions to the field.