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Several additional articles in this issue of Viral Immunology address the host's innate immune response to infection by other viruses. Poxviruses have evolved numerous mechanisms to evade the immune response of the infected host, and many of these mechanisms have not been fully described. Dolega et al. have investigated the innate immune response genes that contribute to susceptibility versus resistance to lethal infection. They show a generalized downregulation of genes in four categories of antiviral innate immune receptors, downstream signaling pathways, and responsive components (Toll-like receptor signaling, nonobese diabetic-like receptor signaling, retinoic acid-inducible gene-I-like receptor signaling, and type I interferon signaling). The data suggest that variations in the expression of these genes contribute to the differences in murine resistance and susceptibility to lethal infection by ectromelia virus. In another article that addresses the host response to a viral infection, Wang et al. point out that the Josephin domain-containing protein 1 (JOSD1) is recognized as a member of the deubiquitinase family, but the biological functions of the protein are largely unknown. The authors show that JOSD1 physically interacts with SOCS1 (a negative regulator of cytokine signaling) and enhances SOCS1 stability. This is the first identification of a deubiquitinating substrate of JOSD1 and highlights a novel biological function of JOSD1. These findings suggest that JOSD1 is a potential target for interferon-based antiviral therapy. Holanda et al. have investigated the role of cellular and viral microRNAs in the modulation of viral and cellular gene expression, as well as the immune response to yellow fever virus. They conclude that the virus infection modulates the proteins involved in microRNA biogenesis and thereby regulates both viral replication and cellular immune response.
Two articles in the issue focus on vaccine development. Lazo Vázquez et al. have developed a vaccine against dengue virus (DENV) based on two different viral regions, the domain III of the envelope protein and the capsid protein. Testing of the vaccine in mice revealed that intranasal immunization with the vaccine favored the generation of DENV-specific cell-mediated immunity, whereas a combined intraperitoneal and intranasal vaccination strategy favored the generation of both functional antibodies and interferon-γ secretion. Abdelhafez et al. have analyzed the immunogenicity of conserved envelope peptides from hepatitis C virus (HCV) in mice. They find that multiple antigenic peptides are more immunogenic and elicit higher levels of neutralizing antibodies than single peptides. These peptides may be valuable additions to HCV vaccines.
Additional two articles in this issue focus on epidemiology. Mansha et al. have assessed the epidemiology of hepatitis B virus and HCV infections among the human immunodeficiency virus (HIV)-infected people who inject drugs in Lahore, Pakistan. Their data show that the incidence of HCV and HBV coinfections among HIV-infected drug users was 55% and 6%, respectively. Woolford et al. note that Canine parvovirus (CPV-2), an important cause of hemorrhagic enteritis in dogs, is associated with two variants (CPV-2a and CPV-2b) in Australia. Here they report the detection of a newly emerging third variant of CPV (CPV-2c) in Australia and recommend further characterization of CPV-2c-associated disease and its prevalence in Australian dogs.
Viral immunology in veterinary diseases was further examined in studies by Mühle et al. as well as Heidari and Delekta. Mühle et al. analyzed sera from feline foamy virus-infected cats and pumas to identify immunodominant epitopes. Gene expression profiles in the skin tissues of Marek's disease virus-infected chickens were determined by Heidari and Delekta. We will devote a future issue of the journal to more fully examining challenges in designing veterinary vaccines for viral infections.
Finally, Zhang et al. have investigated the severity of hemorrhagic fever with renal syndrome associated with Hantaan virus and Seoul virus infection in Asia. Their data indicate that elevated plasma growth arrest-specific 6 (Gas6) protein levels are associated with the severity of disease during infection in humans, suggesting that Gas6 may play an important role in the disease.
I would like to thank all of the authors for their excellent contributions to this issue of Viral Immunology and all of the reviewers for their efforts in maintaining the quality of the published articles.