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Several articles in this issue of Viral Immunology focus on viruses that cause hepatitis B and C. Huang and colleagues point out that the spleen plays a significant role in the development of cirrhosis and hepatocellular carcinoma (HCC), due to hepatitis B virus (HBV). To better understand the role of spleen, the authors investigated how splenectomy impacts cytokine levels in cirrhotic patients. Their data provide new clues to the function of the spleen in cirrhotic patients and suggest that the modulation of cytokine expression may be a potential therapeutic strategy. It is known that circulating follicular helper T cells and circulating follicular regulatory T cells (cTFR) coregulate the reactions of germinal center B cells, but their roles in chronic HBV infection remain limited. To address this issue, Wu et al. have analyzed the frequencies of these cells and the phenotype of circulating CD4+CXCR5+ T cells in HBV-infected patients. The authors show that increased frequencies of cTFR-like T cells and reduced functional impairment of circulating CD4+CXCR5+ T cells may mediate a weakening of the immune response to HBV and contribute to disease progression.
HCC is the second leading cause of cancer-associated deaths. Approximately 50% of all HCC cases are found in high HBV endemic regions, where 70–80% of HCC cases are directly attributable to HBV. Siburian and colleagues have previously shown that Indonesian HBV patients with advanced liver disease exhibit a high prevalence of pre-S2 protein start codon mutations. Since nuclear factor (NF)-κB has been implicated in the disease process, the authors have investigated the involvement of pre-S2 mutations on NF-κB function. Their data show that these mutations had no direct effect on NF-κB activation but may influence an alternative pathway in liver disease progression that involves high expression of the NF-κB subunit, p50. Colucci et al. have also investigated factors that influence the severity of virus-related liver damage. The authors hypothesize that chronic hepatitis C disease results in a deregulation of the chemokine receptor 5 (CCR5) pathway, compromising T cell-dependent antiviral immune responses, and favoring viral persistence. However, their data indicate that CCR5 mutation is not involved in the pathogenesis of chronic hepatitis C disease.
Other articles in this issue of Viral Immunology address other aspects of the relationship between immunity and viral infection. Khopkar et al. present data on the prevalence and burden of genital warts in India. They note that the estimated national prevalence, diagnosis, and treatment costs of genital warts in India were higher for men than for women. Park and colleagues report on the seroprevalence of human parainfluenza virus (HPIV) types 1–4 among healthy children <5 years of age in Korea. Their data suggest that there is an urgent need for HPIV3 vaccination in 1-year-old children in Korea.
Finally, Bavananthasivam et al. have investigated the stimulatory effect of various toll-like receptor (TLR) ligands in reducing Marek's disease virus (MDV) infection in chicken embryo fibroblast cells. Transcriptional analysis of gene expression demonstrated that all TLR ligand treatments in combination with MDV infection significantly increased the expression of type I interferons, interleukin-1β, interferon regulatory factor 7, interferon-induced protein with tetratricopeptide repeats 5, and myxoma-resistance protein. The authors note that further studies are needed to elucidate the underlying mechanism by which TLRs control the replication of MDV in chickens.
I would like to thank all of the authors for their excellent contributions to this issue of the Journal and all of the reviewers who work tirelessly to maintain the high quality of published articles.