Conversely, those who access and complete treatment may subsequently be less likely to transmit the disease. However, the natural history of injection and
potential impact of such heterogeneity is complex.39 Higher risk subpopulations are not necessarily fixed, with IDUs having periods of higher and lower risk at different times during their injection career. Other models have suggested that high risk in the 5-Fluoracil first year of injection or the presence of high-risk groups can limit primary prevention.40 The lack of age-structure in the current model also means that we cannot accurately utilize age-specific death rates.41, 42 These limitations need to be addressed by incorporating more complexity in future model projections and undertaking empirical research to determine the conditions, patient characteristics, and timing under which HCV treatment can be delivered and any associated changes in SVR. The cost-effectiveness of HCV antiviral treatment in terms of reducing morbidity and future liver disease to the individual is established, and our ex/non-IDU model predictions are consistent with these estimates (£3,000-£10,000 per QALY gained depending on treatment regime).12, 15 No other studies, to our knowledge, have examined
the cost-effectiveness of treating injectors Protein Tyrosine Kinase inhibitor including the prevention effect, or compared the cost-effectiveness of different clinical/policy decisions on whether it is justified to treat injectors as well as noninjecting populations, which requires a dynamic model as presented here. Hepatitis C transmission risk remains high among injectors in most populations, even when there is high coverage of prevention interventions such as needle and syringe programs and OST.8, 9 Our research indicates HCV treatment could play a role in prevention among the IDU population,10, 11 and treating IDUs is likely to be cost-effective across a wide range of prevalences. Empirical studies examining the treatment
of IDUs and measuring the effects on prevalence are warranted. Additional Supporting Information may be found in the online version of this article. “
“The immune control of hepatitis B virus (HBV) infection is essential for viral clearance. Therefore, restoring functional anti–HBV clonidine immunity is a promising immunotherapeutic approach to treatment of chronic infection. Plasmacytoid dendritic cells (pDCs) play a crucial role in triggering antiviral immunity through their ability to capture and process viral antigens and subsequently induce adaptive immune responses. We investigated the potential of pDCs to trigger antiviral cellular immunity against HBV. We used a human leukocyte antigen A (HLA–A)*0201+ pDC line loaded with HLA–A*0201-restricted peptides derived from hepatitis B core/hepatitis B surface (HBc/HBs) antigens to amplify specific CD8 T cells ex vivo from chronic HBV patients and established a Hepato-HuPBL mouse model to address the therapeutic potential of the strategy in vivo.