Abstract
Risk factors for hepatitis C virus (HCV) infection vary, and there were an estimated 1.75 million new cases worldwide in 2015. The World Health Organization aims for a 90% reduction in new HCV infections by 2030. An HCV vaccine would prevent transmission, regardless of risk factors, and significantly reduce the global burden of HCV-associated disease. Barriers to development include virus diversity, limited models for testing vaccines, and our incomplete understanding of protective immune responses. Although highly effective vaccines could prevent infection altogether, immune responses that increase the rate of HCV clearance and prevent chronic infection may be sufficient to reduce disease burden. Adjuvant envelope or core protein and virus-vectored nonstructural antigen vaccines have been tested in healthy volunteers who are not at risk for HCV infection; viral vectors encoding nonstructural proteins are the only vaccine strategy to be tested in at-risk individuals. Despite development challenges, a prophylactic vaccine is necessary for global control of HCV.
Highlights
The advent of all oral, interferon-sparing direct-acting antivirals (DAAs) that cure hepatitis C virus (HCV) infection has transformed treatment, in highincome countries
HCV infections are rarely symptomatic before the onset of advanced liver disease, and HCV screening is rare in most parts of the world, so most persons with HCV infection are not identified.[1]
people who inject drugs (PWID), men who have sex with men, health care workers, infants born to HCV-infected mothers, and those living in the many countries with high HCV incidence would be expected to benefit from a preventive HCV vaccine
Summary
Risk factors for hepatitis C virus (HCV) infection vary, and there were an estimated 1.75 million new cases worldwide in 2015. Highly effective vaccines could prevent infection altogether, immune responses that increase the rate of HCV clearance and prevent chronic infection may be sufficient to reduce disease burden. The advent of all oral, interferon-sparing direct-acting antivirals (DAAs) that cure hepatitis C virus (HCV) infection has transformed treatment, in highincome countries. Immunity after effective treatment has been shown to be insufficient to prevent reinfection with HCV in individuals with ongoing risk of infection, including people who inject drugs (PWID), men having sex with men, and health care workers with frequent exposure to blood and bodily fluids.[3,4,5,6] Rates of reinfection in these populations vary, but are high when those most at risk of transmitting infection are treated, in part as a means to interrupt transmission. Abbreviations used in this paper: Ad5, adenovirus serotype 5; bNAb, broadly neutralizing antibodies; CD81bs, CD81 receptor binding site; ChAd, chimpanzee adenovirus; DAA, direct-acting antiviral; HCV, hepatitis C virus; HCVcc, HCV derived from cell culture; HCVpp, HCV pseudoparticles; HVR1, hypervariable region 1; mAbs, monoclonal antibodies; MVA, modified vaccinia Ankara; NAbs, neutralizing antibodies; NS, nonstructural; PD-1, programmed cell death 1; PWID, people who inject drugs; VLP, virus-like particle
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