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Proc Natl Acad Sci U S A. 2014 Aug 19;111(33):12187-92. doi: 10.1073/pnas.1402351111. Epub 2014 Aug 4.

Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections.

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Medical Research Council (MRC) Human Immunology Unit and.
Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, United Kingdom;
Computational Biology Research Group, MRC Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, United Kingdom;
Department of Biochemistry, Birmingham Heartlands Hospital, Birmingham B9 5SS, United Kingdom;
Center for Infectious Diseases, Beijing You'an Hospital, Capital Medical University, Beijing 100069, China;
Department of Medicine, Imperial College, Chelsea and Westminster Hospital, London SW10 9NH, United Kingdom;
MRC International Nutrition Group, London School of Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom;
Centre for Sexual Health and HIV Research, Mortimer Market Centre, University College London, London WC1 6JB, United Kingdom;
Blood Systems Research Institute, San Francisco, CA 94118; andDepartments of Laboratory Medicine andMedicine, University of California, San Francisco, CA 94143.
Medical Research Council (MRC) Human Immunology Unit and
Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, United Kingdom;


During HIV type-1 (HIV-1), hepatitis C virus (HCV), and hepatitis B virus (HBV) infections, altered iron balance correlates with morbidity. The liver-produced hormone hepcidin dictates systemic iron homeostasis. We measured hepcidin, iron parameters, cytokines, and inflammatory markers in three cohorts: plasma donors who developed acute HIV-1, HBV, or HCV viremia during the course of donations; HIV-1-positive individuals progressing from early to chronic infection; and chronically HIV-1-infected individuals (receiving antiretroviral therapy or untreated). Hepcidin increased and plasma iron decreased during acute HIV-1 infection, as viremia was initially detected. In patients transitioning from early to chronic HIV-1 infection, hepcidin in the first 60 d of infection positively correlated with the later plasma viral load set-point. Hepcidin remained elevated in individuals with untreated chronic HIV-1 infection and in subjects on ART. In contrast to HIV-1, there was no evidence of hepcidin up-regulation or hypoferremia during the primary viremic phases of HCV or HBV infection; serum iron marginally increased during acute HBV infection. In conclusion, hepcidin induction is part of the pathogenically important systemic inflammatory cascade triggered during HIV-1 infection and may contribute to the establishment and maintenance of viral set-point, which is a strong predictor of progression to AIDS and death. However, distinct patterns of hepcidin and iron regulation occur during different viral infections that have particular tissue tropisms and elicit different systemic inflammatory responses. The hypoferremia of acute infection is therefore a pathogen-specific, not universal, phenomenon.

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