Short communication High rate of infection and immune disorders in patients with hepatitis C virus after liver transplantation D. Micheloud 1 , M. Salcedo 2 , R. Ban ˜ ares 2 , D. Rinco ´n 2 , J. Jensen 3 , J.J. Rodrı ´guez 3 , E. Ferna ´ ndez-Cruz 3 , J. Carbone Campoverde 3 , S. Resino 4 1 Department of Internal Medicine, Hospital General Universitario ‘Gregorio Maran ˜o ´n’, Madrid, Spain, 2 Liver Transplantation Unit, Hospital General Universitario ‘Gregorio Maran ˜o ´n’, Madrid, Spain, 3 Clinical Immunology Unit, Immunology Division, Hospital General Universitario ‘Gregorio Maran ˜o ´n’, Madrid, Spain, 4 Research Unit, Instituto de Salud ‘Carlos III’, Majadahonda, Madrid, Spain D. Micheloud, M. Salcedo, R. Ban ì ares, D. Rinco¤ n, J. Jensen, J.J. Rodr|¤guez, E. Ferna¤ ndez-Cruz, J. Carbone Campoverde, S. Resino. High rate of infection and immune disorders in patients with hepatitis C virus after liver transplantation. Transpl Infect Dis 2009: 11: 367^372. All rights reserved Abstract: The aim of this prospective study was to analyze the incidence of serious infections and changes in immunological markers after liver transplantation (LT) in a cohort of patients with hepatitis C virus (HCV).This study included 34 patients who had LT, 20 patients with HCVetiology (HCVgroup), and 14 patients with alcoholic etiology (non-HCVgroup). Patients with HCV were more likely to have severe infections (80%) in comparison with patients in the non-HCVgroup (42%) ( P 5 0.05).The HCVgroup had a 3-fold greater likelihood of early severe bacterial infections than the non-HCVgroup. At 1week post LT, the HCVgroup showed higher values of CD19 1 B cells/mL than the non-HCVgroup ( Po0.05). At weeks 4 and 12 post LT, the HCVgroup had lower values of CD19 1 B cells/mL( Po0.05). Our data suggest that HCVrecurrence after LTwas associated with a high incidence of early severe infections and immunological alterations, which may be related to this increased risk.                                                                                                     Infection is an important cause of morbidity after liver transplantation (LT) (1). More than two-thirds of liver trans- plant recipients have infectious complications in the ¢rst year after LT. During the infection, the release of cytokines may have other indirect and negative e¡ects, including allograft injury, opportunistic infections, and malignancy (2). The risk of infection from LT is mainly determined by the intensity of exposure to infectious agents (hospital or community sources) and to the overall level of immunosup- pression. Although it is well recognized that immunosup- pression and surgical issues have a deleterious e¡ect on the immune system, only a few reports have assessed the evolution of humoral and cellular immune parameters (3) and their relationship to infectious complications after LT. Hepatitis C virus (HCV) cirrhosis is one of the major etio- logic causes of LT in several countries. Few reports have studied the incidence of infections in LT recipients with HCVcirrhosis, although many studies have shown the ef- fect of HCV reinfection on the allograft outcome (4). In this study, we have analyzed the incidence of serious infections after LTand the changes of cellular and humoral immunocompetence markers in a cohort of patients with HCVrecurrence. Materials and methods We carried out a prospective study on 46 consecutive pa- tients undergoing LT from January 2005 to June 2006.We r 2009 John Wiley & Sons A/S Transplant Infectious Disease . ISSN 1398-2273 Key words: infections; hepatitis C; liver transplantation; immunoglobulin; T cell; B cell Correspondence to: Dariela Micheloud, Department of Internal Medicine, Hospital General Universitario ‘Gregorio Maran ˜o ´n’, C/Doctor Esquerdo 46, 28007 Madrid, Spain Tel: 3491 586 8423 Fax: 3491 586 6698 E-mail: michelouddary@yahoo.es Received 6 November 2008, revised 24 December 2008, 12 January 2009, accepted for publication 19 January 2009 DOI: 10.1111/j.1399-3062.2009.00408.x Transpl Infect Dis 2009: 11: 367–372 367