HEV in Solid-Organ Transplant Recipients, CME Activity | CDC EID

EID Journal Home > Volume 17, Number 1–January 2011
Volume 17, Number 1–January 2011
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Hepatitis E Virus Infection without Reactivation in Solid-Organ Transplant Recipients, France

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* Describe factors associated with higher risk for HEV seroconversion and development of chronic disease among liver and kidney transplant patients.

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Authors

Disclosures: Florence Legrand-Abravanel, PharmD, PhD; Nassim Kamar, MD, PhD; Karine Sandres-Saune, PharmD, PhD; Sebastien Lhomme, PharmD; Jean-Michel Mansuy, MD; Fabrice Muscari, MD, PhD; Federico Sallusto, MD; Lionel Rostaing, MD, PhD; and Jacques Izopet, PharmD, PhD, have disclosed no relevant financial relationships.
HEV in Solid-Organ Transplant Recipients, CME Activity | CDC EID



EID Journal Home > Volume 17, Number 1–January 2011
Volume 17, Number 1–January 2011
Dispatch
Hepatitis E Virus Infection without Reactivation in Solid-Organ Transplant Recipients, France

Florence Legrand-Abravanel, Comments to Author Nassim Kamar, Karine Sandres-Saune, Sebastien Lhomme, Jean-Michel Mansuy, Fabrice Muscari, Federico Sallusto, Lionel Rostaing, and Jacques Izopet

Author affiliations: Institut National de la Santé et de la Recherche Médicale, Toulouse, France (F. Legrand-Abravanel, N. Kamar, K. Sandres-Saune, S. Lhomme, L. Rostaing, J. Izopet); and Centre Hospitalier Universitaire Toulouse, Toulouse (F. Legrand-Abravanel, N. Kamar, K. Sandres-Saune, S. Lhomme, J.-M. Mansuy, F. Muscari, F. Sallusto, L. Rostaing, J. Izopet)

Suggested citation for this article

Abstract
Infections with hepatitis E virus (HEV) in solid-organ transplant recipients can lead to chronic hepatitis. However, the incidence of de novo HEV infections after transplantation and risk for reactivation in patients with antibodies against HEV before transplantation are unknown. Pretransplant prevalence of these antibodies in 700 solid-organ transplant recipients at Toulouse University Hospital in France was 14.1%. We found no HEV reactivation among patients with antibodies against HEV at the first annual checkup or by measuring liver enzyme activities and HEV RNA. In contrast, we found 34 locally acquired HEV infections among patients with no antibodies against HEV, 47% of whom had a chronic infection, resulting in an incidence of 3.2/100 person-years. Independent risk factors for HEV infection were an age <52 years at transplantation and receiving a liver transplant. Effective prophylactic measures that include those for potential zoonotic infections should reduce the risk for HEV transmission in this population. Large epidemics of hepatitis E have occurred in Asia, Africa, and Latin America where sanitation is suboptimal (1). The numbers of non–travel-associated hepatitis E virus (HEV) infections have also increased in industrialized countries in recent years, and these infections are now considered an emerging infectious disease in Western countries (2). HEV belongs to the family Hepeviridae. At least 4 major genotypes of HEV have been recognized. Genotypes 1 and 2 are restricted to humans and associated with epidemics in developing countries, and genotypes 3 and 4 are zoonotic and infect humans and several other animals in developing and industrialized countries (3). The discovery of animal strains of HEV in pigs, wild boars, deer, and rodents and the finding of other animal species with antibodies against HEV has broadened the host range and diversity of HEV (3). Although HEV is transmitted mainly by the fecal–oral route in developing countries, there are other routes in industrialized countries. These routes include contact with animal reservoirs (4,5) and consumption of undercooked pig, deer, or wild boar meat (6–8). Nosocomial infection and transfusion-transmitted infection have also been reported (9–11). HEV infection generally has a self-limiting symptomatic course or an asymptomatic course that includes acute hepatitis. Fulminant hepatitis may occur in pregnant women and persons with underlying liver disease (1,12,13). HEV can lead to chronic infection in solid-organ transplant (SOT) patients (14–16), in patients who have had chemotherapy (11,17,18), and in patients infected with HIV (19,20). HEV infection can evolve to chronic hepatitis in up to 60% of infected SOT patients (16). Reactivation of an HEV infection was reported recently in a patient in Germany who had acute lymphoblastic leukemia after allogeneic stem cell transplantation (21). This reactivation was diagnosed as acute limited hepatitis E before stem cell transplantation. HEV viremia reappeared 14 weeks after stem cell transplantation with increased aminotransferase activity. Analysis of virus RNA sequences showed reactivation of endogenous HEV genotype 3, which indicated that the virus had persisted despite the recovery of the patient from acute hepatitis E (21). Southwestern France is characterized by a high prevalence of antibodies against HEV in blood donors (22), and several cases of HEV infections have been reported in immunocompetent and immunocompromised patients (23,24). However, the incidence and risk for reactivation of HEV infection in SOT patients in this area are unknown. To identify these factors, we examined a large cohort of immunocompromised patients at Toulouse University Hospital, France, during January 2004–December 2009 to determine the prevalence of antibodies against HEV in SOT recipients before transplantation, the frequency of HEV reactivation, the incidence of HEV infections relative to the organ transplanted, and the risk for HEV transmission from the organ donor or from a blood transfusion. HEV in Solid-Organ Transplant Recipients | CDC EID full-text (large):
HEV in Solid-Organ Transplant Recipients | CDC EID


Suggested Citation for this Article

Legrand-Abravanel F, Kamar N, Sandres-Saune K, Lhomme S, Mansuy J-M, Muscari F, et al. Hepatitis E virus infection without reactivation in solid-organ transplant recipients, France. Emerg Infect Dis [serial on the Internet]. 2011 Jan [date cited]. http://www.cdc.gov/EID/content/17/1/30.htm

DOI: 10.3201/eid1701.100527

Comments to the Authors

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Florence Legrand-Abravanel, Laboratoire de Virologie, Hôpital Purpan, Centre Hospitalier Universitaire, Toulouse 31059, Toulouse CEDEX, France; email: abravanel.f@chu-toulouse.fr