Longitudinal Analysis of Hepatitis E Virus (HEV) in a U.S. Cohort of HIV-Infected Liver and Kidney Transplant Recipients

Publication Type
Conference Paper
Year of Publication
Sherman, KE; Rouster, SD; Boyce, CL; Barin, B; Terrault, N; Kottilil, S; Blackard, JT; Shata, MT
American Association for the Study of Liver Diseases Annual Meeting, 2017
Date Published
Washington, DC
American Association for the Study of Liver Diseases


HEV is an unrecognized cause of acute and chronic hepatitis among immunosuppressed patients with HIV or following solid organ transplantation We evaluated prevalence, incidence, and clinical features of patients with HEV antibody responses in an HIV-infected cohort who underwent liver and/or kidney transplant.


Patients enrolled in the NIH HIV Solid Organ Transplant Study (HIV-TR) were evaluated. Baseline and at least one post-transplant sample were assessed Sera were analyzed for seroconversion, seroreversion, and associated clinical characteristics of those patients were determined at approximately 3, 6, 12, and 24 month intervals following transplant Presence of HEV IgG antibody was determined using an ELISA assay (Wantai, China).


Longitudinal analysis included subjects who received liver (n = 70) or kidney (n = 101) transplantation. In liver recipients, 15/70 (21.4%) had a positive HEV IgG antibody at baseline. Among kidney recipients, 19/101 (18.8%) had a positive HEV antibody indicative of HEV infection prior to transplantation. The overall incidence of seroconversion (new HEV IgG antibody) following organ transplantation was 5.5% in liver recipients and 0% in kidney recipients. Temporary or permanent seroreversion among those positive prior to transplant occurred in 6 of 15 (40%) following liver transplantation and in 6 of 19 (31.6%) in kidney recipients Appearance of anti-HEV IgG was noted at the first available sample after transplant in 2 subjects and at a later evaluation in a third subject In this subject, the appearance of the antibody coincided with an increase in serum ALT to 123 U/ml. A liver biopsy revealed focal centri- zonal necrosis. HCV was the suspected etiology. Among seroconverters, CD4 counts were at/near nadir levels at the time HEV antibody was first noted (mean 75 cells/mm3). AST levels decreased in all liver recipients who had HEV antibody at baseline but subsequently seroreverted, but this pattern was more variable for ALT. 2 of 6 liver recipients who seroreverted had a rejection episode that was treated with increased immunosuppression in the weeks prior to loss of antibody.


Following liver transplantation in HIV-infected persons, 5.5% developed an antibody response to HEV. It is possible that seroconversion occurred in some subjects because of acquisition of antibodies from the donor or from transplant-associated blood transfusions rather than a new infection. Further testing with HEV RNA and HEV IgM is planned. Interestingly, such seroconversions were not observed in kidney recipients. Seroreversion may be influenced by the use of immunosuppression.