Concurrent autochthonous acute hepatitis E and hepatitis B reverse seroconversion in an HIV-1-infected patient: one virus may hide another

Autochthonous hepatitis E is an emerging disease in industrialized countries.1Dalton H.R. Bendall R. Ijaz S. Banks M. Hepatitis E: an emerging infection in developed countries.Lancet Infect Dis. 2008; 8: 698-709Abstract Full Text Full Text PDF PubMed Scopus (549) Google Scholar Very recently, three cases have been described in HIV-infected patients in Germany, France, and the USA.2Thoden J, Venhoff N, Miehle N, Klar M, Huzly D, Panther E, et al. Hepatitis E and jaundice in an HIV-positive pregnant woman. AIDS 2008; 22: 909-10. .Google Scholar, 3Colson P. Dhiver C. Gérolami R. Hepatitis E virus as a newly identified cause of acute viral hepatitis during human immunodeficiency virus infection.Clin Microbiol Infect. 2008; 14: 1176-1180Crossref PubMed Scopus (39) Google Scholar, 4Curry J. Adams N. Crum-Cianflone N. Acute hepatitis E virus infection in an HIV-infected person in the United States.Ann Intern Med. 2009; 150: 226Crossref PubMed Scopus (31) Google Scholar Another reported cause of acute hepatitis in the setting of HIV infection is hepatitis B virus (HBV) reverse seroconversion and reactivation in patients with HBV serology indicating past infection.5Rouphael N.G. Talati N.J. Rimland D. Hepatitis B reverse seroconversion in HIV-positive patients: case series and review of the literature.AIDS. 2007; 21: 771-774Crossref PubMed Scopus (28) Google Scholar, 6Henke-Gendo C. Amini-Bavil-Olyaee S. Challapalli D. Trautwein C. Deppe H. Schulz T.F. et al.Symptomatic hepatitis B virus (HBV) reactivation despite reduced viral fitness is associated with HBV test and immune escape mutations in an HIV-coinfected patient.J Infect Dis. 2008; 198: 1620-1624Crossref PubMed Scopus (22) Google Scholar We present herein a case of concurrent hepatitis E and HBV seroreversion in an HIV-1-infected patient. A 54-year-old HIV-1-infected homosexual male presented in June 2007 with jaundice and asthenia. His alanine aminotransferase (ALT) level was 373 IU/l, bilirubinemia was 52 μmol/l, and prothrombin index (PI) was 56%. The CD4 count was 77 cells/mm3 and plasma HIV-1 RNA was 2.5 log10copies/ml. Tenofovir and emtricitabine, two anti-HIV/HBV drugs, had been interrupted six months earlier. HBV reactivation was diagnosed based on serum HBV DNA-positivity (52 900 000 IU/ml; Cobas TaqMan Roche) and hepatitis B surface antigen (HBsAg) seroreversion (Axsym Abbott assay). Unexpectedly, concurrent hepatitis E was diagnosed based on positive results on IgM anti-hepatitis E virus (HEV) antibody testing (optical density ratios for IgG and IgM anti-HEV antibodies were 0.20 and 10.4, respectively; EIAGen Adaltis kits) and HEV RNA detection and sequencing from serum.7Colson P. Coze C. Gallian P. Henry M. De Micco P. Tamalet C. Transfusion-transmitted hepatitis E in a child in France.Emerging Infect Dis. 2007; 13: 648-649Crossref PubMed Scopus (211) Google Scholar Other major etiologies for acute hepatitis were excluded. Retrospective analysis of a serum sample collected in February 2007 did not detect HEV RNA or HBV DNA, and showed HBsAg positivity, anti-hepatitis B core (HBc) antibody positivity, and anti-hepatitis B surface (HBs) antibodies <10 IU/l. The HEV was genotype 3. This genotype is the most frequently found in autochthonous cases in Europe.1Dalton H.R. Bendall R. Ijaz S. Banks M. Hepatitis E: an emerging infection in developed countries.Lancet Infect Dis. 2008; 8: 698-709Abstract Full Text Full Text PDF PubMed Scopus (549) Google Scholar The patient did not report any recent travel abroad. The patient's health condition, initially poor, was worsening. Digestive B-lymphoma of high-grade malignancy was diagnosed one month after hepatitis onset. The HBV load showed a 3.8-log drop subsequent to tenofovir/emtricitabine re-introduction. ALT normalized (7 IU/l), but PI remained low (54%), and bilirubinemia increased up to 174 μmol/l. The patient died eight weeks after hepatitis onset. IgG anti-HEV antibody testing just before death was still negative, while HEV RNA was still positive in the serum. In the present observation, HBV reactivation might have hidden concurrent hepatitis E if HEV testing had not been systematically performed. Moreover, the HEV diagnosis may have been jeopardized due to the persistent absence of anti-HEV IgG seroconversion, which might have been related to the patient's low CD4 cell count. Indeed, such an atypical feature has previously been described in severely immunosuppressed individuals.8Tamura A. Shimizu Y.K. Tanaka T. Kuroda K. Arakawa Y. Takahashi K. et al.Persistent infection of hepatitis E virus transmitted by blood transfusion in a patient with T-cell lymphoma.Hepatol Res. 2007; 37: 113-120Crossref PubMed Scopus (163) Google Scholar, 9Gérolami R. Moal V. Colson P. Chronic hepatitis E with cirrhosis in a kidney-transplant recipient.N Engl J Med. 2008; 358: 859-860Crossref PubMed Scopus (295) Google Scholar Hence, the present case prompts the inclusion of HEV RNA and IgM anti-HEV antibody testing in routine diagnosis investigations of acute hepatitis in HIV-infected patients, regardless of another identified cause. No conflict of interest to declare.