Probable corticosteroid-induced reactivation of latent hepatitis B virus infection in an HIV-positive patient involving immune escape.

We describe a patient infected with human immunodeficiency virus who possessed a serological profile suggesting a previous cleared acute hepatitis B virus (HBV) infection, including high levels of antibodies against HBV surface antigen (anti-HBs). Following the administration of inhaled glucocorticosteroids combined with protease inhibitor-based antiretroviral treatment, the patient developed an unexpected severe acute hepatitis despite persistence of anti-HBs. A genotype A2 strain emerged with 2 major mutations in the S gene, sK122R and sD144E. Molecular and biological analyses strongly suggested reactivation of a latent HBV infection. The importance and the molecular basis of these 2 epitopes in immune-escape mechanisms and host-virus interactions are discussed.

[1]  F. Josephson Drug–drug interactions in the treatment of HIV infection: focus on pharmacokinetic enhancement through CYP3A inhibition , 2010, Journal of internal medicine.

[2]  F. Tacke,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. , 2008, The Journal of infectious diseases.

[3]  F. Zoulim,et al.  Rolling Circle Amplification, a Powerful Tool for Genetic and Functional Studies of Complete Hepatitis B Virus Genomes from Low-Level Infections and for Directly Probing Covalently Closed Circular DNA , 2008, Antimicrobial Agents and Chemotherapy.

[4]  C. Manegold,et al.  Functional analysis of hepatitis B virus reactivating in hepatitis B surface antigen‐negative individuals , 2005, Hepatology.

[5]  F. Zoulim,et al.  A quasi-monoclonal anti-HBs response can lead to immune escape of 'wild-type' hepatitis B virus. , 2005, The Journal of general virology.

[6]  P. Coursaget,et al.  Genetic Diversity of Hepatitis B Virus Strains Derived Worldwide: Genotypes, Subgenotypes, and HBsAg Subtypes , 2004, Intervirology.

[7]  B. Seong,et al.  Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy , 2003, Journal of medical virology.

[8]  F. Zoulim,et al.  Characterization of two hepatitis B virus populations isolated from a hepatitis B surface antigen–negative patient , 2002, Hepatology.

[9]  T. Berg,et al.  Hepatitis B virus with antigenically altered hepatitis B surface antigen is selected by high‐dose hepatitis B immune globulin after liver transplantation , 1998, Hepatology.

[10]  S. Günther,et al.  A novel method for efficient amplification of whole hepatitis B virus genomes permits rapid functional analysis and reveals deletion mutants in immunosuppressed patients , 1995, Journal of virology.

[11]  L. Poellinger,et al.  The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer. , 1988, Virology.

[12]  P. Tiollais,et al.  Hepatitis B virus. , 1991, Scientific American.

[13]  M. Tong,et al.  Detection of Anti‐HBc IgM Following Prednisone Treatment in Patients with Chronic Active Hepatitis B Virus Infection , 1984, Hepatology.

[14]  C. Trépo,et al.  Deleterious effect of prednisolone in HBsAg-positive chronic active hepatitis. , 1981, The New England journal of medicine.

[15]  E. Sagnelli,et al.  SERUM LEVELS OF HEPATITIS B SURFACE AND CORE ANTIGENS DURING IMMUNOSUPPRESSIVE TREATMENT OF HBsAg-POSITIVE CHRONIC ACTIVE HEPATITIS , 1980, The Lancet.

[16]  A. Williams,et al.  Concurrently circulating hepatitis B surface antigen and heterotypic anti-HBs antibody. , 1976, Journal of immunology.