BACKGROUND: Transfusion-transmitted hepatitis B virus (HBV) infection in recipients with drug-related immunodeficiency is rarely described in endemic areas. Hepatitis B surface antigen (HBsAg)-negative infectious donor blood can be identified by sensitive nucleic acid testing (NAT). Two immunodeficient patients who received blood components from a single seronegative blood donor subsequently found to contain HBV DNA are described. MATERIALS AND METHODS: Multiple samples from the implicated donor and the two recipients were tested for HBV serologic and molecular markers. HBV genome fragments were amplified, sequenced, and phylogenetically analyzed. RESULTS: The implicated donation had low-level HBV DNA due to the donor being in the window period before the donor's seroconversion. Recipient 1 had been vaccinated to HBV and carried anti-HBs but remained negative for all other HBV markers until she developed acute hepatitis B (viral load 2.7 x 10(8) IU/mL and alanine aminotransferase [ALT] level 1744 IU/L) 13 months after transfusion of red cells. Identical HBV sequences from both donor and recipient provided evidence of transfusion-related infection. Recipient 2, who received platelets from the same donation while receiving major chemotherapy, remained uninfected. CONCLUSIONS: In unusual circumstances, HBV incubation time can be considerably prolonged. Both active and passive neutralizing antibodies to HBV likely delayed, but did not prevent, acute infection when the immune system was impaired. HBV NAT may have interdicted the infectious unit, although the donation viral load could not be quantified and odds of detection calculated.
BACKGROUND: Transfusion-transmitted hepatitis B virus (HBV) infection in recipients with drug-related immunodeficiency is rarely described in endemic areas. Hepatitis B surface antigen (HBsAg)-negative infectious donor blood can be identified by sensitive nucleic acid testing (NAT). Two immunodeficientpatients who received blood components from a single seronegative blood donor subsequently found to contain HBV DNA are described. MATERIALS AND METHODS: Multiple samples from the implicated donor and the two recipients were tested for HBV serologic and molecular markers. HBV genome fragments were amplified, sequenced, and phylogenetically analyzed. RESULTS: The implicated donation had low-level HBV DNA due to the donor being in the window period before the donor's seroconversion. Recipient 1 had been vaccinated to HBV and carried anti-HBs but remained negative for all other HBV markers until she developed acute hepatitis B (viral load 2.7 x 10(8) IU/mL and alanine aminotransferase [ALT] level 1744 IU/L) 13 months after transfusion of red cells. Identical HBV sequences from both donor and recipient provided evidence of transfusion-related infection. Recipient 2, who received platelets from the same donation while receiving major chemotherapy, remained uninfected. CONCLUSIONS: In unusual circumstances, HBV incubation time can be considerably prolonged. Both active and passive neutralizing antibodies to HBV likely delayed, but did not prevent, acute infection when the immune system was impaired. HBV NAT may have interdicted the infectious unit, although the donation viral load could not be quantified and odds of detection calculated.
Authors: Angelita Silva de Miranda Corrêa; Letícia Martins Lamarão; Priscilla Cristina Moura Vieira; Renata Bezerra Hermes de Castro; Núbia Caroline Costa de Almeida; Jairo Augusto Américo de Castro; Maria Salete Maciel de Lima; Mauricio Koury Palmeira; Ana Luiza Langanke Pedroso Meireles; Rommel Rodríguez Burbano Journal: PLoS One Date: 2018-12-19 Impact factor: 3.240