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Fırat Üniversitesi Sağlık Bilimleri Tıp Dergisi
2015, Cilt 29, Sayı 2, Sayfa(lar) 087-090
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Vaccine Escape Mutation due to Using Nucleos(t)id Analog at Chronic Hepatitis B: A Case Report
Müge ÖZGÜLER1, Murat SAYAN2
1Elazığ Eğitim Araştırma Hastanesi, Enfeksiyon Hastalıkları Kliniği, Elazığ, TÜRKİYE
2Kocaeli Üniversitesi, Tıp Fakültesi Hastanesi, Merkez Laboratuvarı PCR Ünitesi, Kocaeli, TÜRKİYE
Keywords: Chronic Hepatitis B, vaccine escape mutation, drug resistance

Chronic hepatitis B is a global public health problem that affected 400 million people all around the world. Currently, hepatitis B virus (HBV) strains which escape from the antibodies formed by vaccines started to be detected and are defined as 'antibodies or immune leakage strains. Goal of treatment in chronic hepatitis B is to prevent progression to the formation of decompensated cirrhosis and liver cancer causing a million deaths per year. The developed antibody response against hepatitis B surface antigen, is an important step for hepatitis B virüs infection control. But, even there is a HBsAg loss, HBV DNA can not be eradicated completely with treatment. Interferons and more potent drugs with optimal resistance potentials are suggested in recently published guidelines for treatment of HBV and it is emphasized that entecavir and tenofovir disoproxil fumarate should be the first step in treatment. HBV polymerase (pol) gene completely coincides with envelopes (S) gene. Nucleos(t)ide analog (NA) resistance mutations occuring at pol gene cause changes in overlapping HBsAg genes. The 'a'determinant of the HBsAg is an important target for protective antibodies response, diagnosis and immunoprophylaxis. These strains were identified as antibodies or immune leakage strains with a mutation in 124 to 149 amino acid position on the 'a' determinant of the S gene. HBV surface antigen synthesis and binding to the antibody varies significantly with S gene mutation and leads vaccinated individuals to become susceptible to infection. In this article; we report a patient with chronic hepatitis B infection caused by vaccine escape mutation who is under treatment and not responding to treatment. We found to oral antiviral induced anti-HBV vaccine leakage mutation (T127P, T189, the I195M) in our patient. Although anti-HBs positivity vaccine escape mutations lead to the formation of disease. This condition leads to be a risk for the individual who is vaccinated for hepatitis B infection in the community.

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