Research Article

Identification of a mutation in Hepatitis B virus surface antigen capable of evading ELISA screening

Published: July 15, 2016
Genet. Mol. Res. 15(3): gmr7582 DOI: https://doi.org/10.4238/gmr.15037582
Cite this Article:
(2016). Identification of a mutation in Hepatitis B virus surface antigen capable of evading ELISA screening. Genet. Mol. Res. 15(3): gmr7582. https://doi.org/10.4238/gmr.15037582
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Abstract

Hepatitis B virus (HBV) infection can cause HBV-related cirrhosis, liver failure, and hepatocellular carcinoma. At present, a hepatitis B surface antigen (HBsAg) blood test is the primary clinical and diagnostic marker for the identification of a chronic HBV infection. In the current study, we isolated a novel HBV mutant from a chronic HBV patient, capable of causing a false negative test result for most (7 of 8) commercial HBsAg ELISA kits. DNA sequencing of the HBsAg region of this HBV mutant revealed two novel mutation sites that resulted in a Thr-to-Met substitution at amino acid (aa) position 118 and a Lys to Asn substitution at aa position 122 of HBsAg. Moreover, a mutagenesis assay showed that the aa118 (Thr to Met) mutation was the leading cause of the false negative results from the HBsAg ELISA tests. The false negative result was restored, in that the mutation was correctly detected, when the Thr at aa position 118 of this mutated HBsAg was reconstituted. In conclusion, our study revealed a novel aa118 Met mutation of HBsAg HBV that will benefit the future development of HBV diagnosis.

Hepatitis B virus (HBV) infection can cause HBV-related cirrhosis, liver failure, and hepatocellular carcinoma. At present, a hepatitis B surface antigen (HBsAg) blood test is the primary clinical and diagnostic marker for the identification of a chronic HBV infection. In the current study, we isolated a novel HBV mutant from a chronic HBV patient, capable of causing a false negative test result for most (7 of 8) commercial HBsAg ELISA kits. DNA sequencing of the HBsAg region of this HBV mutant revealed two novel mutation sites that resulted in a Thr-to-Met substitution at amino acid (aa) position 118 and a Lys to Asn substitution at aa position 122 of HBsAg. Moreover, a mutagenesis assay showed that the aa118 (Thr to Met) mutation was the leading cause of the false negative results from the HBsAg ELISA tests. The false negative result was restored, in that the mutation was correctly detected, when the Thr at aa position 118 of this mutated HBsAg was reconstituted. In conclusion, our study revealed a novel aa118 Met mutation of HBsAg HBV that will benefit the future development of HBV diagnosis.

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