HBV mutation literature information.


  Precore/core mutations of hepatitis B virus genotype D arising in different states of infection.
 PMID: 35415256       2022       Clinical and experimental hepatology
Table: S87G


  Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate.
 PMID: 30902704       2019       Antiviral research
Method: The PCR fragment containing the combined 6 core mutations (P5T/S35T/P79Q/E83D/S87G/Q177K) were amplified from pCMVHBV-GYF-L97I and the PCR product was used as primers to mutate pCMVHBV-WT by Q5 mutagenesis, giving rise to plasmid pCMVHBV-WT-6Cmut.
Result: S87G mutation of WT
Result: The mutations within the core protein of GYF mutant include P5T, S35T, P79Q, E83D, S87G, I97L and Q177K.


  The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease.
 PMID: 30406036       2018       Frontiers in cellular and infection microbiology
Table: S87G


  Potential Susceptibility Mutations in C Gene for Hepatitis B-Related Hepatocellular Carcinoma Identified by a Two-Stage Study in Qidong, China.
 PMID: 27727182       2016       International journal of molecular sciences
Discussion: A2159G and A2189Y mutations are missense mutations resulting in an amino acid change of HBcAg codons 87 (S87G) and 97 (I97L/F), respectively.


  Hepatitis B virus core protein variations differ in tumor and adjacent nontumor tissues from patients with hepatocellular carcinoma.
 PMID: 21325784       2012       Intervirology
Abstract: The most frequently occurring mutations in rank were codon P130T (38.8%), I97L (37.8%) and S87G (23.5%).


  [Detection and analysis of gene polymorphism in hepatitis B virus C region].
 PMID: 22097597       2011       Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: Four hepatitis B patients had mutation nt1896 g-->a, and another 4 patients had 2 mutations, namely, S87G and I97F (or 197L) in HBcAg CTL recognition episome.


  Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha.
 PMID: 20959021       2010       Virology journal
Abstract: In this study, we investigated whether HBc protein mutations at hot spots (L60V, S87G and I97L) could still inhibit MxA transcription and the potential significance of this inhibition in virus replication in vitro.
Discussion: Moreover, compared with WT and the other two mutants (L60V, S87G), Discussion: Our data showed that, in Huh7 cells stably expressing WT HBc protein or mutated proteins (L60V, S87G and I97L), IFN-alpha inhibited the extra- and intracellular levels of HBV DNA, and HBsAg secretion to a similar degree to that in the cells transfected with control plasmids.


  [Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. II. Identification of mutations in the core gene by PCR-direct sequencing and ASO probe method].
 PMID: 8952268       1996       Kansenshogaku zasshi
Abstract: The analysis of nucleotide sequences (codon 27-100) of HBV DNA in anti-HBe positive sera showed that there were two hypervariable segments of codon 31-49 and codon 87-97, where amino acid substitutions of L31I, S49T, S87G/N, K96N and I87F/1 frequently occurred regardless of the presence or absence of the mutation in the pre-core region.



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