Evidence map›Paper›PMID 35415256›Full record

ArticleClinical and experimental hepatology2022

Precore/core mutations of hepatitis B virus genotype D arising in different states of infection.

Neda Sanaei, Seyed Mohammad Ali Hashemi, Seyedeh Zahra Salehi Dehno, Mozhde Mahmoudi Asl, Maryam Moini, Seyed Ali Malek-Hosseini, Seyed Younes Hosseini, Jamal Sarvari

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Article in Clinical and experimental hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Neda Sanaei *Shiraz University of Medical Sciences, Iran.
Seyed Mohammad Ali Hashemi *Shiraz University of Medical Sciences, Iran.
Seyedeh Zahra Salehi DehnoShiraz University of Medical Sciences, Iran.
Mozhde Mahmoudi AslShiraz University of Medical Sciences, Iran.
Maryam MoiniShiraz University of Medical Sciences, Iran.
Seyed Ali Malek-HosseiniShiraz University of Medical Sciences, Iran.
Seyed Younes HosseiniShiraz University of Medical Sciences, Iran.
Jamal SarvariShiraz University of Medical Sciences, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aim of the study: Precore/core variations and liver disease progression have been suggested. In this study, we aimed to determine the frequency of precore/core mutations in hepatitis B virus (HBV)-infected patients at various clinical stages. Material and methods: In total, 73 HBV-infected patients including 26 inactive carriers (IC), 20 chronic active (CA), and 27 patients with liver cirrhosis/hepatocellular carcinoma (C/HCC) were randomly selected. The HBV DNA was extracted from the sera and subjected to nested PCR for amplification of precore/core region. The PCR product was then sequenced by the Sanger method. Results: The stop codon of W28*(G1896A) was determined as the most prevalent mutation (55%) of the precore region. The comparison of groups also demonstrated that core substitutions at residues of S21, E40 and I105 (< 0.05) correlated with the development of the inactive carrier state. Furthermore, the total substitutions in Th epitopes (117-131) were significantly higher in the C/HCC group than the IC and CA groups ( Conclusions: Our results indicated a high frequency of W28* mutation in HBV studied patients. Moreover, variations including S21, E40 and I105 and R151 that were mapped onto cellular epitopes might be related to inactive state development.

Indexed as

corehepatitis B virusprecorevariation

Identifiers

PMID35415256
PMCPMC8984791

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