HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers

León, Bernal; Taylor, Lizeth; Vargas, M C; Luftig, Ronald B.; Albertazzi, Federico J.; Herrero, Libia; Visoná, Kirsten A.

doi:10.1186/1743-422x-2-60

Cited by 24 publications

(4 citation statements)

References 35 publications

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“…We identified high frequency of K130M mutation and A1762T/G1764A double-mutation in 47 para-tumor and central-tumor samples, similar to previous reports [20,32,33]. But no statistically significant differences in these mutation sites were observed between central- and para-tumor tissues, although there were differences in entropy between both sequence datasets.…”

Section: Resultssupporting

confidence: 89%

“…This study detected a high frequency of K130M mutation and A1762T/G1764A double-mutation (approximately 2/3), consistent with previous reports [20,32,33]. But by using conventional data analysis method, no difference in the calculated amino acid frequency or selection between central- and para-tumor isolates was found, which is also consistent with previous study [53].…”

Section: Discussionsupporting

confidence: 92%

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A novel mutant 10Ala/Arg together with mutant 144Ser/Arg of hepatitis B virus X protein involved in hepatitis B virus-related hepatocarcinogenesis in HepG2 cell lines

Shi

Wang

Wang³

et al. 2016

Cancer Letters

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Hepatitis B virus (HBV) infection-related hepatocellular carcinoma (HCC) represents a major health problem worldwide. HBV X (HBx) protein is the most common open reading frame that may undergo mutations, resulting in the development of HCC. This study aimed to determine specific HBx mutations that differentiate the central- and para-tumor tissues, and identify their association with HCC development. HBx gene from HCC tumor and para-tumor tissues of 47 HCC patients was amplified, sequenced and statistically analyzed. A novel combination of 2 mutations at residues 10 and 144 was identified which might play a significant role in HCC development. Expression vectors carrying HBx with the specific mutations were constructed and transfected into HepG2 and p53-null HepG2 cells. Compared to wild type (WT) and single mutation of HBx at residue 10 or 144, the 10/144 double mutations strongly up-regulated p21 expression and prolonged G1/S transition in WT- and p53-null HepG2 cells. Apoptosis was also inhibited by HBx harboring 10/44 double-mutation. Binding of 10/144 double-mutant HBx to p53 was lower than WT HBx. Conclusively, the 10/144 double mutation of HBx might play a crucial role in HCC formation.

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Section: Resultssupporting

confidence: 89%

Section: Discussionsupporting

confidence: 92%

A novel mutant 10Ala/Arg together with mutant 144Ser/Arg of hepatitis B virus X protein involved in hepatitis B virus-related hepatocarcinogenesis in HepG2 cell lines

Shi

Wang

Wang³

et al. 2016

Cancer Letters

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“…HBx with mutations in amino acids 130 and 131 have been frequently reported and may be associated with the severity of chronic hepatitis; these mutations have also been detected in HCC (Yotsuyanagi et al, 2002;Iavarone et al, 2003;Leon et al, 2005), and a recent study of serum samples indicated that these mutations arise before the development of HCC (Kuang et al, 2004). However, the functional consequences of these mutated HBx proteins are still unclear.…”

Section: Hbv-related Hcc D Kremsdorf Et Almentioning

confidence: 99%

Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis

et al. 2006

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As discussed in detail in other chapters of this review, chronic hepatitis B (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC). Most HCCs complicate the evolution of an active or inactive cirrhosis. However, some tumors occur on livers with minimal histological changes; the prevalence of such cases varies from one geographical region to the other, being much higher in the southern half of Africa (around 40% of HCCs) than in Asia, America and Europe, where at least 90% of HCCs are associated with the cirrhosis. This heterogeneity is probably a reflection of different environmental and genetic factors. This review will summarize the current knowledge on the mechanisms involved in HBVrelated liver carcinogenesis. It will show in particular how viruses can be viewed as tools to discover and dissect new cellular pathways involved in cancer development and emphasize the potential synergistic effects between HBV and hepatitis C virus, as well as between viral infections and other environmental factors, such as alcohol.

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“…Penentuan asam amino dengan metode deduksi secara manual dibandingkan dengan urutan parsial asam amino RT DNA polimerase dan protein S HbsAg. Genotipe isolat ditentukan dengan membandingkan hasil sekuensing dengan urutan nukleotida homolog yang didapat dari data GenBank, menggunakan program BLAST (Leon et al, 2005).…”

Section: Analisis Hasil Sekuensingunclassified

IDENTIFIKASI MUTASI PADA DAERAH DNA POLIMERASE DAN HBsAg VIRUS HEPATITIS B

Hindarto

Rostinawati

Retnoningrum

2011

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Infeksi virus hepatitis B (HBV) menyebabkan hepatitis akut dan kronis, dengan angka kematian 1,2 juta per tahun di seluruh dunia. Antivirus analog nukleosida dan vaksinHBV dapat menekan perkembangan infeksi HBV namun penggunaan untuk terapi jangkapanjang dilaporkan menginduksi terjadinya mutasi. Mutasi yang menyebabkan timbulmutan resisten-antivirus dan mutan lolos-vaksin menjadi kendala utama dalam pengobatandan pencegahan infeksi HBV. Telah dilakukan penelitian untuk mengidentifikasi mutasipada gen pengkode reverse transcriptase (RT) DNA polimerase dan HBsAg virus hepatitisB. Penelitian menggunakan 24 sampel cetakan HBV yang berasal dari penderita hepatitisB dari Medan (3), Jakarta (10), Bandung (9), Yogyakarta (1), dan Surabaya (1). Metodeyang dilakukan adalah amplifikasi fragmen gen pengkode DNA polimerase dan HBsAg,konfirmasi produk PCR dengan elektroforesis gel agarosa, pemurnian produk PCR dengan GFX column kit, penentuan urutan nukleotida, dan analisis hasil penentuan urutan nukleotida. Hasil penelitian menunjukkan sampel 12273 dari Jakarta mengalami mutasi di daerah gen pengkode RT DNA polimerase. Mutasi tersebut menyebabkan substitusi asam amino M475L, V519L, L526M, dan M550V. Sampel 12273 juga mengalami mutasi pada gen pengkode HBsAg yang menyebabkan substitusi asam amino M120L, V164L, L171M, dan M195V. Mutasi tersebut terjadi di daerah yang tumpang tindih dengan gen pengkode DNA polimerase, dan di luar determinan a. Mutan diklasifikasikan sebagai mutan resistenantivirus dengan substitusi asam amino ganda L526M dan M550V, dan tidak ditemukan mutasi pada daerah DNA pengkode determinan a.Kata kunci : HBV, RT DNA polimerase, HBsAg, Mutasi

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HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers

Cited by 24 publications

References 35 publications

A novel mutant 10Ala/Arg together with mutant 144Ser/Arg of hepatitis B virus X protein involved in hepatitis B virus-related hepatocarcinogenesis in HepG2 cell lines

A novel mutant 10Ala/Arg together with mutant 144Ser/Arg of hepatitis B virus X protein involved in hepatitis B virus-related hepatocarcinogenesis in HepG2 cell lines

Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis

IDENTIFIKASI MUTASI PADA DAERAH DNA POLIMERASE DAN HBsAg VIRUS HEPATITIS B

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