Sequential analysis of hepatitis B virus core promoter and precore regions in cancer survivor patients with chronic hepatitis B before, during and after interferon treatment

Rosa Zampino, A. Marrone, G. Cirillo, E. Miraglia Del Giudice, R. Utili, P. Karayiannis, T. J. Liang, G. Ruggiero

Research output: Contribution to journalArticle

Abstract

We analysed the hepatitis B virus (HBV) core-promoter (CP) and precore (PC) regions before, during and after interferon treatment in young Caucasian cancer survivors who had acquired HBV infection during chemotherapy for malignancies. Fourteen patients with chronic hepatitis B [hepatitis B e antigen (HBeAg) /HBV-DNA positive] received α-2a interferon (IFN), 5 MU/m2 t.i.w. for 12 months. HBV CP and PC region sequences were analysed following polymerase chain reaction (PCR) amplification. Sera from responders were studied at: T0 (before starting IFN), T1 [at alanine aminotransferase (ALT) peak preceding HBeAg seroconversion], T2 (at ALT normalization), T3 (at end of IFN) and T4 (at one year after IFN) and in nonresponders at time points T0, T3 and T4. Amplified HBV-DNA was cloned and sequenced automatically. Six of 14 patients (43%) responded to IFN treatment. Five of the six (83%) responders displayed the double CP mutation A1762T/G1764A always in association with a T1753C change. None of the nonresponders showed these mutations at any time point. The G1896A change creating the PC stop codon mutation was never detected in any of the patients. In our cancer survivors, IFN-induced HBeAg/anti-HBe seroconversion appeared to correlate with CP mutations and was not influenced by previous chemotherapy. These mutations in addition to low HBV DNA levels and elevated ALT can be considered favourable factors of response to IFN-induced anti-HBe seroconversion.

Original languageEnglish (US)
Pages (from-to)183-188
Number of pages6
JournalJournal of Viral Hepatitis
Volume9
Issue number3
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Chronic Hepatitis B
Genetic Promoter Regions
Hepatitis B virus
Interferons
Survivors
Hepatitis B e Antigens
Neoplasms
Mutation
Alanine Transaminase
Therapeutics
DNA
Drug Therapy
Terminator Codon
Virus Diseases
Polymerase Chain Reaction
Serum

Keywords

  • Anti-HBe seroconversion
  • Cancer survivors
  • Chronic hepatitis B
  • Core promoter/precore mutations

ASJC Scopus subject areas

  • Hepatology
  • Virology

Cite this

Sequential analysis of hepatitis B virus core promoter and precore regions in cancer survivor patients with chronic hepatitis B before, during and after interferon treatment. / Zampino, Rosa; Marrone, A.; Cirillo, G.; Del Giudice, E. Miraglia; Utili, R.; Karayiannis, P.; Liang, T. J.; Ruggiero, G.

In: Journal of Viral Hepatitis, Vol. 9, No. 3, 2002, p. 183-188.

Research output: Contribution to journalArticle

Zampino, Rosa ; Marrone, A. ; Cirillo, G. ; Del Giudice, E. Miraglia ; Utili, R. ; Karayiannis, P. ; Liang, T. J. ; Ruggiero, G. / Sequential analysis of hepatitis B virus core promoter and precore regions in cancer survivor patients with chronic hepatitis B before, during and after interferon treatment. In: Journal of Viral Hepatitis. 2002 ; Vol. 9, No. 3. pp. 183-188.
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AU - Zampino, Rosa

AU - Marrone, A.

AU - Cirillo, G.

AU - Del Giudice, E. Miraglia

AU - Utili, R.

AU - Karayiannis, P.

AU - Liang, T. J.

AU - Ruggiero, G.

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N2 - We analysed the hepatitis B virus (HBV) core-promoter (CP) and precore (PC) regions before, during and after interferon treatment in young Caucasian cancer survivors who had acquired HBV infection during chemotherapy for malignancies. Fourteen patients with chronic hepatitis B [hepatitis B e antigen (HBeAg) /HBV-DNA positive] received α-2a interferon (IFN), 5 MU/m2 t.i.w. for 12 months. HBV CP and PC region sequences were analysed following polymerase chain reaction (PCR) amplification. Sera from responders were studied at: T0 (before starting IFN), T1 [at alanine aminotransferase (ALT) peak preceding HBeAg seroconversion], T2 (at ALT normalization), T3 (at end of IFN) and T4 (at one year after IFN) and in nonresponders at time points T0, T3 and T4. Amplified HBV-DNA was cloned and sequenced automatically. Six of 14 patients (43%) responded to IFN treatment. Five of the six (83%) responders displayed the double CP mutation A1762T/G1764A always in association with a T1753C change. None of the nonresponders showed these mutations at any time point. The G1896A change creating the PC stop codon mutation was never detected in any of the patients. In our cancer survivors, IFN-induced HBeAg/anti-HBe seroconversion appeared to correlate with CP mutations and was not influenced by previous chemotherapy. These mutations in addition to low HBV DNA levels and elevated ALT can be considered favourable factors of response to IFN-induced anti-HBe seroconversion.

AB - We analysed the hepatitis B virus (HBV) core-promoter (CP) and precore (PC) regions before, during and after interferon treatment in young Caucasian cancer survivors who had acquired HBV infection during chemotherapy for malignancies. Fourteen patients with chronic hepatitis B [hepatitis B e antigen (HBeAg) /HBV-DNA positive] received α-2a interferon (IFN), 5 MU/m2 t.i.w. for 12 months. HBV CP and PC region sequences were analysed following polymerase chain reaction (PCR) amplification. Sera from responders were studied at: T0 (before starting IFN), T1 [at alanine aminotransferase (ALT) peak preceding HBeAg seroconversion], T2 (at ALT normalization), T3 (at end of IFN) and T4 (at one year after IFN) and in nonresponders at time points T0, T3 and T4. Amplified HBV-DNA was cloned and sequenced automatically. Six of 14 patients (43%) responded to IFN treatment. Five of the six (83%) responders displayed the double CP mutation A1762T/G1764A always in association with a T1753C change. None of the nonresponders showed these mutations at any time point. The G1896A change creating the PC stop codon mutation was never detected in any of the patients. In our cancer survivors, IFN-induced HBeAg/anti-HBe seroconversion appeared to correlate with CP mutations and was not influenced by previous chemotherapy. These mutations in addition to low HBV DNA levels and elevated ALT can be considered favourable factors of response to IFN-induced anti-HBe seroconversion.

KW - Anti-HBe seroconversion

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KW - Core promoter/precore mutations

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