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Articles by Pietro Andreone
Total Records ( 2 ) for Pietro Andreone
  Helen Cooksley , Shilpa Chokshi , Yafit Maayan , Heiner Wedemeyer , Pietro Andreone , Richard Gilson , Thomas Warnes , Simona Paganin , Fabien Zoulim , David Frederick , Avidan U. Neumann , Carol L. Brosgart and Nikolai V. Naoumov
  Weak T-cell reactivity to hepatitis B virus (HBV) is thoughtto be the dominant cause for chronic HBV infection. Treatmentwith adefovir dipivoxil (ADV) increases the rate of HBV e antigen(HBeAg) loss; however, the immune mechanisms associated withthis treatment response are not understood. Serial analysisof HBV-specific CD4+ T-cell reactivity was performed during48 weeks of therapy with ADV and correlated with treatment outcomefor 19 HBeAg-positive patients receiving ADV (n = 13) or theplacebo (n = 6). We tested T-cell reactivity to HBV at sevenprotocol time points by proliferation, cytokine production,and enzyme-linked immunospot assays. A panel of serum cytokineswas quantitated by cytokine bead array. ADV-treated patientsshowed increased CD4+ T-cell responses to HBV and lower serumlevels of cytokines compared to those of placebo-treated patients.Enhanced CD4+ T-cell reactivity to HBV, which peaked at treatmentweek 16, was confined to a subgroup of ADV-treated patientswho achieved greater viral suppression (5.3 ± 0.3 log10copies/ml [mean ± standard error of the mean {SEM}] serumHBV DNA reduction from baseline) and HBeAg loss, but not toADV-treated patients with moderate (3.4 ± 0.2 log10 copies/ml[mean ± SEM]) viremia reduction who remained HBeAg positiveor to patients receiving the placebo. In conclusion, T-cellreactivity to HBV increases in a proportion of ADV-treated patientsand is associated with greater suppression of HBV replicationand HBeAg loss.
  Anthony Tanoto Tan , Elisabetta Loggi , Carolina Boni , Adeline Chia , Adam J. Gehring , Konduru S. R. Sastry , Vera Goh , Paola Fisicaro , Pietro Andreone , Christian Brander , Seng Gee Lim , Carlo Ferrari , Florian Bihl and Antonio Bertoletti
  Repertoire composition, quantity, and qualitative functional ability are the parameters that define virus-specific T-cell responses and are linked with their potential to control infection. We took advantage of the segregation of different hepatitis B virus (HBV) genotypes in geographically and genetically distinct host populations to directly analyze the impact that host and virus variables exert on these virus-specific T-cell parameters. T-cell responses against the entire HBV proteome were analyzed in a total of 109 HBV-infected subjects of distinct ethnicities (47 of Chinese origin and 62 of Caucasian origin). We demonstrate that HBV-specific T-cell quantity is determined by the virological and clinical profiles of the patients, which outweigh any influence of race or viral diversity. In contrast, HBV-specific T-cell repertoires are divergent in the two ethnic groups, with T-cell epitopes frequently found in Caucasian patients seldom detected in Chinese patients. In conclusion, we provide a direct biological evaluation of the impact that host and virus variables exert on virus-specific T-cell responses. The discordance between HBV-specific CD8 T-cell repertoires present in Caucasian and Chinese subjects shows the ability of HLA micropolymorphisms to diversify T-cell responses and has implications for the rational development of therapeutic and prophylactic vaccines for worldwide use.
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