PubMed Health⌕ Search

Biomedical subjects

Francesco Torre

Publications and source records attributed to Francesco Torre.

5 recordsLinked to original sources
PubMed2006

Soluble tumor necrosis factor-related ligand (sTRAIL) levels and kinetics during antiviral treatment in chronic hepatitis C.

Antiviral treatment with pegylated interferon (PEG-IFN) and ribavirin for chronic hepatitis C improved the rates of viral clearance to 56%. An open issue is a better understanding of the factors responsible for the residual lack of response. Our aim was to investigate the effect of antiviral treatments on soluble tumor necrosis factor-related ligand (sTRAIL), which is capable of inducing apoptosis in virus-infected cells. We analyzed sTRAIL levels in 22 naive patients, randomly assigned to receive 6 months of treatment with IFN alone or in combination with amantadine or ribavirin, at baseline, at 6, 12, 24, 30, and 48 h, at days 3, 7, and 14, at 1, 3, and 6 months of treatment, and finally 6 months after the end of treatment. At baseline, the sTRAIL level was significantly higher in patients than in controls (p < 0.0001). The highest sTRAIL release was obtained within the first 12 h, followed by a second peak after the second dose of IFN. There was then a slow decline within the first month. Compared with baseline, high sTRAIL levels were present till day 7 in sustained responders (7 patients) and till the third month of treatment in relapsers or nonresponders (15 patients) (p < 0.02), with no differences related to the type of treatment. The IFN effect on sTRAIL is rapid and intense. The overexpression of TRAIL in viral hepatitis could be seen as a defense mechanism to eliminate infected cells and limit viral replication.

Adult↗
PubMed2005

Interferon beta-1a alone or in combination with ribavirin: a randomized trial to compare efficacy and safety in chronic hepatitis C.

AIM: To compare the efficacy and safety of recombinant human IFN beta-1a alone or in combination with ribavirin in treatment-naive subjects with chronic hepatitis C. METHODS: Open, randomized trial was performed in 6 Italian tertiary centers: 102 of the 108 patients screened were randomized to receive 6 MIU of recombinant human IFN beta-1a subcutaneously daily for 24 wk, alone (Group 1, n = 51) or in combination with ribavirin 1,000 to 1,200 mg/d (Group 2, n = 51). RESULTS: The end-of-treatment virologic response rate was 29.4% in Group 1 and 41.2% in Group 2 (non-significant). Twenty-four weeks after stopping therapy, sustained virologic response rate was 21.6% in Group 1 and 27.4% in Group 2 (non-significant). All subjects in Group 1 completed treatment, while two subjects in Group 2 stopped therapy due to treatment-related adverse events. CONCLUSION: Recombinant human IFN beta-1a, alone or in combination with ribavirin, has an excellent safety profile and, may represent an alternative for chronic hepatitis C patients who are unable to tolerate pegylated alpha-interferon.

Adjuvants, Immunologic↗
PubMed2004

Direct evidence that naturally occurring mutations within hepatitis B core epitope alter CD4+ T-cell reactivity.

Exacerbations of chronic hepatitis B have been associated with accumulation of mutations in the HBV core gene, with amino acid (aa) substitutions clustering between aa 50 and 69. This region of the nucleocapsid protein is known as an immunodominant epitope for CD4+ T-lymphocytes, however the impact of these mutations on T-cell reactivity has not been investigated. For this purpose, we undertook fine mapping of the reactivity of peripheral blood lymphocytes, isolated from patients with acute (n = 8) or chronic hepatitis B (n = 10), against a panel of branched synthetic peptides. The peptide aa sequences corresponded to the wild type HBV (aa 50-69), or contained 1-3 aa changes derived on the basis of naturally occurring mutations. In four of eight patients with acute hepatitis B the wild type peptide 50-69, which corresponded to the core gene sequence of HBV present in these patients, induced a strong T-cell proliferative response. In the same cases, the T-cell response to the mutant peptides was altered at various degrees, depending on the number and the position of aa changes. The most pronounced inhibition of CD4+ T-cell response (between 44 and 92%) was caused by a peptide ligand with two aa substitutions at positions 64 and 67. These results demonstrate that mutations within immunodominant epitopes of the HBV nucleocapsid can affect the CD4+ T-lymphocyte reactivity, which may have a role for the accumulation of certain HBV strains after hepatitis flares during the course of chronic HBV infection.

Adolescent↗