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Carlo Ferrari

Researcher at University of Parma

Publications -  316
Citations -  27180

Carlo Ferrari is an academic researcher from University of Parma. The author has contributed to research in topics: Hepatitis B virus & Antigen. The author has an hindex of 79, co-authored 298 publications receiving 25130 citations. Previous affiliations of Carlo Ferrari include COMSATS Institute of Information Technology & University of Bologna.

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Journal ArticleDOI

Hepatitis B virus immunopathogenesis

TL;DR: Elucidation of the immunological and virological basis for HBV persistence may yield immunotherapeutic and antiviral strategies to terminate chronic HBV infection and reduce the risk of its life-threatening sequellae.
Proceedings ArticleDOI

Planning optimal grasps

TL;DR: Two general optimality criteria that consider the total finger force and the maximum finger force are introduced and discussed and the geometric interpretation of the two criteria leads to an efficient planning algorithm.
Journal ArticleDOI

The hepatitis B virus persists for decades after patients' recovery from acute viral hepatitis despite active maintenance of a cytotoxic T–lymphocyte response

TL;DR: The results suggest that sterilizing immunity to HBV frequently fails to occur after recovery from acute hepatitis and that traces of virus can maintain the CTL response for decades following clinical recovery, apparently creating a negative feedback loop that keeps the virus under control, perhaps for life.
Journal ArticleDOI

Characterization of hepatitis B virus (HBV)-specific T-cell dysfunction in chronic HBV infection.

TL;DR: A broad spectrum of anti-HBV immunity is expressed by patients with chronic HBV infection and this spectrum is proportional to HBV replication levels and can be improved by blocking the PD-1/PD-L1 pathway.
Journal ArticleDOI

The role of virus-specific CD8(+) cells in liver damage and viral control during persistent hepatitis B virus infection.

TL;DR: Results show that in the presence of an effective HBV-specific CD8 response, inhibition of virus replication can be independent of liver damage and may contribute to liver pathology not only directly but by causing the recruitment of nonvirus-specific T cells.