Hepatitis C virus infection, cryoglobulinaemia, and beyond

D. Sansonno, A. Carbone, V. De Re, F. Dammacco

Research output: Contribution to journalArticle

79 Citations (Scopus)

Abstract

Hepatitis C virus (HCV) infection is the major cause of mixed cryoglobulinaemia (MC), an immune complex (IC)-mediated systemic vasculitis mainly involving the small blood vessels. The precise mechanism of cryoprotein production is currently unknown. HCV virions and non-enveloped core protein participate in the formation of cold-insoluble ICs. Cryoglobulinaemic patients represent a distinct HCV-infected population, in that significant HCV enrichment of lymphoid cells is accompanied by evidence of productive virus infection and increased frequency of B cells. Liver, the major target organ of HCV, is the site of accumulation of inflammatory infiltrates that shares many architectural features with lymphoid tissue and reflects a distorted homeostatic balance between factors that enhance cellular recruitment, proliferation and retention, and those that decrease cellularity (cell death and emigration). There is now overwhelming evidence of a direct contribution to B-cell growth and survival through production of a variety of cytokines and chemokines. Liver tissue over-expression and abnormal circulating levels of B-cell activating factor belonging to the TNF family can provide effective costimulatory mechanisms to sustain the B-cell clonal expansion, which constitutes molecular stigmata of MC. Indolent lymphoproliferation might act as the starting point of chronic, multistage lymphomagenesis. An innovative therapeutic strategy is directed to 'eradication of the virus' and deletion of B-cell clonalities.

Original languageEnglish
Pages (from-to)572-578
Number of pages7
JournalRheumatology
Volume46
Issue number4
DOIs
Publication statusPublished - Apr 2007

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Cryoglobulinemia
Virus Diseases
Hepacivirus
B-Lymphocytes
B-Cell Activating Factor
Cryoglobulins
Christianity
Systemic Vasculitis
Liver
Emigration and Immigration
Lymphoid Tissue
Antigen-Antibody Complex
Chemokines
Virion
Blood Vessels
Cell Survival
Cell Death
Cell Proliferation
Lymphocytes
Cytokines

ASJC Scopus subject areas

  • Neuroscience(all)
  • Rheumatology

Cite this

Hepatitis C virus infection, cryoglobulinaemia, and beyond. / Sansonno, D.; Carbone, A.; De Re, V.; Dammacco, F.

In: Rheumatology, Vol. 46, No. 4, 04.2007, p. 572-578.

Research output: Contribution to journalArticle

Sansonno, D. ; Carbone, A. ; De Re, V. ; Dammacco, F. / Hepatitis C virus infection, cryoglobulinaemia, and beyond. In: Rheumatology. 2007 ; Vol. 46, No. 4. pp. 572-578.
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