GBV‐C/HGV and HCV infection in mixed cryoglobulinaemia

Recently, a new, suspected hepatotropic virus has been identified. Named GBV‐C/HGV, this virus shares with the hepatitis C virus (HCV) routes of transmission and molecular organization. Indeed, a proportion of HCV‐infected patients (10–25%) are also carriers of GBV‐C/HGV. Since mixed cryoglobulinaem...

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Published in:British journal of haematology 1999-08, Vol.106 (2), p.510-514
Main Authors: Crovatto, Marina, Mazzaro, Cesare, Mishiro, Shunij, Santini, Gianfranco, Baracetti, Stefano, Zorat, Francesca, Pozzato, Gabriele
Format: Article
Language:English
Subjects:
Biological and medical sciences
Biopsy
Bone Marrow Cells - virology
chronic hepatitis
Cryoglobulinemia - virology
Flaviviridae
Hematologic and hematopoietic diseases
Hematology
Hepatitis C - complications
hepatitis C virus
hepatitis G virus
Hepatitis, Viral, Human - complications
Human viral diseases
Humans
Immunoglobulin M - analysis
Infectious diseases
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Liver Function Tests
Medical sciences
mixed cryoglobulinaemia
non‐Hodgkin's lymphoma
Viral diseases
Viral hepatitis
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Summary:Recently, a new, suspected hepatotropic virus has been identified. Named GBV‐C/HGV, this virus shares with the hepatitis C virus (HCV) routes of transmission and molecular organization. Indeed, a proportion of HCV‐infected patients (10–25%) are also carriers of GBV‐C/HGV. Since mixed cryoglobulinaemia (MC) is closely associated with HCV infection, the aim of this study was to determine the prevalence of GBV‐C/HGV infection in MC patients, and to investigate whether the double infection influenced the clinical and/or laboratory aspects of the disease. 52 patients affected by MC were studied. 100 patients affected by HCV‐positive chronic liver disease (CLD) without MC were used as control group. To determine the prevalence of GBV‐C/HGV infection in general population, 150 blood donors were studied, as well as 80 patients affected by non‐A–E CLD. Among the MC patients, only five (9.6%) were positive for both HCV and GBV‐C/HGV infection. No difference was found between patients with and without double infection as regards main clinical and laboratory aspects. Among HCV‐positive CLD cases, 27 were positive for double infection. Among blood donors, the prevalence of GBV‐C/HGV infection was 8.0%, whereas in cases with cryptogenetic CLD the prevalence was 5.0%. In conclusion, these data show that GBV‐C/HGV infection does not play any role in the pathogenesis of MC.
ISSN:0007-1048
1365-2141
DOI:10.1046/j.1365-2141.1999.01556.x