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GB virus type C infection in patients treated for childhood acute lymphoblastic leukemia
Author(s) -
Aricò Maurizio,
Bissolati Morena,
Bossi Grazia,
Asti Margherita,
Cerino Antonella,
Caselli Désirée,
Ricci Antonio,
Klersy Catherine,
Silini Enrico,
Mondelli Mario U.
Publication year - 1999
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1999.39299154738.x
Subject(s) - gb virus c , medicine , hepatitis c virus , flaviviridae , lymphoma , antibody , gastroenterology , virus , leukemia , viral disease , lymphoblastic leukemia , immunology , virology
BACKGROUND: The purpose of this study was to determine the prevalence of GB virus type C (GBV‐C) infection in subjects treated for childhood acute lymphoblastic leukemia (ALL) or non‐Hodgkin's lymphoma. STUDY DESIGN AND METHODS: One hundred forty patients (82 males) aged 4 to 27 years (median, 11) diagnosed with ALL between 1976 and 1993, were prospectively followed for a median of 5 years (range, 0.1–17) after completion of therapy. Stored sera were tested for antibody to hepatitis C virus (HCV), HCV RNA, antibody to GBV‐C E2 (anti‐E2), and GBV‐C RNA. RESULTS: Thirty‐eight patients (27%) were exposed to GBV‐C: 30 were positive for GBV‐C RNA (mostly type 2) and 8 were positive for anti‐E2. Anti‐E2 and GBV‐C RNA were mutually exclusive: 61 patients (43%) were positive for HCV RNA, 16 (11%) were coinfected with GBV‐C and HCV. Alanine aminotransferase (ALT) levels were increased (>35 mU/mL) in 32 (23%) of 137:3 of 20 who were positive for GBV‐C and negative for HCV, 7 of 15 who were positive for GBV‐C and HCV, 15 of 44 who were negative for GBV‐C and positive for HCV, and 7 of 58 who were negative for GBV‐C and HCV (p<0.001). Median ALT values were significantly higher in patients positive for GBV‐C and HCV than in those who were positive for GBV‐C and negative for HCV (35 vs. 13 mU/mL, p = 0.003). Thirty‐one of 38 patients with GBV‐C markers were re‐tested: GBV‐C RNA was lost in 16 of 30 tested, but 7 were still GBV‐C RNA positive up to 50 months later, 3 tested positive for anti‐E2 up to 27 months later, and 1 was positive for GBV‐C RNA and anti‐E2 26 months later, while 20 tested negative for both. CONCLUSION: GBV‐C did not behave as a liver pathogen, because ALT alterations were unrelated to GBV‐C status, but, rather, were related to HCV infection or coinfection. GBV‐C RNA was frequently lost over a relatively short period, though in some cases, it was retained for a longer time. Anti‐E2 rarely coexisted with GBV‐C RNA and might be short‐term.