GB virus type C infection in patients treated for childhood acute lymphoblastic leukemia

Citation
M. Arico et al., GB virus type C infection in patients treated for childhood acute lymphoblastic leukemia, TRANSFUSION, 39(2), 1999, pp. 212-217
Citations number
35
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
TRANSFUSION
ISSN journal
00411132 → ACNP
Volume
39
Issue
2
Year of publication
1999
Pages
212 - 217
Database
ISI
SICI code
0041-1132(199902)39:2<212:GVTCII>2.0.ZU;2-X
Abstract
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 lymp hoblastic leukemia (ALL) or non-Hodgkin's lymphoma. STUDY DESIGN AND METHODS: One hundred forty patients (82 males) aged 4 to 2 7 years (median, 11) diagnosed with ALL between 1976 and 1993, were prospec tively 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 we re significantly higher in patients positive for GBV-C and HCV than in thos e 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 retested: 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 wa s positive for GBV-C RNA and anti-E2 26 months later, while 20 tested negat ive for both. CONCLUSION: GBV-C did not behave as a liver pathogen, because ALT alteratio ns were unrelated to GBV-C status, but, rather, were related to HCV infecti on or coinfection. GBV-C RNA was frequently lost over a relatively short pe riod, though in some cases, it was retained for a longer time. Anti-E2 rare ly coexisted with GBV-C RNA and might be short-term.