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J. Mellor, G. Haydon, C. Blair, W. Livingstone, P. Simmonds (1998)
Low level or absent in vivo replication of hepatitis C virus and hepatitis G virus/GB virus C in peripheral blood mononuclear cells.The Journal of general virology, 79 ( Pt 4)
X. Zhang, H. Shinzawa, L. Shao, M. Ishibashi, K. Saito, S. Ohno, N. Yamada, H. Misawa, H. Togashi, T. Takahashi (1997)
Detection of hepatitis G virus RNA in patients with hepatitis B, hepatitis C, and non‐A‐E hepatitis by RT‐PCR using multiple primer setsJournal of Medical Virology, 52
H. Alter (1996)
The cloning and clinical implications of HGV and HGBV-C.The New England journal of medicine, 334 23
M. Ikeda, K. Sugiyama, T. Mizutani, T. Tanaka, K. Tanaka, K. Shimotohno, N. Kato (1997)
Hepatitis G virus replication in human cultured cells displaying susceptibility to hepatitis C virus infection.Biochemical and biophysical research communications, 235 3
P. Karayiannis, S. Hadziyannis, J. Kim, J. Pickering, M. Piatak, G. Hess, A. Yun, M. McGarvey, J. Wages, H. Thomas (1997)
Hepatitis G virus infection: clinical characteristics and response to interferonJournal of Viral Hepatitis, 4
tis were HCV positive. We found that only 1 patient positive for Vox Sang 2000;79:247 HGV infection showed chronic hepatitis. HGV RNA was detected in PBMCs of all patients positive for HGV RNA in serum, except for High Prevalence of Hepatitis G Virus in one who showed a faint positivity for the presence of HGV RNA in Multitransfused Sicilian Patients with serum and absence of HGV RNA in PBMCs. Another patient (fig. 1), Beta-Thalassaemia who in 1996 was HGV RNA positive in serum and in PBMCs, tested a a b negative in serum and still faintly positive in PBMCs after treatment Nunzio Cutuli , Gabriella Milana , Salvatore Musumeci for 12 months with recombinant interferon (Roferon Roche) at a dos- Department of Pediatrics, University of Catania, Catania, 2 2 b age of 5 MU/m for 6 months, reduced to 3 MU/m after 6 months. Department of Pediatrics, University of Sassari, Sassari, Italy Our results confirm that polytransfused patients are the most common reservoir of HGV RNA in the world; the transmission of We studied the prevalence of hepatitis G virus (HGV) RNA in this new virus through blood derivates is widely documented [2]. The 100 ß-thalassaemia major patients (46 males, 54 females), aged easy transmissibility of this virus suggests a high viral replication and between 7.5 and 33 years, using a reverse transcription polymerase it seems to help the HCV virus in its cellular introduction [3]. More- chain reaction (RT-PCR) technique in serum and in peripheral blood over, Mellor et al. [4] found a low level of HCV and GBV-C/HGV mononuclear cells (PBMCs) [1]. RNA in PBMCs and suggested that these cells are at most a minor Hepatitis C virus (HCV) antibodies and HCV RNA were found reservoir for virus replication. In our experience, patients HGV RNA in 56 out of 100 patients (56%). HGV RNA was detected in 28 of 100 positive in serum were also HGV RNA positive in PBMCs, except patients (28%). The presence of HGV RNA associated with HCV for 2 cases. In fact, one continued to present a faint positivity of HGV antibodies was detected in 15 of 28 (53.5%) patients. In our experi- RNA only in serum, while the other, negative in the serum after treat- ence, there is no correlation between HGV and chronic hepatitis 2 ment with interferon, was still faintly positive in PBMCs, demon- (¯ = 0.002, p = 0.961), and all patients affected with chronic hepati- strating that the role of interferon therapy in HGV infection is lim- ited [5]. The faint positivity observed in this patient, who was HGV RNA negative in the serum after 3 years from first positivity for HGV RNA with elevation of transaminases, suggests also a role of a reservoir of PBMCs, even if this phenomenon does not have any clin- ical relevance. This has to be confirmed. The high incidence of HGV RNA in the population studied suggests a need for testing donors for HGV RNA even if HGV infection itself does not seem to be a fre- quent cause of chronic liver disease. Acknowledgments This work was supported by a grant of the Sicilian Region (T6/7) for the treatment and prevention of ß-thalassaemia. References 1 Zhang XH, Shinzawa H, Shao L, Ishibashi M, Saito K, Ohno S, Yamada N, Misawa H, Togashi H, Takahashi T: Detection of hepatitis G virus RNA in patients with hepatitis B, hepatitis C and non-A-E hepatitis by RT-PCR using multiple primer sets. J Med Virol 1997;52:385–390. 2 Alter HJ: The cloning and clinical implication of HGV and HGBV. N Engl J Med 1996;334:1536–1537. 3 Ikeda M, Sugiyama K, Mizutani T, Tanaka K, Shimotohono K, Kato N: Hepatitis G virus replication in human cultured cells displaying suscepti- bility to hepatitis C virus infection. Biochem Biophys Res Commun 1997; 235:505–508. 4 Mellor J, Haydon G, Blair C, Livingstone W, Simmonds P: Low level or absent in vivo replication of hepatitis C virus and hepatitis G virus/GB virus C in peripheral blood mononuclear cells. J Gen Virol 1998;79:705– 5 Karayannis P, Hadzyiannis SJ, Kim J, Pickering JM, Piatak M, Hess G, Yun A, McGarvey MJ, Wage J, Thomas HC: Hepatitis G infection: Clini- cal characteristics and response to interferon. J Viral Hepat 1997;4:37–44. Prof. Salvatore Musumeci Department of Pediatrics, University of Sassari Viale S. Pietro, 12, I–01700 Sassari (Italy) Fig. 1. Presence of 229-bp amplified DNA band in the serum (lane 2) and in PBMCs (lane 3) before interferon treatment and in the serum (lane 4) and in PBMCs (lane 5) after interferon treatment. Lane 6 corresponds to PCR negative control and lane 1 and lane 7 to ladder 50-bp GIBCO. Letters to the Editor Vox Sang 2000;79:246–252 247
Vox Sanguinis – Karger
Published: Dec 1, 2000
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