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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2426-2427
CORRESPONDENCE
Evidence Against a Direct Role Played by Transfusion-Transmitted
Virus Infection in Causing Hepatic or Hematologic Manifestations
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LETTER |
To the Editor:
Transfusion-transmitted virus (TTV) is a newly described nonenveloped,
single-stranded DNA virus, recently detected with high prevalence in
Japanese patients with fulminant hepatitis and chronic liver disease of
unknown origin.1 Having a high buoyant density (1.26 g/mL) and a single-stranded DNA genome of at least 3,700 bases,2 TTV resembles the Parvoviridae. It could be
argued that, in analogy to Parvovirus B19, which has a remarkable
tropism for human erythroid progenitor cells, TTV-infected hosts may
have hematologic manifestations, including anemia, leukopenia, or
thrombocytopenia.3 However, whether TTV has any role in
causing hepatic and/or hematologic diseases remains an unsettled issue.
Here we report the results of searching for TTV DNA in fasting serum
samples collected from 250 subjects, belonging to the following four
categories: patients with chronic liver disease (N = 49), patients
with coagulopathy (N = 34), intravenous drug users (N = 50), and
nonremunerated blood donors (N = 117).
TTV DNA sequences, determined by polymerase chain reaction
(PCR),4 were detected in 4 of 117 (3.4%) healthy blood
donors and 15 of 133 (11.3%) patients (P = .019). The
prevalence of TTV DNA seropositivity was similar in the three groups of
patients, being 4 of 34 (11.8%) in patients with coagulopathy, 5 of 50 (10.0%) in intravenous drug users, and 6 of 49 (12.2%) in patients
with chronic liver disease (P = .935). There were no
significant differences between TTV DNA+ and TTV
DNA subjects with regard to age (41.7 ± 17.8
v 39.1 ± 14.1 years, mean ± SD; P = .535) and
gender distribution (male/female ratio 13/6 v 78/153;
P = .846).
The rate of positivity for serum markers of infection by known or
presumed hepatotropic viruses in TTV DNA positive subjects is presented
in Table 1. Serum markers for hepatotropic
viruses were present in 16 of 19 TTV DNA+ patients. Twelve
of 19 TTV DNA+ subjects were anti-HCV
antibody+, in comparison with 90 of 231 TTV
DNA (P = .039). In nonremunerated, regular
blood donors, which are selected for being at low risk for infections
by parenterally transmitted viruses, TTV DNA was found in one HGV RNA
positive subject and in one subject with evidence of previous exposure to HAV.
Table 2 shows the relationship between TTV
DNA seropositivity and abnormal serum alanine aminotransferase (ALT)
concentrations. Although TTV DNA+ subjects had more
commonly ALT >1.5-fold the upper limit of the normal reference range
than TTV DNA patients (P = .010), none of the
seven TTV DNA+, anti-HCV subjects had
abnormal ALT. Hemoglobin values, leukocyte count, and platelet count
were similar in TTV DNA+ and TTV DNA
subjects; moreover, none of TTV DNA+ subjects had
hemoglobin level <110 g/L, leukocyte count <4.0 × 109/L, or platelet count <50 × 109/L.
This report confirms that TTV infection has a worldwide distribution
and a surprisingly high prevalence, both in healthy volunteer blood
donors and in groups traditionally considered at risk for parenterally
transmitted viral infections. However, it also casts doubts that
prospective screening of blood donors for TTV will ever be indicated,
at least for the purpose of avoiding posttransfusion hepatitis. In
fact, none of TTV-infected blood donors had alanine aminotransferases
above normal limits. Moreover, although among subjects belonging to
groups at risk the presence of TTV DNA is accompanied by abnormal
alanine aminotransferase in approximately 40% of cases, this might be
entirely due to the frequent coexistence, in these populations, of
infection by HCV, an agent routinely tested for by blood banks.
Finally, none of the TTV-infected subjects had anemia, leukopenia, or thrombocytopenia.
The risk for viral transmission by transfusion has been reduced
dramatically through improved techniques for selecting and testing
blood donors.5 Initiatives to further improve the safety of
the blood supply, including more stringent donor qualifications, additional testing for infectious disease markers, viral inactivation processes, and refinement of transfusion decisions are possible. However, because the risk for viral transmission by allogeneic transfusion is already low, additional measures will have a predictably limited yield and poor cost-effectiveness.6 Although
efforts to improve the safety of blood supply will continue, to
minimize the risks of transmitting by blood transfusion the next (yet
undiscovered) agent, we will have no other choice than a judicious use
of blood and blood components.
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ACKNOWLEDGMENT |
The authors are grateful to Dario Liani and Tiziana Galai for excellent
technical support.
Pierluigi Toniutto
Carlo Fabris
Edmondo Falleti
Tiziana Lombardelli
Vinicio Gasparini
Giovanni Barillari
Franco Biffoni
Mario Pirisi
Department of
Experimental and Clinical Pathology and Medicine (DPMSC)
University
of Udine
Blood Bank
Udine General Hospital
Udine,
Italy
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REFERENCES |
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A novel DNA virus (TTV) associated with elevated transaminase levels in posttransfusion hepatitis of unknown etiology.
Biochem Biophys Res Commun
241:92, 1997[Medline]
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Okamoto H, Nishizawa T, Kato N, Ukita M, Ikeda H, Iizuka H, Miyakawa Y, Mayumi M:
Molecular cloning and characterization of a novel DNA virus (TTV) associated with post-transfusion hepatitis of unknown aetiology.
Hepatology Res
10:1, 1998
3.
Young N:
Hematologic and hematopoietic consequences of B19 parvovirus infection.
Semin Haematol
25:159, 1988[Medline]
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4.
Naoumov NV, Petrova EP, Thomas MG, Williams R:
Presence of a newly described human DNA virus (TTV) in patients with liver disease.
Lancet
352:195, 1998[Medline]
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Schreiber GB, Busch MP, Kleinman SH, Korelitz JJ:
The risk of transfusion-transmitted viral infections.
N Engl J Med
334:1685, 1996[Abstract/Free Full Text]
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Holland PV:
Viral infections and the blood supply.
N Engl J Med
334:1734, 1996[Free Full Text]
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