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Blood, 15 July 2002, Vol. 100, No. 2, pp. 677-681
TRANSFUSION MEDICINE
Persistence of HTLV-I in blood components after leukocyte
depletion
Joanne Pennington,
Graham
P. Taylor,
Janet Sutherland,
Ricardo E. Davis,
Jerhard Seghatchian,
Jean-Pierre Allain, and
Lorna M. Williamson
From Department of Haematology, Division of Transfusion
Medicine, University of Cambridge; Imperial College/St Mary's
Hospital, London; and National Blood Service, East Anglia and Brentwood
Centres, United Kingdom.
The human T-cell leukemia virus HTLV-I is a
transfusion-transmissible retrovirus targeting T lymphocytes for which
screening is not currently undertaken in United Kingdom blood donors.
The introduction of universal leukocyte depletion (LD) of the United Kingdom blood supply raises the question as to the degree of protection afforded by this procedure against HTLV-I transmission by blood components. HTLV-I viral DNA removal by leukocyte-depleting filters was
assessed in units of whole blood and platelets by real-time quantitative polymerase chain reaction (PCR) and by nested PCR for
HTLV-I Tax DNA. We examined HTLV-I removal by LD filters
using a model system of blood units containing exogenous spiked
HTLV-I-positive MT-2 cells at a relevant concentration and whole blood
donations from asymptomatic HTLV-I carriers. T-lymphocyte removal was
assessed in parallel by measurement of endogenous subset-specific CD3
mRNA. In the MT-2 model system we observed 3.5 log10 to 4 log10 removal of HTLV-I Tax DNA by filtration of whole
blood and 2 log10 to 3 log10 removal across
platelet filters with 13 of 16 whole blood and 8 of 8 platelet units
still positive after filtration. Despite 3 log10 to 4 log10 viral removal, HTLV-I Tax DNA could be detected after
whole blood filtration in asymptomatic carriers with viral loads above
108 proviral DNA copies/L. T-lymphocyte removal was also
between 3.5 log10 and 4.5 log10. HTLV-I
provirus removal was incomplete in the model system and in asymptomatic
carriers with viral loads greater than 108 copies/L. These
results suggest that LD alone may not provide complete protection from
HTLV-I transmission by transfusion.

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