Persistence of HTLV-I in blood components after leukocyte depletion

Author:

Pennington Joanne1,Taylor Graham P.1,Sutherland Janet1,Davis Ricardo E.1,Seghatchian Jerhard1,Allain Jean-Pierre1,Williamson Lorna M.1

Affiliation:

1. 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.

Abstract

Abstract 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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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