Literature DB >> 12091364

Persistence of HTLV-I in blood components after leukocyte depletion.

Joanne Pennington1, Graham P Taylor, Janet Sutherland, Ricardo E Davis, Jerhard Seghatchian, Jean-Pierre Allain, Lorna M Williamson.   

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 log(10) to 4 log(10) removal of HTLV-I Tax DNA by filtration of whole blood and 2 log(10) to 3 log(10) removal across platelet filters with 13 of 16 whole blood and 8 of 8 platelet units still positive after filtration. Despite 3 log(10) to 4 log(10) viral removal, HTLV-I Tax DNA could be detected after whole blood filtration in asymptomatic carriers with viral loads above 10(8) proviral DNA copies/L. T-lymphocyte removal was also between 3.5 log(10) and 4.5 log(10). HTLV-I provirus removal was incomplete in the model system and in asymptomatic carriers with viral loads greater than 10(8) copies/L. These results suggest that LD alone may not provide complete protection from HTLV-I transmission by transfusion.

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Year:  2002        PMID: 12091364     DOI: 10.1182/blood.v100.2.677

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


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