cipient was instigated by undetected HTLV-I in the asymptomatic donor. The possibility of an acquired infection of donor T cells by HTLV-I in the recipient has not been excluded. We propose that the profound immunosuppression attributable to pretransplantation conditioning and prophylaxis against post-transplantation graft-versus-host disease could have accelerated the development of ATL. 2 Even if the donor was a healthy carrier of HTLV-I, proviral integration occurs in only about 0.1 to 1.0 percent of peripheral-blood mononuclear cells. However, although it is "T-cell lymphotropic," HTLV-I can infect extrahematopoietic cell types in vitro.
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Zakowski et al. (2006) studied this question.
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