“…The synergistic severity of disease caused by these infections has been suggested to be due to immunocompromise resulting from HTLV-1 as a result of interferon g expression, and shift from Th2 to Th1 responses, resulting in decreased levels of IL4, IL5, IL13, and IgE [4,[16][17][18][19]. Alternatively, a Strongyloides antigen has been postulated to induce a potent polyclonal T-cell mitogenic response, and reactivation of HTLV-1 expression [1,20].…”