Infection with human T-lymphotropic virus types I and II results in alterations of cellular receptors, including the up-modulation of T-cell counterreceptors CD40, CD54, and CD80 (B7-1).

To examine the phenotypic alterations associated with human T-lymphotropic virus types I and II (HTLV-I and -II) infection, long-term cell lines (n = 12 HTLV-I cell lines; n = 11 HTLV-II cell lines; n = 6 virus-negative cell lines) were analyzed for the cell surface expression of various lineage markers (i.e., myeloid, progenitor, and leukocyte), integrin receptors, and receptor-counterreceptor (R-CR) pairs responsible for cellular activation. As expected, all cell lines expressed the markers characterizing the leukocyte lineage (CD43, CD44, and CD53). Of the progenitor-myeloid markers examined (CD9, CD13, CD33, CD34, and CD63), only the percent expression of CD9 was significantly increased on HTLV-I and -II-infected cell lines as compared with that on virus-negative cell lines. Analysis of the beta 1 integrin subfamily (CD29, CD49b, CD49d, CD49e, and CD49f) showed no significant change, except that CD49e was significantly decreased on the HTLV-infected cell lines. For the beta 2 integrin subfamily, the cell surface density was increased for CD18 and CD11a, while the CD11c molecule was expressed exclusively on the HTLV-I- and HTLV-II-infected cell lines. Analysis of several R-CR pairs (CD2-CD58, CD45RO-CD22, CD5-CD72, CD11a-CD54, gp39-CD40, and CD28-CD80) demonstrated that comparable levels of expression of the Rs (CD2, CD45RO, CD5, and CD28) and of some of the CRs (CD58, CD22, and CD72) were in all cell lines; however, CD54, CD40, and CD80 were expressed constitutively on the HTLV-I- and HTLV-II-infected cell lines. Functionally, the expression of these R-CR pairs did not appear to affect the autologous proliferation since monoclonal antibodies to these R-CR pairs were not able to inhibit proliferation of the infected cell lines. Taken together, our results indicate that HTLV-I and -II can modulate the expression of several T-cell activation molecules and CRs normally expressed on alternate cell types.