Human T-cell leukaemia lymphoma virus type 1 syncytium formation is regulated in a cell-specific manner by ICAM-1, ICAM-3 and VCAM-1 and can be inhibited by antibodies to integrin beta(2) or beta(7)

Human T-cell leukaemia/lymphoma virus type 1 (HTLV-1) is a pathogenic retro virus responsible for a number of inflammatory pathologies and adult T-cell leukaemia. Although T-cell tropic in vivo, HTLV-1 can infect a wide variet y of cell types in vitro, Cell-to-cell spread of HTLV-1 may require specifi c binding of envelope to its cellular receptor, with other cell-surface mol ecules facilitating fusion, Here it is shown that intercellular adhesion mo lecule-1 or -3 (ICAM-1, ICAM-3) or vascular cell adhesion molecule-1 (VCAM- 1) are required for syncytium formation of K562 with HTLV-1-infected MT2 ce lls but not C91-PL cells, The effect of ICAMs and VCAM-1 on MT2-induced fus ion can be blocked by antibodies that bind P-integrins, These fusion co-fac tor molecules are effective only when present in combination with HTLV-1 re ceptor-bearing cells and are not sufficient to mediate syncytium formation alone. The results suggest that engagement of HTLV-l-infected cells with su sceptible target cells requires the simultaneous binding of viral envelope glycoprotein to the cellular receptor and co-factor molecules to P-integrin s. The tissue-specific expression of adhesion molecules might therefore inf luence HTLV-1 virus tropism and pathogenic changes associated with syncytiu m formation.