The conventional explanation for the high fatality rate due to cytomegalovirus (CMV) pneumonitis among allogeneic transplant recipients is that immunosuppression renders the host unable to control replication of this opportunistic agent. However, evidence from studies in man and the murine model of CMV show that virus replication in the lung is unrelated to the development of pathological effects, and that a host immune response is required for the induction of pneumonitis. Thus the hypothesis is that limited CMV replication in the lungs leads to display of a virus-coded protein, which is recognised by host T-cells, and that the pneumonitis is due to an uncontrolled accumulation and recruitment of such cells in the lungs. The reason why CMV is found in the lungs of patients with the acquired immunodeficiency syndrome (AIDS) without producing pneumonitis is probably because these patients cannot mount the pathogenic T-cell response. According to the hypothesis stated here, if the immune capabilities of AIDS patients can be restored, life-threatening CMV pneumonitis may develop.