The acquired immune deficiency syndrome (AIDS) is now recognized as the end stage of a disease caused by human immunodeficiency virus infection (HIV, formerly LAV/HTLV-III). The Centers for Disease Control (CDC) definition of AIDS only identifies those infected individuals with certain opportunistic infections, tumours or associated diseases who have developed a progressive irreversible immune deficiency.' For every case of AIDS, it has been estimated that there are 30 to 300 individuals infected by the virus, who may exhibit acute or chronic features of the infection, or remain asymptomatic.2 The well recognized risk groups reflect the sexual, parenteral and perinatal routes of transmission of the virus.345 HIV is a double-stranded RNA retrovirus, which on penetration ofa susceptible cell bearing a CD4 antigen receptor (CD = cluster differentiation), makes aDNA copy of itself. This process uses a viral reverse transcriptase enzyme. This proviral DNA is then incorporated into the host genetic material where it may remain latent or periodically produce new RNA copies. New viral particles are assembled from the RNA, core and envelope proteins.6 Isolates of HIV show considerable genetic heterogeneity, particularly in the envelope gene region. Recently a similar virus (LAV-2 or HIV-2) has been isolated from patients with AIDS from West Africa, and two Caucasian homosexual men in Paris. Its morphological and biological features are similar to HIV-1 but it differs in some of its antigenic components, notably the envelope glycoprotein.7'8 The primary defect induced by HIV infection is in cellular immunity. The CD4 antigen expressed by the helper/inducer subset of Tlymphocytes makes them most susceptible to infection. These lymphocytes have a pivotal role in the immune response. Their depletion and/or a functional abnormality which results from HIV infection leads not only to a loss ofcytotoxic T-cell responses but also a reduction of natural killer cell and monocyte function and B cell abnormalities with polyclonal B cell activation, hypergammaglobulinaemia and impairment of specific antibody responses to new antigens.9 In addition, HIV has been shown to infect macrophages, B-lymphocyte cell lines and neuroglial cells.'0 Seroconversion for anti-HIV occurs typically 4-12 weeks after acute infection, although longer delays in the development of antibody and a persistent antigenaemia in the absence ofdetectable antibody have been described. The antibodies produced to HIV core and envelope proteins in vivo are a readily detectable marker of exposure, but have only weak in vitro neutralizing activity and therefore coexist with latent infection and productive viral replication.