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As part of the Medical Research Council prospective study of the neurological complications of HIV infection, neurophysiological tests of spinal cord and peripheral nerve function were recorded in a cohort of homosexual or bisexual men. The studies included motor and sensory nerve conduction studies, vibration perception thresholds, somatosensory evoked potentials and motor evoked potentials elicited by magnetic stimulation. The results were compared with markers of immune function. The findings from 114 volunteers were analysed in a cross-sectional study. Fifty-nine were HIV-seropositive but asymptomatic, 26 had progressed to the symptomatic stages of HIV disease and 29 were persistently HIV-seronegative. There was some evidence of a mild sensory axonopathy in the symptomatic HIV-seropositive group. No differences were detected between the asymptomatic HIV-seropositive group and the HIV-seronegative comparison group. There were no consistently significant correlations between the neurophysiological measurements and CD4 counts and ß2-microglobulin levels. On repeated testing, there was no evidence of a trend towards deterioration over a mean period of approximately 3 years in 36 HIV-seropositive subjects who remained asymptomatic compared with 22 HIV-seronegatives. These findings have failed to demonstrate neurophysiological evidence of spinal cord or peripheral nerve dysfunction in the asymptomatic stages of HIV infection.

The purpose of this study was to examine by proton spectroscopy for any difference in cerebral metabolites in patients taking part in the Concorde study (comparing the efficacy of immediate versus deferred treatment with zidovudine on asymptomatic HIV infected individuals). Forty seven HIV positive male patients [29 immediate, 18 deferred zidovudine] were examined in the last 9 months of the therapeutic trial. Magnetic resonance imaging and proton spectroscopy were performed at 1.5 Tesla using a single voxel placed in the parieto-occipital white matter. No significant difference was found in metabolite ratios comparing immediate versus deferred zidovudine (NA/NA+Cho+Cr 0.52 vs. 0.52). High quality spectra were acquired in relatively large numbers of patients and logistically spectroscopy may be applied to clinical therapeutic studies.

Thirteen patients with AIDS or ARC on continuous zidovudine therapy (800–1200 mg daily), who developed severe anaemia (median Hb 7.9g dl−1range 4.9–9.4) after 66 days of treatment (median, range 35–258) were then treated with an intermittent regimen in an open study. The regimen consisted of cycles of 4 weeks on treatment (600–100 mg daily) followed by 2 weeks off. Intermittent treatment was tolerated for a significantly longer period of time (median 257 days range 72–603) and a higher cumulative does (P< 0.001). Four patients discontinued intermittent therapy in the period of follow-up, three due to bone marrow suppression. Eight of 13 patients needed red cell transfusions on continuous therapy compared to only one on the intermittent regimen. On intermittent therapy median haemoglobin concentration and neutrophil counts remained stable (Hb median 11.9g dl−1range 9.1–14.8, neut. median 1.7 × 109I−1range 0.6–4.3). Ten patients had detectable levels of P24 antigen which decreased from a median of 128 pg ml−1(range 15–242) to 24 pg ml−1(range 0–53) on continuous therapy. Subsequently, in eight of these patients on the intermittent regimen, levels of P24 Ag remained below 50% of initial pretreatment values (median 28 pg ml−1range 0–178) or below 50 pg ml−1.

The epidemiological, immunological and early virological observations on the acquired immune deficiency syndrome (AIDS) suggested that an agent was involved which was sexually, parenterally and perinatally transmitted and perhaps tropic for T helper lymphocytes. A new subgroup of human T lymphotropic retroviruses have been identified and seroepidemiological studies suggest that they are aetiologically related to AIDS. The syndrome is characterised by the development of tumours: such as Kaposi's sarcoma and non-Hodgkins lymphoma. with an aggressive clinical course and infection by a wide spectrum of opportunistic organisms, Both the tumours and the infections commonly involve the gut.

Four patients with acquired immunodeficiency syndrome (AIDS) (CDC group IV) were investigated for biliary disease because of the presence of both severe upper abdominal pain and raised levels of serum alkaline phosphatase. None was clinically jaundiced. Upper abdominal ultrasound was abnormal in three. All had endoscopic retrograde cholangiographic evidence of both an intrahepatic sclerosing cholangitis suggestive of primary sclerosing cholangitis and an irregular suprapapillary common bile duct dilation suggestive of papillary stenosis. Three had evidence of gastrointestinal cryptosporidiosis and two of disseminated cytomegalovirus infection. Endoscopic sphincterotomy, performed in two patients, gave good pain relief. We propose the name 'AIDS sclerosing cholangitis' for this form of secondary cholangitis. The cause of this disorder remains unclear. Recent evidence is discussed which suggests that it is not due to HIV itself but to an opportunistic infection. Cryptosporidium appears to be the most likely candidate.

Atevirdine is a nonnucleoside reverse transcriptase inhibitor of human immunodeficiency virus type 1 (HIV-1). In this study we investigated the effect of atevirdine in asymptomatic antiretroviral naive HIV-infected patients with CD4+ cell counts of between 200 and 750 cells per mm3. Patients were randomized to receive 600 mg of atevirdine (n = 15) or a placebo (n = 15) three times a day for 12 weeks. There was no statistically significant effect of atevirdine on viral loads (HIV p24 antigen and HIV-1 RNA levels by PCR) or CD4+ cell counts. The data do not support the use of atevirdine as a monotherapy in the treatment of HIV-infected patients.

Lymph node biopsy was performed in 39 homosexual men with unexplained persistent generalized lymphadenopathy (PGL). Thirtyseven (95 per cent) of these patients had antibodies to human Tlymphotropic virus type III (HTLV-III), at the time of biopsy. Histology in all but one showed only follicular hyperplasia, the exception showed caseating granulomata typical of tuberculosis. Clinical differentiation between lymphadenopathy associated with HTLV-III and other causes of generalized lymphadenopathy is difficult; however, the presence of antibodies to HTLV-III probably identifies patients in whom surgical biopsy will only occasionally reveal a specific histological diagnosis. It is suggested that the presence of antibodies to HTLV-III in patients with PGLjustifies a more selective approach to lymph node biopsy.