Background Studies have suggested that HIV-1 may develop thymidine analogue mutations (TAMs) by one of two distinct pathways – the TAM1 pathway (including mutations 41L, 210W and 215Y) or the TAM2 pathway (including mutations 67N, 70R and 219E/Q) – under the pressure of a not fully suppressive thymidine-analogue-containing regimen. Methods Frozen plasma samples stored in the EuroSIDA repository were selected and sent to two central laboratories for genotypic analysis. We considered 733 patients with at least one genotypic test showing ≥1 TAMs (the first of these tests in chronological order was used). TAM1 and TAM2 genotypic profiles were defined in accordance with previous literature. Statistical modelling involved logistic regression and linear regression analysis for censored data. Results The observed frequencies of patterns classifiable as TAM1 or TAM2 profiles were markedly higher than the probabilities of falling into these classifications by chance alone. The chance of detecting a TAM2 profile increased by 25% per additional year of exposure to zidovudine. We found that mutations 67N and 184V were not associated with a particular TAM profile. In the presence of TAM2 profiles, the adjusted mean difference in the 6-month viral reduction was 0.96 log10 copies/ml (95% confidence interval: 0.20; 1.73) higher in patients who started stavudine-containing regimens instead of zidovudine-containing regimens. Conclusions This study provides evidence that the suggested TAM clustering is a real phenomenon and that it may be driven by which thymidine analogue the patients has used. In patients with TAM2-resistant viruses, stavudine appears to retain greater viral activity than zidovudine.

Fever, loss of weight, anaemia, hepatosplenomegaly and lymphadenopathy developed in two HIV-infected patients. At first malignant lymphoma with septicaemia was thought to be the cause. In both patients Salmonella enteritidis was isolated by blood culture and found to be sensitive against the antibiotics that were given (5 g azlocillin and 2 g cefotaxime, three times daily each; additionally in case 2, metronidazole, 500 mg three times daily). Because bone-marrow biopsy demonstrated acid-fast rods, antimycobacterial treatment was started (isoniazid 300 mg/d, rifampicin 600 mg/d, ethambutol 1,200 mg/d and pyrazinamide 2 g/d). Despite this the patients died of septic shock. Histological examination revealed massive amounts of acid-fast rods in spleen, liver, gut and bone marrow. Polymerase chain reaction and sequencing identified the structure as that of the recently discovered M. genavense.

A 40-year-old male chimpanzee had multiple intestinal polyps associated with immature male oxyurid parasites. The gross and histologic characteristics of these lesions were identical to those produced by Nochtia nochti in the stomach and esophagus of Old World primates. It was theorized that the lesions resulted from hypersensitivity to oxyurid infection in an aberrant host.

Nephritis and uremia were diagnosed in an 11-yearold, female chimpanzee. The primary pathologic change was a severe, diffuse glomerulonephritis, and lesions attributable to severe uremia were seen in the pericardium, stomach, small intestine, tongue, thyroid and eyes. The glomerulonephritis was considered probably the post-infectious type.

A 37-year-old woman in acute right heart failure had experienced systemic venous thromboses for 17 years, five miscarriages and repeated pulmonary emboli. For the last 7 years she had been treated symptomatically for pulmonary hypertension. The platelet count was 62,000/microliters, thromboplastin time under phenprocoumon was 22%, partial thromboplastin time was 72 s. Despite anticoagulation with phenprocoumon and heparin (7,500 IU two times daily subcutaneously) new pulmonary emboli occurred and platelet count fell to 12,000/microliters. An increased titre for anticardiolipin antibodies (IgG > 320 GPL U/l, IgM 8 MPL U/l), antinuclear (1:640) and anti-ds-DNA antibodies (> 200 IU/ml) with simultaneous complement consumption suggested secondary antiphospholipid syndrome associated with lupus erythematodes. Treatment with prednisolone (150 mg/d), immunoglobulins (20 mg/d intravenously for 5 days) and heparin (25,000 IU/24 h intravenously) achieved an increase in platelet count to 200,000/microliters within 10 days, but fell again when the prednisolone dose was reduced, recovering under azathioprine, 150 mg/d. Four weeks later the patient died of renewed acute right heart failure.