Infants who developed NEC had an increased incidence of norovirus detection in their stool following diagnosis. This further strengthens the case for an etiologic role of norovirus in the pathogenesis of NEC.

ObjectiveTo survey the Aboriginal community of the Northern Territory for antibodies to human T‐lymphotropic virus type I (HTLV‐I) and to describe the distribution of the virus. DesignA sero‐epidemiological study using the Serodia particle‐agglutination assay, indirect immunofluorescence and western blot. Evidence of HTLV‐I‐related diseases was sought through clinicians, and by searching the cancer register and medical records. SeraSamples from 1897 Aborigines, including 1569 sera received by the Royal Darwin Hospital Pathology Department for syphilis serology between March and July 1988. Most of the specimens were from public health surveys and antenatal screening. ResultsNinety‐four samples (5.0%) were positive by the particle‐agglutination assay method but only 36 (1.9%) were positive by both particle‐agglutination assay and indirect immunofluorescence. After confirmation by western blot, the seroprevalence of HTLV‐I was 1.7% (95% confidence interval, 1.2‐2.3%). Western blot positivity was higher in samples from the "Cattle Country" and Alice Springs regions (i.e., 4.7% and 13.9% respectively). ConclusionHTLV‐I is endemic among Aborigines in inland Australia. These serological findings are supported by the recognition of two cases of adult T‐cell leukaemia/lymphoma in this population.

This study tested isolates of human immunodeficiency virus, obtained before and after zidovudine therapy from 10 patients, for susceptibility to the drug in vitro. The isolates collected after therapy were less susceptible to zidovudine as assessed by replication in MT-2 cells and production of reverse transcriptase activity by infected mononuclear leucocytes in the presence of the drug. Furthermore, pretherapy isolates were sensitive to a range of zidovudine concentrations when 100% inhibition was used as the end point. The loss of zidovudine susceptibility did not correlate with any clinical or virologic consequences in this small group of patients.

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