SUMMARYThe morphogenesis of yellow fever virus replication was examined in infected Vero cell cultures. Penetration and uncoating occurred by endocytosis with the formation of coated vesicles, similar to that demonstrated for other enveloped and unenveloped viruses. Inclusion bodies associated with newly formed nucleocapsids were evident in the perinuclear region during the growth cycle. No evidence of RNA synthesis in the vicinity of the inclusion bodies was obtained by autoradiography, suggesting that genome replication and assembly of viral nucleocapsids occur at separate cytoplasmic sites. An excessive proliferation of membrane-bound organelles involving both vacuoles and endoplasmic reticula was the most striking feature of virus-infected cells late in infection. No morphological changes in the appearance of nuclei or mitochondria were detected. Virus release appeared to occur by movement of nascent virions through the proliferated endoplasmic reticula followed by exocytic fusion of virus-containing vesicles with the plasmalemma. A possible mechanism whereby the internal nucleocapsid acquires an outer envelope is discussed.

We report the first case of a non-Enterocytozoon bieneusi microsporidial infection in the small intestine of a European AIDS patient with diarrhoea. It

Fifty nine patients seropositive for human immunodeficiency virus

further radioactive substance being given, emission computed tomography of the kidneys was then performed using the same gamma camera connected to an image analysis computer (Gamma-il, Digital Equipment Go) in its rotation mode. Data were collected for 20 s at each of 64 views equally spaced through 360. around the patient. Sagittal sections were then computed (fig 2d,e), which clearly showed that in the left kidney the functioning cortical tissue extended across the middle of the kidney. The radiographs were then reviewed and another ultrasound investigation done, after which it was concluded that the left kidney showed partial reduplication of the collecting system with interposed solid tissue having the characteristics of normal renal parenchyma. The renal abnormality was therefore a hypertrophied column of Bertin. DiscussionThe column of Bertin may be a source of considerable confusion in radiographic investigation of the kidney since it may simulate a renal tumour on an excretion urogram and may require angiography for diagnosis.4 Ultrasonography may be unhelpful, not only if the patient yields poor-quality images owing to, for example, obesity but also because the calyceal appearance in healthy kidneys varies considerably and a small amount of distortion is therefore easily missed. Conventional radionuclide images may also, as in this case, be unhelpful. The usual procedure to determine the nature of the suspected lesion would then be to proceed to selective renal angiography.4 In this case the necessity for this invasive investigation of a healthy kidney was obviated by the clear tomographic radionuclide images obtained. In other patients we have found that emission tomographic imaging of the kidney can be a useful adjunct to other non-invasive studies.5We are grateful to Dr P G Rose, consultant radiologist, for his advice and opinion on this case. Progressive degeneration of the ependymal cell liberates trypomastigotes back into the perivascular space, from which re-entry into the blood may occur. Re-entry to the blood does not take place from any tissues other than the brain and its membranes. References