PubMed · 297000
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M L Green, B L Green. 1979. Aggressive curettage.. https://pubmed.ncbi.nlm.nih.gov/297000/
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OBJECTIVE: To directly infect human fetal intestine with HIV in vitro. DESIGN: Human fetal intestinal explant cultures were exposed to HIV-1 and monitored for evidence of infection by biochemical assay, immunohistochemistry and in situ hybridization. METHODS: Human fetal intestinal explants (14-21 weeks) were established in culture and exposed to HIV-1. Tissue culture fluid was assayed for p24 antigen and reverse transcriptase activity over a 14-day period. Explants were removed from culture on days 4, 7, 10 and 14 postinoculation and subjected (1) to immunohistochemistry to detect p24 and gp160/41 antigens, and (2) to in situ hybridization to detect HIV-1 RNA. Explant tissue culture fluid was cocultured with Jurkat T-cells to detect infectious viral particles. RESULTS: Reverse transcriptase activity and p24 antigen levels in fetal explant culture fluid rose between 7 and 14 days after viral inoculation. Jurkat T-cell cocultures confirmed the presence of infectious virus. Cells in the lamina propria resembling lymphocytes and macrophages of both small intestine and colon stained positively for the viral proteins p24 and gp41. The same type of cells also stained positively for HIV-1 RNA using in situ hybridization. Dual-label immunohistochemistry, combined immunohistochemistry and in situ hybridization confirmed the presence of viral protein and RNA in cells bearing the CD3, CD4 (lymphocyte) or CD68 (macrophage) surface markers. There was no evidence at any time of HIV-1 infection of epithelial cells. CONCLUSIONS: Cells of the lamina propria of the small intestine and colon, bearing lymphocyte or macrophage markers, can be directly infected by and support the replication of HIV-1. Such infection may be implicated in the pathogenesis of HIV enteropathy.
We report the case of a 61-year-old male who presented with a febrile illness accompanied by arthralgia and myalgia. Two months later he developed multiple subcutaneous nodules and enlarged parotid glands. Later two erythematous plaques, clinically compatible with erythema nodosum (EN), were observed. Laboratory investigations revealed abnormal levels of angiotensin converting enzyme and chest radiography showed bilateral hilar enlargement. The biopsy of the cutaneous lesions demonstrated multiple non-caseating granulomas in the subcutaneous tissue without any alterations in the epidermis and the dermis. The cultures for Mycobacteria and fungi were both negative. The clinical picture and histopathological findings were compatible with subcutaneous nodular sarcoidosis. The response to steroid treatment was satisfactory.
A thin horizontal linear area of hyperattenuation that extends laterally from the mediastinal surface of the lung within the area between the inferior pulmonary vein and the diaphragm is a common observation on computed tomographic (CT) scans of the chest. To determine the anatomic basis for this structure, the authors examined four normal human lungs (two right and two left lungs) fixed in an inflated state at pathologic and histologic examination and at CT. The structure in question was identified in one right and two left lungs. The linear area of hyperattenuation seen at CT is a septum of thin, loose intraparenchymal connective tissue that is bounded medially by the base of the pulmonary ligament, where the two sleeves of the visceral pleura appose one another, and laterally by a vertically oriented vein. The septum was identified in 39 of 50 (78%) normal chest CT scans. The pulmonary ligament often appeared to look like a beak at the mediastinal side of the lung. The septum, when visible (n = 39), was bounded medially by the beak in 28 CT scans (72%) and laterally by a vein in 24 scans (62%).