The pathology of respiratory syncytial virus (RSV) infection was evaluated 1 day after an outpatient diagnosis of RSV in a child who died in a motor vehicle accident. We then identified 11 children with bronchiolitis from the Vanderbilt University autopsy log between 1925 and 1959 who met criteria for possible RSV infection in the preintensivist era. Their tissue was re-embedded and evaluated by routine hematoxylin and eosin and PAS staining and immunostaining with RSV-specific antibodies. Tissue from three cases was immunostain-positive for RSV antigen and was examined in detail. Small bronchiole epithelium was circumferentially infected, but basal cells were spared. Both type 1 and 2 alveolar pneumocytes were also infected. Although, not possible for archival cases, tissue from the index case was evaluated by immunostaining with antibodies to define the cellular components of the inflammatory response. Inflammatory infiltrates were centered on bronchial and pulmonary arterioles and consisted of primarily CD69 þ monocytes, CD3 þ double-negative T cells, CD8 þ T cells, and neutrophils. The neutrophil distribution was predominantly between arterioles and airways, while the mononuclear cell distribution was in both airways and lung parenchyma. Most inflammatory cells were concentrated submuscular to the airway, but many cells traversed the smooth muscle into the airway epithelium and lumen. Airway obstruction was a prominent feature in all cases attributed to epithelial and inflammatory cell debris mixed with fibrin, mucus, and edema, and compounded by compression from hyperplastic lymphoid follicles. These findings inform our understanding of RSV pathogenesis and may facilitate the development of new approaches for prevention and treatment.

Human 15S-lipoxygenase-2 (15-LOX-2) is a recently identified lipoxygenase that has approximately 40% sequence identity to the known human 5S-, 12S-, and 15S-lipoxygenases. 15-LOX-2 has a limited tissue dis-Arachidonic acid (AA) metabolites are important mediators of a variety of physiological processes and inflammatory reactions. In addition, alterations in AA metabolism may potentially mediate key steps in certain neoplastic processes. 1-3 AA is metabolized via cyclooxygenase to prostaglandins, prostacyclin, and thromboxane, 4 and via lipoxygenases (LOX) to hydroxyeicosatetraenoic acids (HETEs) or leukotrienes (5-LOX pathway). 5,6 Until recently, three lipoxygenases were recognized in humans: a 5S-LOX found in leukocytes, a 12S-LOX found in platelets and certain epithelia, and a 15S-LOX in reticulocytes, eosinophils, macrophages, and skin. 7 Recently, in studying lipoxygenase expression in human skin, Brash et al 8 discovered a second 15S-lipoxygenase (herein referred to as 15-LOX-2). The cDNA-derived amino acid sequence of 15-LOX-2 showed only 44% identity to 5-LOX and 38% to 39% identity to 12-LOX and the reticulocyte type of 15-LOX

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