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Virus-induced elaboration of proinflammatory cytokines is mediated by virus-induced oxidative stress. The purpose of these studies was to determine the source of the virus-induced oxidative stress. Inhibition of viral replication with antibody to intercellular adhesion molecule-1 had no effect on virus-induced oxidative stress or interleukin-8 (IL-8) response (597+/-88 vs. 668+/-78 pg/mL in control cells). Treatment of cells with diphenylene iodonium inhibited virus-induced oxidative stress and IL-8 elaboration, but allopurinol, ibuprofen, and rotenone had no effect. Studies in cell lines produced from a patient with gp91-phox deficiency revealed normal responses. In contrast, the oxidative response was decreased and the IL-8 concentration was 227+/-36 pg/mL in cells from a patient with p47-phox deficiency, compared with 664+/-48 pg/mL in control cells. These studies suggest that the stimulation of reactive oxygen species by viral challenge occurs at the cell surface even in the absence of viral replication and involves a flavoprotein that may act in concert with p47-phox.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Rhinovirus‐Induced Oxidative Stress and Interleukin‐8 Elaboration Involves p47‐<i>phox</i>but Is Independent of Attachment to Intercellular Adhesion Molecule–1 and Viral Replication

Rhinovirus‐Induced Oxidative Stress and Interleukin‐8 Elaboration Involves p47‐phoxbut Is Independent of Attachment to Intercellular Adhesion Molecule–1 and Viral Replication