Increased apoptosis and expression of tumor necrosis factor-α caused by infection of cultured human monocytes with dengue virus

• Published in: The American journal of tropical medicine and hygiene Vol. 68; no. 1; pp. 48 - 53
• Main Authors: ESPINA, Luz M, VALERO, Nereida J, HERNANDEZ, Janeth M, MOSQUERA, Jesus A
• Format: Journal Article
• Language: English
• Published: Lawrence, KS Allen Press 2003
• Subjects: Antigens, Viral - analysis; Apoptosis; Arboviroses; Biological and medical sciences; Cells, Cultured; Dengue fevers; Dengue Virus - immunology; Dengue Virus - physiology; Dengue Virus - ultrastructure; Enzyme-Linked Immunosorbent Assay; Fluorescent Antibody Technique, Direct; Human viral diseases; Humans; In Situ Nick-End Labeling; Infectious diseases; Medical sciences; Microscopy, Electron; Monocytes - cytology; Monocytes - immunology; Monocytes - virology; Nitric Oxide - biosynthesis; Tropical medicine; Tropical viral diseases; Tumor Necrosis Factor-alpha - biosynthesis; Viral diseases; Virus; Human; Cell culture; Monocyte; Pathophysiology; Cell death; Dengue group virus; Flaviviridae; Dengue virus; Flavivirus; Tumor necrosis factor α; Apoptosis
• ISSN: 0002-9637; 1476-1645
• DOI: 10.4269/ajtmh.2003.68.48

Dengue (DEN) virus is responsible for one of the most significant viral diseases in tropical countries. Monocytes/macrophages (Mo/Mphi) are the major target cells for DEN virus. To determine the effects of the interaction between DEN virus and Mo/Mphi, human monocyte cultures were infected with DEN virus type 2. Apoptosis and production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide were measured in control and infected cultures. Virus was taken up by phagocytosis, but no membrane-coated pits at the virus attachment sites were observed. Increased number of apoptotic cells and increased production of TNF-a were observed in infected monocyte cultures. No increase in production of nitric oxide was observed. These results may be related to early primary viral infection, in which virus could induce apoptosis in monocytes, but monocytes may contribute to host defense mechanisms against virus by viral phagocytosis, phagocytosis of infected apoptotic cells, and the release of proinflammatory cytokines.