Depression of neutrophil function induced by viruses and its role in secondary microbial infections.
A large body of evidence has accumulated indicating that viruses can predispose animal and human hosts to secondary local and systemic bacterial and fungal disease. The mechanism by which viruses cause these superinfections involves both a direct effect of viruses on the tissues at the site of infection and alterations in cells involved in immune surveillance. The effect of viruses on lymphocytes, monocytes, and macrophages has recently been reviewed. A number of viruses have been shown to depress various functions of polymorphonuclear leukocytes, which are critical for controlling bacterial and fungal infections. The alterations in functions of polymorphonuclear leukocytes induced by different viruses include abnormalities of adherence, chemotaxis, phagocytic, oxidative, secretory, and bactericidal activities. The effect of various viruses on neutrophils and the role that virus-induced neutrophil dysfunction has in predisposing the host to secondary infections are reviewed.
D000818:Animals; D001424:Bacterial Infections / Q000209:etiology*; D006678:HIV / Q000502:physiology; D006518:Hepatitis Viruses / Q000502:physiology; D006564:Herpesviridae / Q000502:physiology; D006801:Humans; D009181:Mycoses / Q000209:etiology*; D009504:Neutrophils / Q000276:immunology*; D009975:Orthomyxoviridae / Q000502:physiology; D010252:Paramyxoviridae / Q000502:physiology; D014777:Virus Diseases / Q000150:complications*; D018406:Virus Physiological Phenomena