Respiratory viruses predisposing to bacterial infections: role of neuraminidase

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Abstract
Viral-bacterial coinfections in humans are well-documented. Viral infections often lead to bacterial superinfections. In vitro and animal models for influenza, as well as molecular microbiology study of viruses and bacteria, provide an understanding of the mechanisms that explain how respiratory viruses and bacteria combine to cause disease. This article focuses on viral and bacterial combinations, particularly synergism between influenza and Streptococcus pneumoniae. Potential mechanisms for synergism between viruses and bacteria include: virus destruction of respiratory epithelium may increase bacterial adhesion; virus-induced immunosuppression may cause bacterial superinfections; and inflammatory response to viral infection may up-regulate expression of molecules that bacteria utilize as receptors. Influenza and parainfluenza viruses possess neuraminidase (NA) activity, which appears to increase bacterial adherence after viral preincubation. Experimental studies demonstrate that viral NA exposes pneumococcal receptors on host cells by removing terminal sialic acids. Other studies show that inhibition of viral NA activity reduces adherence and invasion of S. pneumoniae, independently of effects on viral replication. Clinical studies reveal that influenza vaccination reduces the incidence of secondary bacterial respiratory tract infections. Detection of viral factors (e.g. high NA activity) that increase the likely potential of epidemic/pandemic influenza strains for causing morbidity and mortality from secondary bacterial infections provides new possibilities for intervention. Additional study is needed to identify the mechanisms for the development of bacterial complications after infections with respiratory syncytial virus and other important respiratory viruses that lack NA activity. Prevention of bacterial superinfection is likely to depend on effective antiviral measures.