The immunology of influenza virus-associated bacterial pneumonia.
Infection with influenza virus has been a significant cause of morbidity and mortality for more than a hundred years. Severe disease and increased mortality often results from bacterial super-infection of patients with influenza virus infection. Preceding influenza infection alters the host's innate and adaptive immune responses, allowing increased susceptibility to secondary bacterial pneumonia. Recent advances in the field have helped to define how influenza alters the immune response to bacteria through the dysregulation of phagocytes, antimicrobial peptides, and lymphocytes. Viral-induced interferons play a key role in altering the phenotype of the immune response. Potential genetic modifiers of disease will help to define additional immunologic mechanisms that predispose to viral, bacterial super-infection with the overarching goal of developing effective therapeutic strategies to prevent and treat disease.
Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA 15261, USA.
Keven M
KM
Robinson
Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA. 15224, USA; Richard K. Mellon Foundation Institute, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, USA. Electronic address: jay.kolls@chp.edu.
Jay K
JK
Kolls
Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA. 15224, USA. Electronic address: john.alcorn@chp.edu.
John F
JF
Alcorn
D000818:Animals; D006801:Humans; D007251:Influenza, Human / Q000150:complications* / Q000276:immunology* / Q000382:microbiology; D009975:Orthomyxoviridae / Q000502:physiology; D009976:Orthomyxoviridae Infections / Q000150:complications / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D010586:Phagocytes / Q000276:immunology; D018410:Pneumonia, Bacterial / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000502:physiology*; D013296:Streptococcus pneumoniae / Q000502:physiology*