Innate Immune Response-Mediated Inflammation in Viral Pneumonia

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Objective This study aims to investigate the intricate interactions between viral infections, specifically within the context of community-acquired pneumonia. We seek to shed light on the underestimation of viral pneumonia cases, utilizing advancements in molecular diagnostic testing.

Methods The investigation involves a comprehensive review of existing literature to explore the prevalence and impact of various viruses causing pneumonia in both children and adults. Our focus spans parainfluenza virus, respiratory syncytial virus, human bocavirus, human metapneumovirus, and rhinoviruses in children and coronaviruses, rhinoviruses, and influenza viruses in adults. The study further delves into the host's innate immune response, emphasizing the roles of pattern recognition receptors (PRRs), type I interferons (IFNs), proinflammatory cytokines, and other immune cells during viral infections.

Results The analysis reveals a substantial global burden of viral community-acquired pneumonia, estimating approximately 200 million cases annually in children and adults combined. This study underscores viruses' significant, previously underestimated role in causing pneumonia. Insights into specific viruses affecting different age groups and their prevalence in various geographical settings are provided.

Conclusion In conclusion, this review emphasizes the necessity of recognizing the substantial contribution of viral infections to community-acquired pneumonia cases. The host's innate immune response, mediated by PRRs, type I IFNs, and other immune mediators, is pivotal in preventing viral invasion and replication. The study accentuates the importance of continued research into understanding the innate immune mechanisms involved in viral infections and the resulting inflammation.

Keywords inflammation - innate immune response - pneumonia - viral infection Publication History

Received: 09 August 2023

Accepted: 27 December 2023

Article published online:
11 March 2024

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