Abstract
Cigarette smoking has been shown to increase the risk of respiratory infection, resulting in the exacerbation of infectious disease outcomes. Influenza viruses are a major respiratory viral pathogen, which are responsible for yearly epidemics that result in between 20,000 and 50,000 deaths in the US alone. However, there are limited general summaries on the impact of cigarette smoking on influenza pathogenic outcomes. Here, we will provide a systematic summarization of the current understanding of the interplay of smoking and influenza viral infection with a focus on examining how cigarette smoking affects innate and adaptive immune responses, inflammation levels, tissues that contribute to systemic chronic inflammation, and how this affects influenza A virus (IAV) disease outcomes. This summarization will: (1) help to clarify the conflict in the reports on viral pathogenicity; (2) fill knowledge gaps regarding critical anti-viral defenses such as antibody responses to IAV; and (3) provide an updated understanding of the underlying mechanism behind how cigarette smoking influences IAV pathogenicity.
Highlights
As of 2018, the CDC estimates that current cigarette smokers represent 14% of the US population, representing 34 million Americans [1]
It is important that further studies conducted on the effects of cigarette smoke (CS) on viral loads and clearance standardize a set CS exposure amount and virus type, while titrating viral doses. This would determine whether CS affects viral burden and clearance with a single influenza A virus (IAV) strain, but may help parse the effects of smoking in both mild and severe infections. If we examine the latter option of how CS affects infection, it is possible that, similar to chronic disease, CS exposure may exacerbate infection outcomes by exaggerated inflammatory responses to pulmonary insults
Airway epithelial cells harvested from smokers have lower levels of Type I and II IFN in response to IAV infection compared to healthy cells [57], while exposure to CS extract results in lower type I and type II IFN, IP-10, IL-6, and RIG-I transcription and expression [61,62], suggesting CS has an inhibitory effect on innate immune responses to viral insult in humans
Summary
As of 2018, the CDC estimates that current cigarette smokers represent 14% of the US population, representing 34 million Americans [1]. Besides the direct damage cigarette smoke (CS) can inflict on the pulmonary system, it is a well-known risk factor for the development and exacerbation of infectious diseases such as influenza virus [2,3,4,5]. A direct complicating factor for this study of CS induced disease and complications is that CS is comprised of over 4000 different compounds and toxins This high number of chemicals makes isolation of a single causative agent for pathologies induced by CS extremely difficult and time-consuming. The etiology of smoking’s impact on infection outcomes remains relatively understudied Despite this hurdle, a common thread in the CS induced exacerbation of chronic and infectious disease appears to be acute and chronic (dubbed “low-grade”) inflammation. We will examine the known impact of CS exposure on immune responses critical to influenza infection, the exacerbation of inflammation (local and systemic) during infection in smokers and smoking models, potential CS induced changes in virus replication due to changes in immune response, and potential impacts of low-grade inflammation on influenza disease outcomes
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