Immune Response to Respiratory Viral Infections

Abstract

The respiratory system is constantly exposed to viral infections that are responsible for mild to severe diseases. In this narrative review, we focalized the attention on respiratory syncytial virus (RSV), influenza virus, and severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infections, responsible for high morbidity and mortality in the last decades. We reviewed the human innate and adaptive immune responses in the airways following infection, focusing on a particular population: newborns and pregnant women. The recent Coronavirus disease-2019 (COVID-19) pandemic has highlighted how our interest in viral pathologies must not decrease. Furthermore, we must increase our knowledge of infection mechanisms to improve our future defense strategies.

Keywords: RSV; SARS-CoV-2; immune response; influenza; newborns; pregnant women; respiratory viral infection.

Figure 1

Representation of the immune response during respiratory viral infections. First, the virus activates an innate immune response constituted by structural cells (i.e., epithelial and mesenchymal cells), chemical barriers (mucus produced by goblet cells), and several immune cells (i.e., alveolar macrophages (AMs), innate lymphoid cells (ILCs), dendritic cells (DCs), neutrophils). Interferons (IFNs), cytokines (such as IL-6 and TNF-α), and chemokines (such as CCL2 and CCL3) also promote viral clearance. The adaptive immune response starts in the draining lymph nodes after interacting with specific cells (i.e., T CD4 and T CD8 cells, B cells) and the antigen-presenting cells (APCs).

Figure 2

Role of cytokines and chemokines during respiratory viral infections in particular populations (newborns and pregnant women). RSV inhibits IFN-α/β signaling, while it induces upregulation of some cytokines (i.e., IL-6, TNF-α) and chemokines (i.e., CXCL10, CXCL8, CCL2, CCL3, CCL5). During influenza type-1, IFNs, and TNF-α are crucial in limiting viral replication. SARS-CoV-2 infection in newborns was related to high levels of IL-1β, IL-6, and IFN-γ.