Disease severity in respiratory syncytial virus infection: Role of host genetic variation

Abstract

Summary Respiratory syncytial virus (RSV) infection is the most common cause of bronchiolitis and pneumonia in the pediatric population worldwide. The immunopathology of RSV infection varies considerably and severe disease occurs only in a minority of the population. There are many factors (host, viral, and environmental) that contribute to the complicated disease phenotype. In this regard, host factors are decisive for pulmonary susceptibility to RSV infection. Host genetic diversity certainly affects the balance between control of viral replication and tissue damage during RSV infection, consequently impacting on diseases outcome. In this review, we discuss the role of host genetic variation in disease caused by RSV aiming to highlight genetic risk factors for one of the most common diseases in early childhood. Our findings clearly indicate that the response of each individual to infection is influenced by genetic diversity mainly linked to the regulation of host immune responses. Future genetic association and functional studies using more powerful and consistently reproducible approaches will likely be able to confirm, refine, and expand our developing concept of RSV disease pathogenesis.

Transmission of SARS-CoV-2 in domestic cats imposes a narrow bottleneck

“…For example, an infection founded by 1,000 genetically identical viruses would be categorized as resulting from a narrow genetic bottleneck but a relatively large inoculation dose, or population bottleneck. Furthermore, levels of viral genetic diversity have been linked to pathogenesis or clinical outcomes in the context of other viruses (e.g., influenza A virus, polio, and respiratory syncytial virus) and because narrow transmission bottlenecks reduce viral genetic diversity, bottlenecks may play an essential role in the outcome of individual infections in this way as well [48][49][50][51][52] . The relationship between SARS-CoV-2 viral genetic diversity and COVID-19 severity has been discussed, but remains unclear 53,54 .…”

Respiratory syncytial virus infection‐induced mucus secretion by down‐regulation of miR‐34b/c‐5p expression in airway epithelial cells

“…The immune response and clinical manifestations after RSV infection vary greatly among children after RSV infection 6,7 . Moreover, airway obstruction is one of the main clinical manifestations of hospitalization for severe RSV infection 8 .…”

In vivo comparison of a laboratory-adapted and clinical-isolate-based recombinant human respiratory syncytial virus

“…To predict which infants will develop severe LRT disease, it is crucial to understand viral, environmental and host factors that promote or inhibit early viral dissemination. These could include viral or bacterial co-infections [6,7], differences in the respiratory microbiome [8,9] or single nucleotide polymorphisms in immune-associated genes [10].…”