Epidemiology and Immunopathogenesis of Virus Associated Asthma Exacerbations

Abstract

Asthma is a common airway disease, affecting millions of people worldwide. Although most asthma patients experience mild symptoms, it is characterized by variable airflow limitation, which can occasionally become life threatening in the case of a severe exacerbation. The commonest triggers of asthma exacerbations in both children and adults are viral infections. In this review article, we will try to investigate the most common viruses triggering asthma exacerbations and their role in asthma immunopathogenesis, since viral infections in young adults are thought to trigger the development of asthma either right away after the infection or at a later stage of their life. The commonest viral pathogens associated with asthma include the respiratory syncytial virus, rhinoviruses, influenza and parainfluenza virus, metapneumovirus and coronaviruses. All these viruses exploit different molecular pathways to infiltrate the host. Asthmatics are more prone to severe viral infections due to their unique inflammatory response, which is mostly characterized by T2 cytokines. Unlike the normal T1 high response to viral infection, asthmatics with T2 high inflammation are less potent in containing a viral infection. Inhaled and/or systematic corticosteroids and bronchodilators remain the cornerstone of asthma exacerbation treatment, and although many targeted therapies which block molecules that viruses use to infect the host have been used in a laboratory level, none has been yet approved for clinical use. Nevertheless, further understanding of the unique pathway that each virus follows to infect an individual may be crucial in the development of targeted therapies for the commonest viral pathogens to effectively prevent asthma exacerbations. Finally, biologic therapies resulted in a complete change of scenery in the treatment of severe asthma, especially with a T2 high phenotype. All available data suggest that monoclonal antibodies are safe and able to drastically reduce the rate of viral asthma exacerbations.

Viral infections causing asthma exacerbations in the age of biologics and the COVID-19 pandemic

“…Individuals with asthma, especially those with Th2 endotypes, have impaired antiviral responses making them more susceptible to respiratory viral infections [ 3 , 4 ▪ ]. Moreover, concomitant exposure to allergens and respiratory viruses has a deleterious synergistic effect in clinical outcomes [ 5 ]. At least two mechanisms for this synergy have been identified: allergen-bound immunoglobulin E (IgE) inhibits the type I interferon production by the plasmacytoid dendritic cell and suppressor of cytokine signaling 1 (SOCS-1) produced by type 2 T helper (Th2) and innate lymphoid cells (ILC-2) inhibits the production of antiviral interferons by type 1 T helper (Th1) cells and epithelial cells [ 6 ].…”