Respiratory viruses, such as respiratory syncytial virus (RSV), parainfluenza, influenza, coronavirus, and metapneumovirus, have been linked to asthma attacks, new-onset asthma, and a variety of other respiratory conditions, according to research. These viruses cause upper respiratory tract infections such as pneumonia, bronchitis, colds, and asthma. Because respiratory viruses rarely cause asthma in people who lack asthma genes, 90% of the population is immune to virus-induced asthma.
Asthma affects between 5% and 10% of children. Recurrent wheezing, dyspnea, and cough are caused by airway inflammation, excessive mucous production, bronchial hyperreactivity, and reversible airflow obstruction. Asthma exacerbation is increased by viral infections, particularly rhinovirus and RSV. Bronchiolitis affects 20% to 30% of infants in their first year and 10% to 20% in their second.
Understanding the risk factors that lead to asthma progression from infant wheezing to asthma development is critical for targeted prevention and anticipatory guidance after an initial wheezing episode. RSV and RV recurrent wheezing is the most significant risk factor for asthma, according to the majority of data. Wheezing is strongly linked to RSV in infants with severe infections but no history of atopy. There are distinct risk factors for allergic and nonallergic asthma.
Respiratory viruses turn airway epithelial cells into virus factories. Infected cells release inflammatory mediators into the bloodstream, resulting in additional infection. These mediators cause airway inflammation by releasing fluid into intracellular spaces, trapping viruses, and causing cold, allergy, and asthma symptoms. They indirectly attract granulocytes to the airways, where they secrete more mediators, worsening inflammation and cold and asthma symptoms.
Although the cause of RSV and asthma is unknown, one-third of children experience wheezing. The severity of RSV infection is likely the most important risk factor for asthma development after wheezing because of the various disease mechanisms involved in the antiviral response. Viral infections, sensitization, and environmental exposures can all contribute to the development of asthma in susceptible hosts.
Direct infiltration, indirect infiltration, and parasympathetic nerve stimulation can all cause influenza-related asthma. During indirect infiltration, viruses enter the lower airways directly, causing bronchospasm and asthma. By increasing acetylcholine, viruses cause reflex bronchospasm and parasympathetic nerve stimulation. RSV, influenza, and parainfluenza cause epithelial cell damage and the release of inflammatory markers when they infect the lower airways directly.
Viruses, particularly those that affect young children, can alter the immune system and increase the risk of allergies and asthma. Airway secretions contain more Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae after RV infections. Respiratory viruses and the airway bacterial biome may interact to cause or worsen disease.
Understanding how viral infections cause asthma and reducing asthma exacerbations are prevention and treatment goals. Bronchiolitis and wheezing are less common in premature infants who have RSV monoclonal antibodies. In children with RV, eczema, or both, oral steroids given to hospitalized infants with their first wheeze can reduce the risk of recurrent wheeze and asthma. The FDA has approved Omalizumab (Xolair), Mepolizumab (Nucala), Reslizumab (Cinqair), Benralizumab (Fasenra), Dupilumab (Dupixent), and Tezepelumab to treat severe asthma. These monoclonal antibodies have been shown to effectively treat moderate to severe asthma, reducing asthma exacerbations and seasonal variation.
Neutrophils play an important role in the interaction of viral respiratory infections and asthma. The influx of neutrophils into the airway epithelium is high in infants hospitalized with RSV and other viruses. RV infection and allergic inflammation cause asthma and asthma exacerbations. Researchers are looking into genetic factors that may contribute to asthma after a respiratory viral infection. We must first understand these differences to develop primary prevention strategies and novel therapeutics to prevent viral-induced wheeze, asthma, and atopy.
The content of this post is provided for informational purposes only and is not intended as medical advice, or as a substitute for the medical advice of your physician.