Abstract
BACKGROUND: Viral-respiratory infections are the most prevalent illness among humans. A viral infection affecting lower respiratory tract infections (LRTI) is a critical health concern worldwide. The COVID-19 pandemic has significantly impacted respiratory health, particularly in individuals with asthma. Other viral respiratory infections and asthma are critical concerns, either. The current study aimed to discuss how elevated IgE levels can influence viral LRTI and potentially exacerbate asthma symptoms, as well as biological treatments targeting IgE in managing asthma. MATERIALS AND METHODS: The search was conducted in electronical databases (including PubMed, Scopus, Google Scholar, and so on). all obtained documents were listed and reviewed by two independent authors. All relevant studies were included and used for final assessment and data collection. RESULTS: IgE is a crucial mediator in the pathophysiology of asthma, particularly in type 2-high (T2-high) asthma, where it drives allergic responses and airway inflammation. The interaction between COVID-19 and asthma has illustrated that asthmatic patients may experience increased respiratory symptoms following COVID-19 infection. Interestingly, T2-high asthmatics may have had some protection against severe COVID-19 outcomes, highlighting the need for a nuanced understanding of asthma management during and after the pandemic. CONCLUSION: Viral infections, particularly those caused by human rhinoviruses, are a significant trigger for asthma exacerbations. These infections can lead to heightened serum IgE levels, which play a vital role in the immune response and the worsening of asthma symptoms. The Th2 inflammatory pathway is frequently upregulated during these infections, associated with increased production of cytokines such as IL-4, IL-5, and IL-13, which aggravate asthma symptoms. Additionally, viral infections can compromise the airway epithelium, resulting in greater exposure to allergens and irritants, and disrupt the balance between Th1 and Th2 cytokines, leading to more severe exacerbations.