The influenza virus is a significant cause of morbidity in children. Severe infection most often develops in children under 5 years of age and is accompanied by wheezing and crackles that require oxygen support. In some cases, respiratory failure becomes the cause of death.
An early innate immune response is a critical factor in protection against the influenza virus. Type I interferons (IFN-I) are immune signaling proteins that initiate antiviral defense mechanisms in response to infection. The most extensively studied IFN-I subtypes are IFN-α and IFN-β.
The influenza virus can suppress IFN-I production. A deficiency in type I interferon increases the severity of influenza infection.
For a long time, it remained unclear whether a child would develop a severe form of influenza requiring hospitalization or experience a mild illness managed on an outpatient basis. In 2019, Brazilian researchers identified an association between IFN-I levels in the nasal epithelium of children and the severity of influenza infection.
Study Design
The study included 100 children admitted to the emergency department. During diagnostic evaluation, each child was assessed for clinical signs of influenza, and the final diagnosis was confirmed by PCR testing.
Nasal secretion samples were also collected from all children to determine nasal IFN-I levels. The nasal compartment was of particular interest because it represents the primary site of influenza virus entry. Previous studies had shown a weak correlation between interferon levels in the nasal mucosa and in blood serum.
Based on disease severity, children were divided into three groups:
- children with severe influenza requiring hospitalization;
- children with mild flu managed on an outpatient basis;
- control group – children receiving treatment for other conditions.
Results
Children with mild influenza had significantly higher levels of interferon alpha in the nasal cavity – 263.2 pg/mL – compared with undetectable levels in the other two groups. A similar pattern was observed for interferon beta.
The researchers concluded that children with mild influenza produce substantial amounts of IFN-I in the nasal mucosa, which alleviates disease severity. Previous studies have shown that insufficient endogenous production of type I interferon predisposes individuals to more severe influenza infection.
The researchers also noted that hospitalization was required only for children younger than 6 months. This finding is likely related to the innate immune system’s immaturity at this age.
Taken together, these results indicate that nasal type I interferon levels may serve as a novel prognostic test for influenza severity in children. Such a test could support the development of more effective treatment strategies and reduce the frequency of complications. In addition, this study may guide future research aimed at correcting IFN-I deficiency in children.
Conclusions
High nasal IFN-I levels are associated with less severe influenza infection in children. Hospitalized children exhibit undetectable levels of nasal type I interferon. Measurement of IFN-I in the nasopharynx may help identify the risk of severe influenza and enable early initiation of appropriate treatment. Correction of IFN-I deficiency in children is a potential strategy to prevent severe flu.
Reference
Evaluation of nasal levels of interferon and clinical severity of influenza in children
