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Short-term repeated HRV-16 exposure results in an attenuated immune response in vivo in humans. | LitMetric

AI Article Synopsis

  • The study examines how repeated exposure to human rhinovirus (HRV) affects immune responses, focusing on innate immunity after an initial infection.
  • Researchers conducted an experiment with 40 healthy subjects, who were first inoculated with HRV-16 and then re-exposed a week later to assess immune response changes.
  • Results show that while primary infection heightened certain immune markers, the second exposure resulted in a weaker immune response, suggesting potential immunological tolerance that might increase susceptibility to future infections.

Article Abstract

Introduction: Naturally, development of adaptive immunity following HRV infection affects the immune response. However, it is currently unclear whether or not HRV re-exposure within a short time frame leads to an altered innate immune response. The "experimental cold model" is used to investigate the pathogenesis of HRV infection and allows us to investigate the effects of repeated exposure on both local and systemic innate immunity.

Methods: 40 healthy male and female (1:1) subjects were nasally inoculated with HRV-16 or placebo. One week later, all subjects received HRV-16. Baseline seronegative subjects (n = 18) were included for further analysis.

Results: Infection rate was 82%. Primary HRV infection induced a marked increase in viral load and IP-10 levels in nasal wash, while a similar trend was observed for IL-6 and IL-10. Apart from an increase in IP-10 plasma levels, HRV infection did not induce systemic immune effects nor lower respiratory tract inflammation. With similar viral load present during the second HRV challenge, IP-10 and IL-6 in nasal wash showed no increase, but gradually declined, with a similar trend for IL-10.

Conclusion: Upon a second HRV challenge one week after the first, a less pronounced response for several innate immune parameters is observed. This could be the result of immunological tolerance and possibly increases vulnerability towards secondary infections.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813921PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191937PLOS

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