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

Short-term repeated HRV-16 exposure results in an attenuated immune response in vivo in humans.
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Koch RM, Kox M, van den Kieboom C, Ferwerda G, Gerretsen J, Ten Bruggencate S, van der Hoeven JG, de Jonge MI, Pickkers P,


Koch RM, Kox M, van den Kieboom C, Ferwerda G, Gerretsen J, Ten Bruggencate S, van der Hoeven JG, de Jonge MI, Pickkers P, (click to view)

Koch RM, Kox M, van den Kieboom C, Ferwerda G, Gerretsen J, Ten Bruggencate S, van der Hoeven JG, de Jonge MI, Pickkers P,

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PloS one 2018 02 1513(2) e0191937 doi 10.1371/journal.pone.0191937

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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