Effects of serostatus and gender on the HRV-16-induced local immune response

Koch, Rebecca M.; Kox, Matthijs; Pickkers, Peter; Jonge, Marien I. de; Kieboom, Corné van den; Ferwerda, Gerben; Gerretsen, Jelle; Bruggencate, Sandra ten; Hoeven, Johannes G. van der

doi:10.1016/j.vaccine.2016.06.076

Cited by 1 publication

(5 citation statements)

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“…In our study, we only included seronegative subjects, because previous work has demonstrated that serostatus alters both HRV-induced symptom scores[ 16 , 39 ] as well as the HRV-induced immune response, which we showed to be virtually nullified in seropositive subjects[ 29 ]. As such, next to the pathophysiological consequences, our results indicate that a crossover design is neither feasible using a short interval, due to a suppressed innate immune response, nor using a longer interval, due to antibody formation that starts approximately one week after HRV infection[ 16 ] and severely impacts the immune response[ 29 ].…”

Section: Discussionmentioning

confidence: 99%

“…This randomized, placebo-controlled study was part of a larger trial also investigating effects of serostatus and gender on the HRV-induced immune response[ 29 ]. This study is registered at ClinicalTrials.gov (NCT01823640, participant recruitment and follow-up: March-May 2013).…”

Section: Methodsmentioning

confidence: 99%

“…Seven days later, all 40 subjects underwent challenge with HRV-16. For the analyses described in this manuscript, only seronegative subjects were included, as serostatus was shown to exert profound effects on the HRV-induced immune response, which was virtually absent in seropositive subjects[ 29 ]. Furthermore, we did not stratify our analyses for gender, as we found no differences in any parameters between males and females[ 29 ].…”

Section: Methodsmentioning

confidence: 99%

“…We previously showed that the HRV-16 batch used in this study does not result in significant induction of cold symptoms[ 29 ]. Therefore, we focused on lower respiratory tract and systemic symptoms in the current study.…”

Section: Methodsmentioning

confidence: 99%

“…A one-week interval was chosen, as at this time point the innate immune response induced by the first infection is expected to be largely resolved and specific antibodies have not yet been produced to a large extent[ 16 , 27 , 28 ]. We recently demonstrated that seropositivity for HRV is associated with a virtually nullified immune response upon HRV challenge [ 29 ]. Therefore, we only analyzed data from seronegative subjects in the current study.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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IntroductionNaturally, 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.Methods40 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.ResultsInfection 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.ConclusionUpon 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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