scholarly journals An Overview of Innate Immune Response to Human Rhinovirus Infection

2021 ◽  
Vol 2 (3) ◽  
pp. 75-85
Author(s):  
Shuaibu Abdullahi Hudu
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Human Rhinovirus ◽  
Rhinovirus Infection

The suppression of innate immune response by human rhinovirus C

2017 ◽  
Vol 490 (1) ◽  
pp. 22-28 ◽  
Author(s):  
Li-li Pang ◽  
Xin-hui Yuan ◽  
Chang-sheng Shao ◽  
Mao-zhong Li ◽  
Ying Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Human Rhinovirus ◽  
Rhinovirus C

259 Antagonism of the innate immune response by human rhinovirus 1a

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 301
Author(s):  
Jennifer Drahos ◽  
Vincent Racaniello
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Human Rhinovirus

scholarly journals Cleavage of IPS-1 in Cells Infected with Human Rhinovirus

2009 ◽  
Vol 83 (22) ◽  
pp. 11581-11587 ◽  
Author(s):  
Jennifer Drahos ◽  
Vincent R. Racaniello
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Sendai Virus ◽  
Innate Immune ◽  
Human Rhinovirus ◽  
Type I ◽  
Human Pathogens ◽  
Infected Cells ◽  
In Cells

ABSTRACT Rhinoviruses are prevalent human pathogens that are associated with life-threatening acute asthma exacerbations. The innate immune response to rhinovirus infection, which may play an important role in virus-induced asthma induction, has not been comprehensively investigated. We examined the innate immune response in cells infected with human rhinovirus 1a (HRV1a). Beta interferon (IFN-β) mRNA was induced in HRV1a-infected cells at levels significantly lower than in cells infected with Sendai virus. To understand the basis for this observation, we determined whether components of the pathway leading to IFN-β induction were altered during infection. Dimerization of the transcription factor IRF-3, which is required for synthesis of IFN-β mRNA, is not observed in cells infected with HRV1a. Beginning at 7 h postinfection, IPS-1, a protein that is essential for cytosolic sensing of viral RNA, is degraded in HRV1a-infected cells. Induction of apoptosis by puromycin led to the cleavage of IPS-1, but treatment of HRV1a-infected cells with the pan-caspase inhibitor, zVAD, did not block cleavage of IPS-1. IPS-1 is cleaved in vitro by caspase-3 and by the picornaviral proteinases 2Apro and 3Cpro. Expression of HRV1a and polioviral 2Apro and 3Cpro led to degradation of IPS-1 in cells. These results suggest that IPS-1 is cleaved during HRV1a infection by three different proteases. Cleavage of IPS-1 may be a mechanism for evasion of the type I IFN response, leading to a more robust infection.

scholarly journals Rhinovirus infection results in stronger and more persistent genomic dysregulation: Evidence for altered innate immune response in asthmatics at baseline, early in infection, and during convalescence

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0178096 ◽  
Author(s):  
Peter W. Heymann ◽  
Huyen-Tran Nguyen ◽  
John W. Steinke ◽  
Ronald B. Turner ◽  
Judith A. Woodfolk ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Rhinovirus Infection

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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