Human Rhinovirus 2 Induces the Autophagic Pathway and Replicates More Efficiently in Autophagic Cells

Klein, Kathryn A.; Jackson, William T.

doi:10.1128/jvi.00316-11

Cited by 57 publications

(67 citation statements)

References 30 publications

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“…Tissue culture studies of poliovirus (Jackson et al, 2005), CVB (Wong et al, 2008; Yoon et al, 2008), human rhinoviruses (Brabec-Zaruba et al, 2007; Klein and Jackson, 2011) and enterovirus 71 (Huang et al, 2009) have found only minor changes in virus titer when autophagy is modulated, and there is no clear understanding of precisely which stage(s) of the enterovirus lifecycle are affected. The data in Figure 2 reveal a far greater effect in vivo ; in the absence of intact Atg5, pancreatic CVB3 titers early in infection are reduced by ~3 logs.…”

Section: Resultsmentioning

confidence: 99%

Pancreatic Acinar Cell-Specific Autophagy Disruption Reduces Coxsackievirus Replication and Pathogenesis In Vivo

Alirezaei

Flynn

Wood

et al. 2012

Cell Host & Microbe

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Section: Resultsmentioning

confidence: 99%

Pancreatic Acinar Cell-Specific Autophagy Disruption Reduces Coxsackievirus Replication and Pathogenesis In Vivo

Alirezaei

Flynn

Wood

et al. 2012

Cell Host & Microbe

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“…(Jackson et al, 2005) This is true for other picornaviruses, and a large number of viruses, particularly positive-strand RNA viruses, have been shown to benefit from some aspect of the autophagic pathway. (S.-C. Huang et al, 2009; Klein and Jackson, 2011; O'Donnell et al, 2011; Yoon et al, 2008) For poliovirus, the DMVs can act as a substrate for RNA replication, although they play other important roles, discussed below. For Hepatitis C Virus (HCV), autophagy appears be required for initiation of, but not maintenance of, viral replication.…”

Section: Viral Proteins That Trigger the Autophagy Pathwaymentioning

confidence: 99%

Viruses and the autophagy pathway

2015

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Studies of the cellular autophagy pathway have exploded over the past twenty years. Now appreciated as a constitutive degradative mechanism that promotes cellular homeostasis, autophagy is also required for a variety of developmental processes, cellular stress responses, and immune pathways. Autophagy certainly acts as both an anti-viral and pro-viral pathway, and the roles of autophagy depend on the virus, the cell type, and the cellular environment. The goal of this review is to summarize, in brief, what we know so far about the relationship between autophagy and viruses, particularly for those who are not familiar with the field. With a massive amount of relevant published data, it is simply not possible to be comprehensive, or to provide a complete “parade of viruses”, and apologies are offered to researchers whose work is not described herein. Rather, this review is organized around general themes regarding the relationship between autophagy and animal viruses.

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“…For example, human Tollip is required for the proper clearance of Huntington's disease-linked polyQ proteins through the ubiquitin-dependent autophagy [19]. As autophagy participates in the anti-RV response in a normal setting [10, 20], Tollip may also serve as a novel mechanism to modulate host responses to RV infection in a type 2 cytokine milieu (e.g., IL-13), a major feature of airway allergic inflammation.…”

Section: Introductionmentioning

confidence: 99%

Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection

Huang

Jiang

Francisco

et al. 2016

Clin Experimental Allergy

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Background Rhinovirus (RV) infection in asthma induces varying degrees of airway inflammation (e.g., neutrophils), but the underlying mechanisms remain unclear. Objective The major goal was to determine the role of genetic variation (e.g., single nucleotide polymorphisms [SNPs]) of Toll-interacting protein (Tollip) in airway epithelial responses to RV in a type 2 cytokine milieu. Methods DNA from blood of asthmatic and normal subjects was genotyped for Tollip SNP rs5743899 AA, AG and GG genotypes. Human tracheobronchial epithelial (HTBE) cells from donors without lung disease were cultured to determine pro-inflammatory and anti-viral responses to IL-13 and RV16. Tollip knockout and wild-type mice were challenged with house dust mite (HDM) and infected with RV1B to determine lung inflammation and anti-viral response. Results Asthmatic subjects carrying the AG or GG genotype (AG/GG) compared with the AA genotype demonstrated greater airflow limitation. HTBE cells with AG/GG expressed less Tollip. Upon IL-13 and RV16 treatment, cells with AG/GG (versus AA) produced more IL-8 and expressed less anti-viral genes, which was coupled with increased NF-κB activity and decreased expression of LC3, a hallmark of the autophagic pathway. Tollip co-localized and interacted with LC3. Inhibition of autophagy decreased anti-viral genes in IL-13 and RV16 treated cells. Upon HDM and RV1B, Tollip knockout (versus wild-type) mice demonstrated higher levels of lung neutrophilic inflammation and viral load, but lower levels of anti-viral gene expression. Conclusions and Clinical Relevance Our data suggest that Tollip SNP rs5743899 may predict varying airway response to RV infection in asthma.

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Human Rhinovirus 2 Induces the Autophagic Pathway and Replicates More Efficiently in Autophagic Cells

Abstract: In this study, we tested HRV-2-infected cells for activation of autophagic signaling and changes in virus growth in response to changes in autophagy levels. Our data indicate that HRV-2 induces and subverts the autophagic machinery to promote its own replication.

Cited by 57 publications

References 30 publications

Pancreatic Acinar Cell-Specific Autophagy Disruption Reduces Coxsackievirus Replication and Pathogenesis In Vivo

Pancreatic Acinar Cell-Specific Autophagy Disruption Reduces Coxsackievirus Replication and Pathogenesis In Vivo

Viruses and the autophagy pathway

Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection

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