Helminth–virus interactions: determinants of coinfection outcomes

Desai, Pritesh; Diamond, Michael S.; Thackray, Larissa B.

doi:10.1080/19490976.2021.1961202

Cited by 22 publications

(25 citation statements)

References 98 publications

(167 reference statements)

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“…In addition to bacteria, other viruses, fungi, and helminths can determine host immunity and virus infection. These trans-kingdom interactions described by Pfeiffer and Virgin [ 49 ] demonstrate both protective and detrimental outcomes. For example, the induction of an IFN response by helminths had a positive effect on respiratory viral infection whilst enteric helminths could enhance susceptibility to systemic viral infections that also had tropism for the GI tract [ 50 ].…”

Section: Causes Of Deviant Immune Response In Viral Infectionsmentioning

confidence: 99%

Understanding Immune Responses to Viruses—Do Underlying Th1/Th2 Cell Biases Predict Outcome?

Howard

Kwan

Winder

et al. 2022

Viruses

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Emerging and re-emerging viral diseases have increased in number and geographical extent during the last decades. Examples include the current COVID-19 pandemic and the recent epidemics of the Chikungunya, Ebola, and Zika viruses. Immune responses to viruses have been well-characterised within the innate and adaptive immunity pathways with the outcome following viral infection predominantly attributed to properties of the virus and circumstances of the infection. Perhaps the belief that the immune system is often considered as a reactive component of host defence, springing into action when a threat is detected, has contributed to a poorer understanding of the inherent differences in an individual’s immune system in the absence of any pathology. In this review, we focus on how these host factors (age, ethnicity, underlying pathologies) may skew the T helper cell response, thereby influencing the outcome following viral infection but also whether we can use these inherent biases to predict patients at risk of a deviant response and apply strategies to avoid or overcome them.

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Section: Causes Of Deviant Immune Response In Viral Infectionsmentioning

confidence: 99%

Understanding Immune Responses to Viruses—Do Underlying Th1/Th2 Cell Biases Predict Outcome?

Howard

Kwan

Winder

et al. 2022

Viruses

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“…With the recent discovery of thymic tuft cells in humans, the role of tuft cells in human tolerance and autoimmunity will likely bring critical insights into the human immune system [ 104 ]. As reduced helminth burdens and dysregulated microbiomes in human populations are correlated with increases in autoimmunity and allergy, it will be compelling to see whether tuft cells support anti-helminth immune responses or bacterial microflora in humans and how this relates to allergy and autoimmunity [ 123 , 124 ]. Finally, how tuft cells interact with human enteric viruses remains to be seen.…”

Section: Discussionmentioning

confidence: 99%

“…Taken together, these findings suggest that tuft cells may modulate viral persistence and the CD8+ adaptive immune response. Despite high rates of norovirus and flavivirus infection in countries with endemic helminth burden and previous reports of coinfection, the role of tuft cells in helminth–virus coinfection in humans is unclear [ 122 – 124 ].…”

Section: Tuft Cells In Host–microbe Interactionsmentioning

confidence: 99%

Tuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces

Strine

Wilen

2022

PLoS Pathog

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Although tuft cells were discovered over 60 years ago, their functions have long been enigmatic, especially in human health. Nonetheless, tuft cells have recently emerged as key orchestrators of the host response to diverse microbial infections in the gut and airway. While tuft cells are epithelial in origin, they exhibit functions akin to immune cells and mediate important interkingdom interactions between the host and helminths, protists, viruses, and bacteria. With broad intra- and intertissue heterogeneity, tuft cells sense and respond to microbes with exquisite specificity. Tuft cells can recognize helminth and protist infection, driving a type 2 immune response to promote parasite expulsion. Tuft cells also serve as the primary physiologic target of persistent murine norovirus (MNV) and promote immune evasion. Recently, tuft cells were also shown to be infected by rotavirus. Other viral infections, such as influenza A virus, can induce tuft cell–dependent tissue repair. In the context of coinfection, tuft cells promote neurotropic flavivirus replication by dampening antiviral adaptive immune responses. Commensal and pathogenic bacteria can regulate tuft cell abundance and function and, in turn, tuft cells are implicated in modulating bacterial infiltration and mucosal barrier integrity. However, the contribution of tuft cells to microbial sensing in humans and their resulting effector responses are poorly characterized. Herein, we aim to provide a comprehensive overview of microbial activation of tuft cells with an emphasis on tuft cell heterogeneity and differences between mouse and human tuft cell biology as it pertains to human health and disease.

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“…However, when mice are first treated with Schistosoma mansoni eggs, then challenged with MHV68 intranasally 14-days later, the virus replicates less in the lung ( 17 ). Species of helminth, timing of infection, immune response to the pathogens, and tissue tropism all play a role in whether the coinfection helps or hinders the host response to the virus ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Coinfection with Intestinal Parasite Expands Resident Macrophages and Impairs Control of Chronic Herpesvirus Infection

Zarek

Dende

Coronado

et al. 2022

Preprint

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In addition to a range of homeostatic functions, resident macrophages are essential for immune surveillance in tissues. Therefore, anything that alters the phenotype or function of these cells potentially impacts their response to infectious challenges. Parasite infections cause proliferation of large peritoneal macrophages (LPMs), which are the resident macrophages of the peritoneal cavity. However, the functional consequences of LPM expansion on the control of secondary infectious challenge is unknown. Using a coinfection model with the intestinal parasite Heligmosomoides polygyrus (HP) and the virus, murine gammaherpesvirus-68 (MHV68), we investigated the impact of LPM expansion on viral infection. We determined that LPM expansion induced by HP required retinoic acid signaling. When we challenged HP-infected mice with MHV68, we observed increased herpesvirus infection and latency. Coinfection of mice with macrophage-specific deletion of GATA6, the retinoic acid-responsive transcription factor that drives LPM transcriptional programming, eradicated the increase in viral infection. In addition to increased MHV68 infection, parasite coinfected mice displayed increased herpesvirus reactivation from latency, indicating impaired control of chronic herpesvirus infection. Elimination of dietary vitamin A, which depletes retinoic acid and LPMs, abolished the increased MHV68 reactivation in parasite coinfected mice. These results indicate that parasite- and retinoic acid-mediated resident macrophage expansion drives increased herpesvirus infection, latency, and reactivation.

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Helminth–virus interactions: determinants of coinfection outcomes

Cited by 22 publications

References 98 publications

Understanding Immune Responses to Viruses—Do Underlying Th1/Th2 Cell Biases Predict Outcome?

Understanding Immune Responses to Viruses—Do Underlying Th1/Th2 Cell Biases Predict Outcome?

Tuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces

Coinfection with Intestinal Parasite Expands Resident Macrophages and Impairs Control of Chronic Herpesvirus Infection

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