scholarly journals Zika Virus–Infected Decidual Cells Elicit a Gestational Age–Dependent Innate Immune Response and Exaggerate Trophoblast Zika Permissiveness: Implication for Vertical Transmission

2020 ◽  
Vol 205 (11) ◽  
pp. 3083-3094
Author(s):  
Ozlem Guzeloglu-Kayisli ◽  
Xiaofang Guo ◽  
Zhonghua Tang ◽  
Nihan Semerci ◽  
Asli Ozmen ◽  
...  
Keyword(s):  
Immune Response ◽  
Vertical Transmission ◽  
Innate Immune Response ◽  
Gestational Age ◽  
Zika Virus ◽  
Innate Immune ◽  
Decidual Cells ◽  
Age Dependent

scholarly journals Zika virus dynamics: Effects of inoculum dose, the innate immune response and viral interference

2021 ◽  
Vol 17 (1) ◽  
pp. e1008564
Author(s):  
Katharine Best ◽  
Dan H. Barouch ◽  
Jeremie Guedj ◽  
Ruy M. Ribeiro ◽  
Alan S. Perelson
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Natural Infection ◽  
Innate Immune ◽  
Viral Dynamics ◽  
Viral Production ◽  
Viral Interference ◽  
Inoculum Dose ◽  
Better Than

Experimental Zika virus infection in non-human primates results in acute viral load dynamics that can be well-described by mathematical models. The inoculum dose that would be received in a natural infection setting is likely lower than the experimental infections and how this difference affects the viral dynamics and immune response is unclear. Here we study a dataset of experimental infection of non-human primates with a range of doses of Zika virus. We develop new models of infection incorporating both an innate immune response and viral interference with that response. We find that such a model explains the data better than models with no interaction between virus and the immune response. We also find that larger inoculum doses lead to faster dynamics of infection, but approximately the same total amount of viral production.

Innate immune response in patients with acute Zika virus infection

2019 ◽  
Vol 208 (6) ◽  
pp. 703-714 ◽  
Author(s):  
Marcelo Henrique Matias da Silva ◽  
Raiza Nara Cunha Moises ◽  
Brenda Elen Bizerra Alves ◽  
Hannaly Wana Bezerra Pereira ◽  
Anne Aline Pereira de Paiva ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Innate Immune ◽  
Zika Virus Infection

The innate immune response in Zika virus infection

2020 ◽  
Author(s):  
Jorge Rodrigues de Sousa ◽  
Raimunda do Socorro da Silva Azevedo ◽  
Juarez Antônio Simões Quaresma ◽  
Pedro Fernando da Costa Vasconcelos
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Innate Immune ◽  
Zika Virus Infection

scholarly journals Zika virus alters centrosome organization to suppress the innate immune response

2020 ◽  
Author(s):  
Andrew Kodani ◽  
Kristeene A. Knopp ◽  
Elizabeth Di Lullo ◽  
Hanna Retallack ◽  
Arnold R. Kriegstein ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Nonstructural Protein ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Zikv Infection ◽  
Centrosomal Proteins ◽  
Nonstructural Protein Ns3

AbstractZika virus (ZIKV) is a flavivirus transmitted via mosquitoes and sex to cause congenital neurodevelopmental defects, including microcephaly. Inherited forms of microcephaly (MCPH) are associated with disrupted centrosome organization. Similarly, we found that ZIKV infection disrupted centrosome organization. ZIKV infection disrupted the organization of centrosomal proteins including CEP63, a MCPH-associated protein. The ZIKV nonstructural protein NS3 bound CEP63, and expression of NS3 was sufficient to alter centrosome architecture and CEP63 localization. Loss of CEP63 suppressed ZIKV-induced centrosome disorganization, indicating that ZIKV requires CEP63 to disrupt centrosome organization. ZIKV infection or loss of CEP63 decreased the centrosomal localization and stability of TANK-binding kinase 1 (TBK1), a regulator of the innate immune response. ZIKV infection or loss of CEP63 also increased the centrosomal accumulation of the CEP63 interactors, Mindbomb1 (MIB1) and DTX4, ubiquitin ligases that respectively activate and degrade TBK1. Therefore, we propose that ZIKV NS3 binds CEP63 to increase centrosomal DTX4 localization and destabilization of TBK1, thereby tempering the innate immune response. In addition to identifying a mechanism by which CEP63 controls the innate immune responses in ZIKV infection, we propose that the altered centrosomal organization caused by altered CEP63 function may contribute to ZIKV-associated microcephaly.

scholarly journals Predominant role of IPS-1 over TRIF adaptor proteins in early innate immune response against Zika virus in mice

2018 ◽  
Vol 99 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Jocelyne Piret ◽  
Julie Carbonneau ◽  
Chantal Rhéaume ◽  
Mariana Baz ◽  
Guy Boivin
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Adaptor Proteins ◽  
Innate Immune ◽  
Predominant Role

The innate immune response during Zika virus infection

2021 ◽  
pp. 19-29
Author(s):  
Manuela Sales Lima Nascimento ◽  
Wilo Victor dos Santos ◽  
Amanda Costa Ayres Salmeron ◽  
Josélio Maria Galvão de Araújo ◽  
José Veríssimo Fernandes ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Zika Virus ◽  
Innate Immune ◽  
Zika Virus Infection

scholarly journals The Innate Immune Response to Herpes Simplex Virus 1 Infection Is Dampened in the Newborn Brain and Can Be Modulated by Exogenous Interferon Beta To Improve Survival

mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Daniel Giraldo ◽  
Douglas R. Wilcox ◽  
Richard Longnecker
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Newborn Brain ◽  
Age Dependent ◽  
Simplex Virus ◽  
Increased Susceptibility ◽  
Hsv 1

ABSTRACT Newborns are particularly susceptible to severe forms of herpes simplex virus 1 (HSV-1) infection, including encephalitis and multisystemic disseminated disease. The underlying age-dependent differences in the immune response that explain this increased susceptibility relative to the adult population remain largely understudied. Using a murine model of HSV-1 infection, we found that newborn mice are largely susceptible to intracranial and intraperitoneal challenge while adult mice are highly resistant. This age-dependent difference correlated with differential basal-level expression of components of innate immune signaling pathways, which resulted in dampened interferon (IFN) signaling in the newborn brain. To explore the possibility of modulating the IFN response in the newborn brain to recapitulate the adult phenotype, we administered exogenous IFN-β in the context of disseminated HSV-1 infection. IFN-β treatment resulted in significantly increased survival and delayed viral neuroinvasion in the newborn. These effects were associated with changes in the type I IFN response in the brain, reduced viral replication in the periphery, and the stabilization of the blood-brain barrier (BBB). Our study reveals important age-dependent differences in the innate immune response to HSV-1 infection and suggests a contribution of the BBB and the brain parenchyma in mediating the increased susceptibility to HSV-1 infection observed in the newborn. These results could provide the basis for potential new therapeutic strategies for life-threatening HSV-1 infection in newborns. IMPORTANCE Herpes simplex virus (HSV) is a ubiquitous human pathogen affecting 50 to 80% of the population in North America and Europe. HSV infection is commonly asymptomatic in the adult population but can result in fatal encephalitis in the newborn. Current treatment with acyclovir has improved mortality in the newborn; however, severe neurologic sequelae are still a major concern following HSV encephalitis. For this reason, there is a critical need to better understand the underlying differences in the immune response between the two age groups that could be used to develop more effective treatments. In this study, we investigated differences in the innate immune response to viral infection in the brains of newborn and adult mice. We found that, similar to humans, newborn mice are more susceptible to HSV infection than the adult. Increased susceptibility was associated with dampened innate immune responses in the newborn brain that could be rescued by administering interferon beta.

scholarly journals Aberrant overexpression of CD14 on granulocytes sensitizes the innate immune response in mDia1 heterozygous del(5q) MDS

Blood ◽  
2014 ◽  
Vol 124 (5) ◽  
pp. 780-790 ◽  
Author(s):  
Ganesan Keerthivasan ◽  
Yang Mei ◽  
Baobing Zhao ◽  
Ling Zhang ◽  
Chad E. Harris ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Innate Immune Response ◽  
Knockout Mice ◽  
Innate Immune ◽  
Chronic Stimulation ◽  
Key Points ◽  
Age Dependent ◽  
A Cell ◽  
Stimulation Of

Key Points mDia1 deficiency led to a cell-autonomous overexpression of CD14 on granulocytes and a hypersensitive innate immune response. mDia1 heterozygous and knockout mice developed age-dependent MDS that was accelerated by chronic stimulation of the innate immunity.

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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