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

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.

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 ◽  
...  

2020 ◽  
Author(s):  
Jorge Rodrigues de Sousa ◽  
Raimunda do Socorro da Silva Azevedo ◽  
Juarez Antônio Simões Quaresma ◽  
Pedro Fernando da Costa Vasconcelos

2020 ◽  
Author(s):  
Andrew Kodani ◽  
Kristeene A. Knopp ◽  
Elizabeth Di Lullo ◽  
Hanna Retallack ◽  
Arnold R. Kriegstein ◽  
...  

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.


2018 ◽  
Vol 99 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Jocelyne Piret ◽  
Julie Carbonneau ◽  
Chantal Rhéaume ◽  
Mariana Baz ◽  
Guy Boivin

Author(s):  
Manuela Sales Lima Nascimento ◽  
Wilo Victor dos Santos ◽  
Amanda Costa Ayres Salmeron ◽  
Josélio Maria Galvão de Araújo ◽  
José Veríssimo Fernandes ◽  
...  

2010 ◽  
Vol 80 (12) ◽  
pp. 1955-1972 ◽  
Author(s):  
Patricia Vandevenne ◽  
Catherine Sadzot-Delvaux ◽  
Jacques Piette

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

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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