Dynamic causal modelling of immune heterogeneity

Abstract An interesting inference drawn by some COVID-19 epidemiological models is that there exists a proportion of the population who are not susceptible to infection—even at the start of the current pandemic. This paper introduces a model of the immune response to a virus. This is based upon the...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Thomas Parr, Anjali Bhat, Peter Zeidman, Aimee Goel, Alexander J. Billig, Rosalyn Moran, Karl J. Friston
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
R
Q
Acceso en línea:https://doaj.org/article/c5a0622510dd4edd9d484209203bee98
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:c5a0622510dd4edd9d484209203bee98
record_format dspace
spelling oai:doaj.org-article:c5a0622510dd4edd9d484209203bee982021-12-02T18:24:53ZDynamic causal modelling of immune heterogeneity10.1038/s41598-021-91011-x2045-2322https://doaj.org/article/c5a0622510dd4edd9d484209203bee982021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-91011-xhttps://doaj.org/toc/2045-2322Abstract An interesting inference drawn by some COVID-19 epidemiological models is that there exists a proportion of the population who are not susceptible to infection—even at the start of the current pandemic. This paper introduces a model of the immune response to a virus. This is based upon the same sort of mean-field dynamics as used in epidemiology. However, in place of the location, clinical status, and other attributes of people in an epidemiological model, we consider the state of a virus, B and T-lymphocytes, and the antibodies they generate. Our aim is to formalise some key hypotheses as to the mechanism of resistance. We present a series of simple simulations illustrating changes to the dynamics of the immune response under these hypotheses. These include attenuated viral cell entry, pre-existing cross-reactive humoral (antibody-mediated) immunity, and enhanced T-cell dependent immunity. Finally, we illustrate the potential application of this sort of model by illustrating variational inversion (using simulated data) of this model to illustrate its use in testing hypotheses. In principle, this furnishes a fast and efficient immunological assay—based on sequential serology—that provides a (1) quantitative measure of latent immunological responses and (2) a Bayes optimal classification of the different kinds of immunological response (c.f., glucose tolerance tests used to test for insulin resistance). This may be especially useful in assessing SARS-CoV-2 vaccines.Thomas ParrAnjali BhatPeter ZeidmanAimee GoelAlexander J. BilligRosalyn MoranKarl J. FristonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-17 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Thomas Parr
Anjali Bhat
Peter Zeidman
Aimee Goel
Alexander J. Billig
Rosalyn Moran
Karl J. Friston
Dynamic causal modelling of immune heterogeneity
description Abstract An interesting inference drawn by some COVID-19 epidemiological models is that there exists a proportion of the population who are not susceptible to infection—even at the start of the current pandemic. This paper introduces a model of the immune response to a virus. This is based upon the same sort of mean-field dynamics as used in epidemiology. However, in place of the location, clinical status, and other attributes of people in an epidemiological model, we consider the state of a virus, B and T-lymphocytes, and the antibodies they generate. Our aim is to formalise some key hypotheses as to the mechanism of resistance. We present a series of simple simulations illustrating changes to the dynamics of the immune response under these hypotheses. These include attenuated viral cell entry, pre-existing cross-reactive humoral (antibody-mediated) immunity, and enhanced T-cell dependent immunity. Finally, we illustrate the potential application of this sort of model by illustrating variational inversion (using simulated data) of this model to illustrate its use in testing hypotheses. In principle, this furnishes a fast and efficient immunological assay—based on sequential serology—that provides a (1) quantitative measure of latent immunological responses and (2) a Bayes optimal classification of the different kinds of immunological response (c.f., glucose tolerance tests used to test for insulin resistance). This may be especially useful in assessing SARS-CoV-2 vaccines.
format article
author Thomas Parr
Anjali Bhat
Peter Zeidman
Aimee Goel
Alexander J. Billig
Rosalyn Moran
Karl J. Friston
author_facet Thomas Parr
Anjali Bhat
Peter Zeidman
Aimee Goel
Alexander J. Billig
Rosalyn Moran
Karl J. Friston
author_sort Thomas Parr
title Dynamic causal modelling of immune heterogeneity
title_short Dynamic causal modelling of immune heterogeneity
title_full Dynamic causal modelling of immune heterogeneity
title_fullStr Dynamic causal modelling of immune heterogeneity
title_full_unstemmed Dynamic causal modelling of immune heterogeneity
title_sort dynamic causal modelling of immune heterogeneity
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/c5a0622510dd4edd9d484209203bee98
work_keys_str_mv AT thomasparr dynamiccausalmodellingofimmuneheterogeneity
AT anjalibhat dynamiccausalmodellingofimmuneheterogeneity
AT peterzeidman dynamiccausalmodellingofimmuneheterogeneity
AT aimeegoel dynamiccausalmodellingofimmuneheterogeneity
AT alexanderjbillig dynamiccausalmodellingofimmuneheterogeneity
AT rosalynmoran dynamiccausalmodellingofimmuneheterogeneity
AT karljfriston dynamiccausalmodellingofimmuneheterogeneity
_version_ 1718378122854793216