Santa Fe Institute Collaboration Platform

COMPLEX TIME: Adaptation, Aging, & Arrow of Time

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Contact: Caitlin Lorraine McShea, Program Manager, cmcshea@santafe.edu

Aging and Adaptation in Infectious Diseases III

From Complex Time

Category: Application Area Application Area: Infectious Diseases

Date/Time: January 14, 2020 - January 17, 2020

Location: Santa Fe Institute (Noyce Conference Room)

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Organizers

  • Jean Carlson (UCSB)

  • Mercedes Pascual (Univ. Chicago)

  • Meeting Highlight

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    Attendees

    Agenda/Schedule
    Click each agenda item's title for more information.
    Tuesday, January 14, 2020
    8:30 am - 9:00 am Day 1 Continental Breakfast (outside SFI Noyce Conference Room)
    9:00 am - 9:30 am Welcome, Introductions and Workshop Overview - Jean Carlson (UCSB), Mercedes Pascual (Univ. Chicago)
    9:30 am - 12:00 pm Session I: Immune System: Innate/Adaptive collaboration

    (20 minute presentations+10 minute discussion; general discussion at the end)   

    Moderator: Mercedes Pascual

    1. Fast & Slow Immunology: Can we frame predictable temporal trajectories in immunity? Review and Perspectives A - Micaela Martinez (Columbia Univ.)
    2. Review and Perspectives B - Andrea L. Graham (Princeton)
    3. Immunosenosence in Coupled Models of Innate/Adaptive Immune Responses A - Jean Carlson (UCSB), Eric Jones (UCSB)
    4. Immunosenosence in Coupled Models of Innate/Adaptive Immune Responses B - Shenshen Wang (UCLA), Jiming Sheng (UCLA)
    12:00 pm - 1:00 pm Day 1 Lunch (outside SFI Noyce Conference Room)
    1:00 pm - 3:30 pm Session II: Diversity, adaptive immunity, and age

    (20 minute presentations+10 minute discussion; general discussion at the end)

    Moderator: Jean Carlson   

    1. Allometically scaled immune response - Andrew P. Dobson (Princeton), Chris Kempes (SFI)
    2. Immune imprinting and antigenic maps revisited - Sarah Cobey (Univ. Chicago), Pamela Martinez (Harvard), Katie Gostic (UCLA)
    3. Frequency-dependent selection and prediction of strain dynamics in a bacterial pathogen - Pamela Martinez (Harvard)
    4. Diversity threshold and epidemiological models for parasites with extreme antigenic variation - Mercedes Pascual (Univ. Chicago), Qixin He (Univ. Chicago)
    3:30 pm - 4:00 pm Day 1 PM Break
    4:00 pm - 5:00 pm Day 1 Discussion, development of themes, and structure of breakout groups for the rest of the week
    6:00 pm Group Dinner
    Wednesday, January 15, 2020
    8:30 am - 9:00 am Day 2 Continental Breakfast (outside SFI Noyce Conference Room)
    9:00 am - 11:00 am Session III: Disease History, Aging, and Complex Time

    (20 minute presentations+10 minute discussion; 30 minutes general discussion at the end)

    Moderator: Mercedes Pascual   

    1. How many diseases can one pathogen cause - the shape of disease responses in mice as a species - David Schneider (Stanford)
    2. Identifying variants from influenza A H1N1 that exhibit birth-cohort immune escape signatures - Katia Koelle (Emory Univ.)
    3. The Tempo of Our Planet: Biological Rhythms & Health - Micaela Martinez (Columbia Univ.)
    11:00 am - 12:00 pm Day 2 Group Discussion and Working Group Planning Sessions
    12:00 pm - 1:00 pm Day 2 Lunch (outside SFI Noyce Conference Room)
    1:00 pm - 2:30 pm Discussion: Plans for an SFI publication / Presentation from SFI Press
    2:30 pm - 4:30 pm Day 2 Working Group Breakout Sessions
    4:30 pm - 5:00 pm Re-assembling: Brief updates and plans for Day 3
    Thursday, January 16, 2020
    8:30 am - 9:00 am Day 3 Continental Breakfast (outside SFI Noyce Conference Room)
    9:00 am - 12:00 pm Day 3 Working Group Breakout Sessions I
    12:00 pm - 1:00 pm Day 3 Lunch (outside SFI Noyce Conference Room)
    1:00 pm - 3:00 pm Day 3 Working Group Breakout Sessions II
    3:00 pm - 3:30 pm Day 3 PM Break
    3:30 pm - 5:00 pm Day 3 Working Group Breakout Sessions III
    Friday, January 17, 2020
    8:30 am - 9:00 am Day 4 Continental Breakfast (outside Noyce Conference Room)
    9:00 am - 12:00 pm Breakout Group Presentations
    12:00 pm - 1:00 pm Day 4 Lunch (outside SFI Noyce Conference Room)
    1:00 pm - 1:30 pm Closing and next steps
    1:30 pm - 5:00 pm Optional additional Working Group Sessions (for those staying that afternoon)

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    Meeting Synopsis

    Our working group aims to explore the role of aging and adaptation in infectious diseases operating over multiple organizational and temporal scales. General areas include immune system dynamics and age, host-pathogen co-adaptation in chronic vs. acute infections, pathogen antigenic diversity and endemism, effects of age on infectious diseases in human and non-human hosts. Overarching themes include memory, (co)adaptation, diversity, feedback, robustness and fragility. We are interested in aging as increasing fragility to infection, and in complex biological time as related to individual variation in disease progression and recovery. We are also interested in aging of the pathogen in terms of its ability to persist and withstand intervention efforts, and how this robustness is in turn related to pathogen (antigenic) diversity. In all these areas, the dynamic acquisition and loss of information through the immune system plays a central role at the individual and population levels. The goal of this third working group is to reunite participants from the first and second meetings to update progress and develop our next set of objectives for collaborative research on the questions that emerged from our previous discussions. These questions include the interaction of the adaptive and innate immune system in the dynamics of infection, the role of early-childhood exposure (‘imprinting’) in later immune protection and in defining the temporal changes of the antigenic map, and the allometric scaling of the immune system dynamics with organism size.

    Abstracts by Presenters

    Jean Carlson (UCSB), Eric Jones (UCSB) - Adaptive collaboration[edit source]

    While participating in the Aging and Adaptation in Infectious Diseases working group, we refined our mathematical model of the immune system based on expert feedback from other participants. In particular, we discussed parameterizing our model based on existing experimental data of how human memory and naive cell populations change with age. We received several recommendations for relevant studies that we were unaware of before the meeting. Additionally, we discussed how our understanding of the immune model could be improved by a thorough bifurcation analysis, and in particular how this analysis might indicate sensitive parameters that can help quantify immune risk. We discussed how our model could be modified in future work to be applicable to influenza: in particular, influenza rapidly mutates and so considerations of cross-reactive antibodies need to be considered (which our model does not currently include). Future work could also focus on the coevolving feedbacks between our immune model and pathogen strains, and in particular how the evolutionary pressures of an adaptive immune response drive can drive the evolution of diversity of pathogens. Participants expressed interest in studying how chronic infections affect immune outcomes, focusing in particular on cytomegalovirus and its debilitating effect on a host's immune response. Lastly, we have entered into exciting new discussions with Chris Kempes and Andy Dobson regarding how immune system responses scale with host size, which might reveal how immune behaviors are conserved across species' size and age.

    Post-meeting Reflection by Presenter

    Katie Gostic (UCLA) Link to the source page[edit source]

    Immunity to antigenically variable pathogens arises from an individual's history of exposures to multiple strains. The success of a new strain in turn depends on how strongly it is recognized by immune responses generated against previous strains. Traditionally, cross-reactivity between two strains is thought to depend on the similarity between their antigenic structures. Antigenic maps are a widely used visualization tool in which the distance between strains (represented as points in Euclidean space) provides a measure of their antigenic similarity, and potential for cross-reactivity.  

    However, the concept of a fixed antigenic distance between two strains implies that all hosts, regardless of their age and exposure history, would gain the same degree of cross-protection against strain B, given exposure to or vaccination with strain A. This contradicts a growing body of experimental and epidemiological evidence, showing that individuals with different exposure histories can exhibit vastly different levels of cross-protection against the same viral challenge.

    We are developing an individual-based model which we will use to explore how differences in individual exposure history can cause hosts to perceive different antigenic distances between strains. We will use this model to explore how history-specific differences in immunity arise, and to what extent they cause immunity to differ from the predictions of existing maps, which assume a fixed distance between strains.

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    Post-meeting Reflection by Non-presenting Attendees

    Reference Materials by Presenting Attendees[edit source]

    Reference Materials by Non-presenting Attendees

    None.

    General Meeting Reference Material[edit source]