Return to homepagePandemic Pact

The role of IL-2 therapy for Relapsing-Remitting Chikungunya Arthritis

  • Funded by National Institutes of Health (NIH)
  • Total publications:0 publications

Grant number: 1K23AR076505-01

Grant search

Key facts

  • Disease

    Chikungunya haemorrhagic fever
  • Start & end year

    2020
    2023
  • Known Financial Commitments (USD)

    $155,174
  • Funder

    National Institutes of Health (NIH)
  • Principal Investigator

    ASSOCIATE PROFESSOR Aileen Chang
  • Research Location

    United States of America
  • Lead Research Institution

    GEORGE WASHINGTON UNIVERSITY
  • Research Priority Alignment

    N/A
  • Research Category

    Clinical characterisation and management

  • Research Subcategory

    Disease pathogenesis

  • Special Interest Tags

    N/A

  • Study Type

    Non-Clinical

  • Clinical Trial Details

    N/A

  • Broad Policy Alignment

    Pending

  • Age Group

    Not Applicable

  • Vulnerable Population

    Not applicable

  • Occupations of Interest

    Not applicable

Abstract

ABSTRACT Chikungunya virus (CHIKV) is an alphavirus spread by mosquitos that causes persistent arthritis in approximately one-fourth of patients. There is currently no evidence-based standard treatment for CHIKV chronic arthritis. In the current proposal, we seek to identify a therapeutic target for relapsing-remitting arthritis associated with CHIKV infection. Our Colombian cohort (n = 500) of patients affected by CHIKV affords a unique opportunity to further understand the immunology of CHIKV arthritis flares. Our preliminary data suggest that alteration of regulatory T cell (Treg) function may play a role in CHIKV arthritis pathogenesis. Novel low-dose interleukin-2 (IL-2) based therapies for autoimmune disease have been shown to up-regulate Tregs and may be of use in CHIKV arthritis flares. Our main goal is to further understand the role of IL-2 in Treg populations in CHIKV arthritis. Our central hypothesis is that chronic CHIKV arthritis activity is associated with deficient IL-2 mediated Treg levels and low-dose IL-2 is a potential therapeutic. This hypothesis will be evaluated in two specific aims. In Aim 1, we will describe the role of IL-2 in Treg expansion and corresponding arthritis severity during CHIKV arthritis flare vs. remission compared to non-arthritic controls. In Aim 2, we will determine the role of IL-2 therapy in the treatment of CHIKV arthritis in a mouse model. The impact of this research will determine the correlation between Tregs and CHIKV-associated arthralgia. It may provide a pre-clinical evaluation of low-dose IL-2 therapy for CHIKV arthritis and insights into the use of this novel therapeutic for viral arthritis in general.