Oral Presentation 14th Lorne Infection and Immunity 2024

Developing a functional cure for HTLV1 in a humanized mouse model (#24)

James Cooney 1 , Cody Allison 2 , Simon Preston 2 , Damian Purcell 3 , Lloyd Einsiedel 3 , Marcel Doerflinger 1 , Marc Pellergini 1
  1. Walter and Eliza Hall Institute for Medical Research, Parkville, VIC, Australia
  2. Walter and Eliza Hall Institute, Parkville, VIC, Australia
  3. Department of Microbiology and Immunology, Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville

Satisfactory preventative or therapeutic drugs are lacking for HTLV-1, a retrovirus closely related to HIV.  As a result infected individuals frequently present with serious complications including rapidly progressive Adult T Cell Leukaemia (ATL), inflammation of the spinal cord (HTLV-1-assocaited myelitis, HAM) and chronic bronchiectasis. HTLV-1 subtype c (HTLV-1c) is highly prevalent in indigenous communities in Central Australia, with infection rates unparalleled globally. Novel approaches that both inhibit viral replication and reduce the number of HTLV-1 infected cells are urgently required.

We investigated the efficacy of antiretroviral and pro-apoptotic BH3 mimetic compounds as preventative and therapeutic agents in a humanised mouse model of HTLV-1 subtype c (HTLV-1c) infection, the first of its kind. We characterised infection in this model and compared disease to the globally prevalent HTLV-1 subtype a (HTLV-1a). Tenofovir, a reverse transcriptase inhibitor, significantly reduced HTLV-1 transmission in vivo at clinically relevant doses and attenuated de novo viral spread and disease progression during early infection in combination with dolutegravir, an integrase inhibitor. HTLV-1 infection was associated with dysregulation of the intrinsic apoptotic pathway at the transcriptional level, and we found that pharmacological inhibition of MCL-1, but not BCL-2, BCL-xL or BCL-w, killed HTLV-1-infected cells in vitro and in vivo, significantly delaying disease progression in combination with tenofovir and dolutegravir. Our data demonstrate that combination antiretroviral and MCL-1 antagonism may represent an effective, clinically relevant, curative strategy against HTLV-1. We are now expanding our efforts towards next-generation therapeutics with decreased treatment off-target effects and increased cell specificity by utilizing precsion targeting of T cells by LNP-based delivery of RNA therapeutics against MCL-1.