The Role of Receptor-Interacting Serine/Threonine-Protein Kinase 1 (RIPK1) in CD4+ T Cell Necroptosis in HIV Patients: A Narrative Literature Review
DOI:
https://doi.org/10.37275/bsm.v8i10.1096Keywords:
Apoptosis, CD4 T cells, HIV, Necroptosis, RIPK1Abstract
The human immunodeficiency virus (HIV) remains a global health challenge, with its ability to deplete CD4+ T cells, leading to acquired immunodeficiency syndrome (AIDS). While apoptosis has been extensively studied in CD4+ T cell depletion, recent research has highlighted the significant role of necroptosis, a regulated form of necrosis, in this process. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) has emerged as a central player in necroptosis, regulating both cell death and inflammatory responses. This review delves into the intricate mechanisms by which RIPK1 orchestrates necroptosis in CD4+ T cells during HIV infection. We explore the structural intricacies of RIPK1, its interactions with other signaling molecules, and the downstream events that culminate in necroptotic cell death. Additionally, we discuss the therapeutic potential of targeting RIPK1 to mitigate CD4+ T cell loss and control HIV disease progression. Understanding the multifaceted role of RIPK1 in HIV-induced necroptosis may pave the way for novel therapeutic interventions to combat this devastating disease.
Authors
- Asima Juliyana Siregar1*
- Harun Hudari2
- 1Faculty of Medicine, Universitas Sriwijaya, Palembang, Indonesia
- 2Division of Internal Medicine, Dr. Mohammad Hoesin General Hospital, Palembang, Indonesia
Corresponding author Asima Juliyana Siregar — asimajuliyanasiregar250790@gmail.com
Article history
- Submitted
- Accepted
- Published
Downloads
Published
Issue
Section
License
Copyright and licensing
Copyright in each article remains with the author(s). Authors grant Bioscientia Medicina: Journal of Biomedicine and Translational Research a non-exclusive right of first publication and the right to identify itself as the original publisher. No exclusive transfer of copyright is required.
All articles are published under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0): https://creativecommons.org/licenses/by-nc-sa/4.0/. Users may copy, redistribute, remix, transform, and build upon the material for non-commercial purposes, provided appropriate attribution is given, a link to the license is supplied, changes are indicated, and adaptations are distributed under the same license.
The license applies to the article's scholarly content unless a credit line states otherwise. Third-party material may be subject to separate rights. Authors retain patent, trademark, moral, and research-data rights. The copyright year follows the article's publication date.











