Associate Professor Suraj Parihar
Affiliations
- Full Member, Institute of Infectious Disease and Molecular Medicine
- Division of Medical Microbiology, Institute of Infectious Diseases and Molecular Medicine (IDM),Department of Pathology, Faculty of Health Sciences, UCT
- Contributing Investigator to the Basic Science Platform, Centre for Infectious Disease Research in Africa (CIDRI-Africa), Department of Pathology, Faculty of Health Sciences, UCT
- Honorary Extraordinary Associate Professor, Human Metabolomics, North-West University, Potchefstroom, South Africa
Key Expertise
Bacterial Infections, Non-communicable Disease, Omics, Pathogenesis, T-and B-cell Immunology, TB, Vaccine Development
Main Research Focus
Associate Professor Suraj Parihar's research focuses on the complex interactions between bacterial infections (specifically Listeria monocytogenes and Mycobacterium tuberculosis), diabetes, and host immune responses. His work aims to uncover novel gene functions that contribute to protective mechanisms, with the ultimate goal of developing alternative or adjunctive therapies.
Using a loss-of-function approach, Parihar's research identifies novel host factors exploited by intracellular pathogens to evade immune defences and survive in animal models. He also evaluates the translational potential of these factors in C3HeB/FeJ (Kramnik) mice, human macrophages, and patient samples. His methods include omics technologies (transcriptomics, proteomics, metabolomics), cellular immunometabolism studies, repurposed drugs/inhibitors, gene-deficient animal models, and investigations into adjuvant strategies to enhance BCG vaccine efficacy.
Most Significant Paper Authored in 2024
Julius, Chia & Rousseau, Robert & Ozturk, Mumin & Poswayo, Sibongiseni & Lucas, Rodney & Brombacher, Frank & Parihar, Suraj. (2024).
This study provides critical insights into the dual role of IL-4Rα signaling in immune regulation. It reveals that diminished IL-4Rα signaling impairs Foxp3+ Treg functionality, enhancing Th1 responses and survival during Listeria monocytogenes infection, while showing no survival benefit in Mycobacterium tuberculosis. This study underscores the context-dependent nature of cytokine signaling in infectious diseases and highlights potential therapeutic avenues for modulating immune responses. The findings are significant for advancing our understanding of host-pathogen interactions and refining strategies for immunotherapy.