New Delhi: A newly-identified gene could hold the answer to the prevention of Candidiasis - a fungal infection that may affect ICU patients, cancer patients, and those on immunosuppressive therapy. Known as CSA6, the gene has been identified in a fungal species known as Candida albicans responsible for causing high morbidity and mortality due to immune-compromised conditions such as AIDS or cancer. It resides in the mucosal lining of the gastrointestinal and urogenital tract of healthy people and turns into a pathogen under immune-compromised conditions breathing the host defense thereby causing a life-threatening infection.
According to a recent collaborative study by Professor Kaustuv Sanyal's group at Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR), Bangalore, India, and Christophe d'Enfert's group at Institut Pasteur, Paris, France (Jaitley t al, 2022), experts conducted large-scale screening to identify the chromosome stability regulators in C. Albicans, a clinically-relevant fungal model system.
Experts from the JNCASR, an institute of the Department of Science and Technology (DST), screened the effect of overexpression of over a thousand genes of C. albicans on genome stability and successfully identified a set of six chromosome stability genes that are a must for maintaining integrity. While five of the CSA genes are necessary for cell division in other species and the sixth gene encoded a protein that is a must for viability in C. albicans. They discovered that the sixth one was a critical regulator of cell cycle progression - its deletion and overexpression may hamper the growth of C. albicans cells.
The study published in Nature Communications journal is the first-ever report of such extensive screening of the human fungal pathogen. It elucidates the functions of a novel regulator or chromosome stability exclusively found in medically-relevant human fungal pathogens. It also provides a systemic scheme for the identification of genes whose products may serve as therapeutic interventions for infection by causing fewer side effects on humans. Therefore, the small molecule moderators alter expression levels of a gene known as Csa6 that may offer new avenues for treating humans sans side effects.