Candida glabrata ( Nakaseomyces glabratus ), a prevalent opportunistic pathogenic yeast of humans, has been classified as a fungal pathogen of high priority by the World Health Organization. C. glabrata is the leading cause of invasive Candida infections in hospitalized and immunocompromised patients and displays co-resistance to azole and echinocandin drugs. C. glabrata is known for its distinct virulence attributes that facilitate infections of the host in the absence of classical virulence factors, viz. filament formation and secreted toxin. The inability of C. glabrata to induce a strong inflammatory response contributes to its persistence in the host. However, the molecular underpinnings that define the C. glabrata –host relationship are not well-understood. In this review, we summarize the findings on the interplay between C. glabrata and different host cell types and outline the molecular strategies that play a pivotal role in the establishment of C. glabrata infections. Our goal is to expand our knowledge of C. glabrata –host crosstalk and underscore the vital questions whose resolution is essential to effectively manage C. glabrata infections.
Ghosh et al. (Fri,) studied this question.