Abstract
Burkholderia pseudomallei is a causative agent of melioidosis that can infect humans and animals in endemic countries, specifically in Southeast Asia and tropical Australia. A fundamental component for the pathogenesis of Burkholderia pseudomallei is the capability of the bacterium to enter, survive, replicate, and cause disease in a host cell by inducing the host cell fusion. Cell fusion results in multinucleated-giant cell formation, thus enabling the dissemination of Burkholderia pseudomallei intracellularly. cGAS reacts to Burkholderia pseudomallei infection by activating the cGAS-STING pathway and subsequently limiting host’s aberrant cell division and cellular replication by inducing autophagic cell death. In this review, we discuss the host-pathogen interactions between the type VI secretion system 5 (T6SS-5) of Burkholderia pseudomallei and human cGAS pathway in melioidosis infections. Since T6SS-5 is a main virulent factor in Burkholderia pseudomallei and the cGAS pathway is vital for host immune response, elucidating their functions is important for better understanding the pathogenesis of Burkholderia pseudomallei.
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