Table 1.
Comparison of morphological attributes between 70 clinical isolates of cryptococci from HIV/AIDS patients in Botswana-Africa (adapted from [37] and summarized).
Fig 1.
Micrograph showing the budding nature of C. deuterogattii yeast (left panel) vs. titan (right panel) cells [44].
Scale bar = 5 μm.
Fig 2.
The role of Dectin-3 in host response to C. deuterogattii infection in vitro and in vivo.
(A) The C-type lectin receptor, Dectin-3, recognises C. deuterogattii (Cd) capsular glucuronoxylomannan (GXM) [64]. The recognition of GXM leads to the activation of NF-κB and ERK signalling pathways to drive proinflammatory cytokine production. (B) Dectin-3 deficient mice showed increased susceptibility to C. deuterogattii infection [64]. Figure created with BioRender.com.
Table 2.
List of virulence-related phenotypic traits whose underlying molecular, genetic, and metabolic mechanism has been studied in C. neoformans but not C. gattii.
Fig 3.
Schematic diagram illustrating CGSC distinct phenotypic virulence traits as compared to C. neoformans.
Upon inhalation from the environment, CGSC yeast cells/spores responds to the lung extracellular niche by exhibiting phenotypic traits including larger capsule (with less immunogenic properties), larger cell body (with higher degree of homogeneity), and thinner but more compacted cell wall with higher chitosan content than C. neoformans. The manner in which CGSC strains exhibit these host-adaptive traits is perhaps responsible for its low affinity to dissemination from the lungs to the brain. Within the host macrophage, the intracellular phenotypes (mitochondrial fusion and “division of labour” proliferation mechanism mediated by extracellular vesicles) exhibited by C. deuterogattii (which drives the fatal Pacific Northwest outbreak) are absent in C. neoformans.