Pathogenic fungi constitute a vast and diverse kingdom of eukaryotic organisms that interact with an equally vast and diverse collection of hosts. Despite this extraordinary diversity, unrelated fungi have strikingly similar needs and interests: nutrient acquisition, growth, niche establishment, and reproduction. To support these activities, fungi have evolved remarkably sophisticated mechanisms for interacting with host organisms, and modulating the speed, timing, and magnitude of these interactions. In the case of opportunistic human fungal pathogens, these mechanisms have often emerged as a consequence of the expansion of specific gene families and clusters that confer flexibility in nutrient acquisition, host recognition, and adhesion. These evolutionary adaptations do not generally support the destruction of the host, but rather, modulate homeostasis in the host to the advantage of the fungus (Figure 1). This scenario is analogous to what happens in plant pathogens as well. Biotrophs, which do not kill their hosts and require living cells for growth, co-opt homeostasis in the host to create an advantage for the fungus. Understanding the mechanisms by which fungi modulate biological activities in both plant and animal hosts remains an area of significant research interest and practical importance. Here, we describe four themes that emerge from a consideration of common mechanisms by which plant and animal fungi resist, subvert, or evade host defenses to ultimately thrive. Figure 1 Tipping the balance for control in host–pathogen interactions; generalized schematic.
No takes yet. Share an insight, caveat, or question.
Dickman et al. (2011) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: