Abstract
Cryptococcosis is a globally distributed invasive fungal infection that is caused by species within the genus Cryptococcus which presents substantial therapeutic challenges. Although natural human-to-human transmission has never been observed, recent work has identified multiple virulence mechanisms that enable cryptococci to infect, disseminate within and ultimately kill their human host. In this Review, we describe these recent discoveries that illustrate the intricacy of host-pathogen interactions and reveal new details about the host immune responses that either help to protect against disease or increase host susceptibility. In addition, we discuss how this improved understanding of both the host and the pathogen informs potential new avenues for therapeutic development.
Original language | English (US) |
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Pages (from-to) | 106-117 |
Number of pages | 12 |
Journal | Nature Reviews Microbiology |
Volume | 14 |
Issue number | 2 |
DOIs | |
State | Published - Feb 1 2016 |
Bibliographical note
Funding Information:The authors gratefully acknowledge the help of S. Kannambath in preparing Figure 3 and apologize to those colleagues in the field whose work could not be included in this Review owing to space constraints. R.C.M. is supported by funding from the European Research Council, Medical Research Council, Lister Institute and Royal Society. D.L.W. received support from the US National Institutes of Health (NIH) T32 training grant AI007313, a University of Minnesota Doctoral Dissertation Fellowship and a Dennis W. Watson Fellowship. K.N. is supported by funding from the NIH. T.B. is supported by funding from the Wellcome Trust and the Medical Research Council (UK). N.R.H.S. is supported by a Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology to the University of Aberdeen
Funding Information:
The authors gratefully acknowledge the help of S. Kannambath in preparing Figure 3 and apologize to those colleagues in the field whose work could not be included in this Review owing to space constraints. R.C.M. is supported by funding from the European Research Council, Medical Research Council, Lister Institute and Royal Society. D.L.W. received support from the US National Institutes of Health (NIH) T32 training grant AI007313, a University of Minnesota Doctoral Dissertation Fellowship and a Dennis W. Watson Fellowship. K.N. is supported by funding from the NIH. T.B. is supported by funding from the Wellcome Trust and the Medical Research Council (UK). N.R.H.S. is supported by a Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology to the University of Aberdeen.
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