ArticleThe American journal of pathology2012
Virulence factors identified by Cryptococcus neoformans mutant screen differentially modulate lung immune responses and brain dissemination.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- The phenotype of the Cryptococcus-specific CD4+ memory T-cell response is associated with disease severity and outcome in HIV-associated cryptococcal meningitis.The Journal of infectious diseases · 2013Trial
- From microtubule remodeling to clinical translation: the multifaceted roles of vasohibin-1 in disease modulation.Frontiers in immunology · 2026Review
- Cryptococcus exploits delayed microglial activation, and microglial osteopontin/Spp1 impairs peripheral host control.Cell host & microbe · 2025Article
- Cryptococcal nutrient acquisition and pathogenesis: dining on the host.Microbiology and molecular biology reviews : MMBR · 2025Review
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- Transcriptional Changes in Pulmonary Phagocyte Subsets Dictate the Outcome Following Interaction With The Fungal PathogenFrontiers in immunology · 2021Article
- Clinical Aspects of Immune Damage in Cryptococcosis.Current fungal infection reports · 2019Article
- Sensitive bioluminescence imaging of fungal dissemination to the brain in mouse models of cryptococcosis.Disease models & mechanisms · 2019Article
- Identification of T helper (Th)1- and Th2-associated antigens of Cryptococcus neoformans in a murine model of pulmonary infection.Scientific reports · 2018Article
- It's not all about us: evolution and maintenance of Cryptococcus virulence requires selection outside the human host.Yeast (Chichester, England) · 2017Article
- Exploitation of Scavenger Receptor, Macrophage Receptor with Collagenous Structure, byFrontiers in immunology · 2017Article
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- Systemic Approach to Virulence Gene Network Analysis for Gaining New Insight into Cryptococcal Virulence.Frontiers in microbiology · 2016Article
- Cryptococcal heat shock protein 70 homolog Ssa1 contributes to pulmonary expansion of Cryptococcus neoformans during the afferent phase of the immune response by promoting macrophage M2 polarization.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- New technology and resources for cryptococcal research.Fungal genetics and biology : FG & B · 2015Review
- Role of dendritic cell-pathogen interactions in the immune response to pulmonary cryptococcal infection.Future microbiology · 2015Review
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- Cryptococcus neoformans: historical curiosity to modern pathogen.Yeast (Chichester, England) · 2014Review
- The intracellular life of Cryptococcus neoformans.Annual review of pathology · 2014Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Deletions of cryptococcal PIK1, RUB1, and ENA1 genes independently rendered defects in yeast survival in human CSF and within macrophages. We evaluated virulence potential of these genes by comparing wild-type Cryptococcus neoformans strain H99 with deletant and complement strains in a BALB/c mouse model of pulmonary infection. Survival of infected mice; pulmonary cryptococcal growth and pathology; immunological parameters; dissemination kinetics; and CNS pathology were examined. Deletion of each PIK1, RUB1, and ENA1 differentially reduced pulmonary growth and dissemination rates of C. neoformans and extended mice survival. Furthermore, pik1Δ induced similar pathologies to H99, however, with significantly delayed onset; rub1Δ was more efficiently contained within pulmonary macrophages and was further delayed in causing CNS dissemination/pathology; whereas ena1Δ was progressively eliminated from the lungs and did not induce pathological lesions or disseminate into the CNS. The diminished virulence of mutant strains was associated with differential modulation of pulmonary immune responses, including changes in leukocyte subsets, cytokine responses, and macrophage activation status. Compared to H99 infection, mutants induced more hallmarks of a protective Th1 immune response, rather than Th2, and more classical, rather than alternative, macrophage activation. The magnitude of immunological effects precisely corresponded to the level of virulence displayed by each strain. Thus, cryptococcal PIK1, RUB1, and ENA1 differentially contribute to cryptococcal virulence, in correlation with their differential capacity to modulate immune responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.