Kristan Alexander Schneider received a B.S. degree (first diploma) in Mathematics (2001), an M.S. degree (Mag.rer.nat) in Mathematics (2002), and a Ph.D. (Dr.rer.nat) in Mathematics (2005) at the University of Vienna, Austria. During his M.S. and Ph.D. initially specialized as in mathematical population genetics with applications to theoretical ecology and shifted to infectious diseases during a two year postdoctoral appointment at Arizona State University. He completed his habilitation (venia legendi) in Mathematics at University of Vienna in 2010. He was appointed as a full professor for modelling and simulation for 12 years in Germany, before transitioning to UNM in 2024.
Research Areas
Epidemiology, infectious disease modelling, biostatistics, bioinformatics, molecular surveillance of drug resistance in malaria
Research Identifiers
ORCID iD:
https://orcid.org/0000-0003-4138-1180
Keywords
Malaria
Population genetics
Mathematics
Education and qualifications (3)
University of Vienna: Vienna, AT
Organization identifiers
University of Vienna : Vienna, AT
Other organization identifiers provided by ROR
GRID:
grid.10420.37 (preferred)
ISNI:
0000000122861424
WIKIPEDIA_URL:
http://en.wikipedia.org/wiki/University_of_Vienna (preferred)
Department
Department of Mathematics
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
University of Vienna: Vienna, AT
2003-01-03 to 2005-06-27 |
Doktor der Naturwissenschaften (Dr. rer. nat.) (Department of Mathematics)
Education
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Organization identifiers
University of Vienna : Vienna, AT
Other organization identifiers provided by ROR
GRID:
grid.10420.37 (preferred)
ISNI:
0000000122861424
WIKIPEDIA_URL:
http://en.wikipedia.org/wiki/University_of_Vienna (preferred)
Department
Department of Mathematics
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
University of Vienna: Vienna, AT
1999-10-01 to 2002-11-22 |
Magister der Naturwissenschaften (Mag. rer. nat) (Department of Mathematics)
Education
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Organization identifiers
University of Vienna : Vienna, AT
Other organization identifiers provided by ROR
GRID:
grid.10420.37 (preferred)
ISNI:
0000000122861424
WIKIPEDIA_URL:
http://en.wikipedia.org/wiki/University_of_Vienna (preferred)
Department
Department of Mathematics
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
Detecting Opioid Use Disorder in Health Claims Data With Positive Unlabeled Learning
IEEE Journal of Biomedical and Health Informatics
2025-02 | Journal article
Contributors:
Praveen Kumar; Fariha Moomtaheen; Scott A. Malec; Jeremy J. Yang; Cristian G. Bologa (and 9 more)
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Contributors
Praveen Kumar
(Author)
Fariha Moomtaheen
(Author)
Scott A. Malec
(Author)
Jeremy J. Yang
(Author)
Cristian G. Bologa
(Author)
Kristan A Schneider
(Author)
Yiliang Zhu
(Author)
Mauricio Tohen
(Author)
Gerardo Villarreal
(Author)
Douglas J. Perkins
(Author)
Elliot M. Fielstein
(Author)
Sharon E. Davis
(Author)
Michael E. Matheny
(Author)
Christophe G. Lambert
(Author)
External identifiers
Added
2025-02-10
Last modified
2025-02-10
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Crossref
Crossref
Transcriptomic and Proteomic Insights into Host Immune Responses in Pediatric Severe Malarial Anemia: Dysregulation in HSP60-70-TLR2/4 Signaling and Altered Glutamine Metabolism
Pathogens
2024-10-03 | Journal article
Contributors:
Clinton O. Onyango; Samuel B. Anyona; Ivy Hurwitz; Evans Raballah; Sharely A. Wasena (and 8 more)
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Contributors
Clinton O. Onyango
(Author)
Samuel B. Anyona
(Author)
Ivy Hurwitz
(Author)
Evans Raballah
(Author)
Sharely A. Wasena
(Author)
Shamim W. Osata
(Author)
Philip Seidenberg
(Author)
Benjamin H. McMahon
(Author)
Christophe G. Lambert
(Author)
Kristan A. Schneider
(Author)
Collins Ouma
(Author)
Qiuying Cheng
(Author)
Douglas J. Perkins
(Author)
External identifiers
Added
2024-10-03
Last modified
2024-10-03
Source:
Crossref
Crossref
Entire expressed peripheral blood transcriptome in pediatric severe malarial anemia
Nature Communications
2024-06-12 | Journal article
Contributors:
Samuel B. Anyona; Qiuying Cheng; Sharley A. Wasena; Shamim W. Osata; Yan Guo (and 9 more)
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Contributors
Samuel B. Anyona
(Author)
[ORCID: 0000-0001-5813-4018]
Qiuying Cheng
(Author)
[ORCID: 0000-0002-1343-1171]
Sharley A. Wasena
(Author)
Shamim W. Osata
(Author)
[ORCID: 0000-0002-1067-2818]
Yan Guo
(Author)
Evans Raballah
(Author)
[ORCID: 0000-0002-3304-6836]
Ivy Hurwitz
(Author)
[ORCID: 0000-0003-1566-1111]
Clinton O. Onyango
(Author)
[ORCID: 0000-0002-4197-5336]
Collins Ouma
(Author)
[ORCID: 0000-0001-8205-8887]
Philip D. Seidenberg
(Author)
Benjamin H. McMahon
(Author)
Christophe G. Lambert
(Author)
[ORCID: 0000-0003-1994-2893]
Kristan A. Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
Douglas J. Perkins
(Author)
[ORCID: 0000-0001-9390-6255]
External identifiers
ISSN:
2041-1723
Abstract
AbstractThis study on severe malarial anemia (SMA: Hb < 6.0 g/dL), a leading global cause of childhood morbidity and mortality, compares the entire expressed whole blood host transcriptome between Kenyan children (3-48 mos.) with non-SMA (Hb ≥ 6.0 g/dL, n = 39) and SMA (n = 18). Differential expression analyses reveal 1403 up-regulated and 279 down-regulated transcripts in SMA, signifying impairments in host inflammasome activation, cell death, and innate immune and cellular stress responses. Immune cell profiling shows decreased memory responses, antigen presentation, and immediate pathogen clearance, suggesting an immature/improperly regulated immune response in SMA. Module repertoire analysis of blood-specific gene signatures identifies up-regulation of erythroid genes, enhanced neutrophil activation, and impaired inflammatory responses in SMA. Enrichment analyses converge on disruptions in cellular homeostasis and regulatory pathways for the ubiquitin-proteasome system, autophagy, and heme metabolism. Pathway analyses highlight activation in response to hypoxic conditions [Hypoxia Inducible Factor (HIF)−1 target and Reactive Oxygen Species (ROS) signaling] as a central theme in SMA. These signaling pathways are also top-ranking in protein abundance measures and a Ugandan SMA cohort with available transcriptomic data. Targeted RNA-Seq validation shows strong concordance with our entire expressed transcriptome data. These findings identify key molecular themes in SMA pathogenesis, offering potential targets for new malaria therapies.
Added
2024-06-20
Last modified
2024-06-20
Source:
Kristan Schneider
Kristan Schneider
A Meta Algorithm for Interpretable Ensemble Learning: The League of Experts
Machine Learning and Knowledge Extraction
2024-04-09 | Journal article
DOI:
10.3390/make6020038
Contributors:
Richard Vogel; Tobias Schlosser; Robert Manthey; Marc Ritter; Matthias Vodel (and 2 more)
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Richard Vogel
(Author)
[ORCID: 0009-0006-4306-0769]
Tobias Schlosser
(Author)
[ORCID: 0000-0002-0682-4284]
Robert Manthey
(Author)
[ORCID: 0009-0007-4243-5343]
Marc Ritter
(Author)
[ORCID: 0009-0004-0204-8275]
Matthias Vodel
(Author)
[ORCID: 0000-0002-5669-9872]
Maximilian Eibl
(Author)
[ORCID: 0000-0002-9519-2708]
Kristan Alexander Schneider
(Author)
External identifiers
DOI:
10.3390/make6020038
ISSN:
2504-4990
Abstract
Background. The importance of explainable artificial intelligence and machine learning (XAI/XML) is increasingly being recognized, aiming to understand how information contributes to decisions, the method’s bias, or sensitivity to data pathologies. Efforts are often directed to post hoc explanations of black box models. These approaches add additional sources for errors without resolving their shortcomings. Less effort is directed into the design of intrinsically interpretable approaches. Methods. We introduce an intrinsically interpretable methodology motivated by ensemble learning: the League of Experts (LoE) model. We establish the theoretical framework first and then deduce a modular meta algorithm. In our description, we focus primarily on classification problems. However, LoE applies equally to regression problems. Specific to classification problems, we employ classical decision trees as classifier ensembles as a particular instance. This choice facilitates the derivation of human-understandable decision rules for the underlying classification problem, which results in a derived rule learning system denoted as RuleLoE. Results. In addition to 12 KEEL classification datasets, we employ two standard datasets from particularly relevant domains—medicine and finance—to illustrate the LoE algorithm. The performance of LoE with respect to its accuracy and rule coverage is comparable to common state-of-the-art classification methods. Moreover, LoE delivers a clearly understandable set of decision rules with adjustable complexity, describing the classification problem. Conclusions. LoE is a reliable method for classification and regression problems with an accuracy that seems to be appropriate for situations in which underlying causalities are in the center of interest rather than just accurate predictions or classifications.
Added
2024-05-07
Last modified
2024-05-07
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Kristan Schneider
Kristan Schneider
Estimating multiplicity of infection, allele frequencies, and prevalences accounting for incomplete data
PLOS ONE
2024-03-21 | Journal article
Contributors:
Meraj Hashemi; Kristan A. Schneider
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Meraj Hashemi
(Author)
[ORCID: 0000-0001-7151-439X]
Kristan A. Schneider
(Author)
External identifiers
ISSN:
1932-6203
Abstract
Background
Molecular surveillance of infectious diseases allows the monitoring of pathogens beyond the granularity of traditional epidemiological approaches and is well-established for some of the most relevant infectious diseases such as malaria. The presence of genetically distinct pathogenic variants within an infection, referred to as multiplicity of infection (MOI) or complexity of infection (COI) is common in malaria and similar infectious diseases. It is an important metric that scales with transmission intensities, potentially affects the clinical pathogenesis, and a confounding factor when monitoring the frequency and prevalence of pathogenic variants. Several statistical methods exist to estimate MOI and the frequency distribution of pathogen variants. However, a common problem is the quality of the underlying molecular data. If molecular assays fail not randomly, it is likely to underestimate MOI and the prevalence of pathogen variants.
Methods and findings
A statistical model is introduced, which explicitly addresses data quality, by assuming a probability by which a pathogen variant remains undetected in a molecular assay. This is different from the assumption of missing at random, for which a molecular assay either performs perfectly or fails completely. The method is applicable to a single molecular marker and allows to estimate allele-frequency spectra, the distribution of MOI, and the probability of variants to remain undetected (incomplete information). Based on the statistical model, expressions for the prevalence of pathogen variants are derived and differences between frequency and prevalence are discussed. The usual desirable asymptotic properties of the maximum-likelihood estimator (MLE) are established by rewriting the model into an exponential family. The MLE has promising finite sample properties in terms of bias and variance. The covariance matrix of the estimator is close to the Cramér-Rao lower bound (inverse Fisher information). Importantly, the estimator’s variance is larger than that of a similar method which disregards incomplete information, but its bias is smaller.
Conclusions
Although the model introduced here has convenient properties, in terms of the mean squared error it does not outperform a simple standard method that neglects missing information. Thus, the new method is recommendable only for data sets in which the molecular assays produced poor-quality results. This will be particularly true if the model is extended to accommodate information from multiple molecular markers at the same time, and incomplete information at one or more markers leads to a strong depletion of sample size.
Added
2024-05-07
Last modified
2024-05-07
Source:
Kristan Schneider
Kristan Schneider
Repurposing FDA‐approved drugs to target malaria through inhibition of dihydrofolate reductase in the folate biosynthesis pathway: A prospective approach
Journal of Cellular Biochemistry
2024-03 | Journal article
DOI:
10.1002/jcb.30533
Contributors:
Kanika Verma; Rini Chaturvedi; Ayush K. Lahariya; Anil K. Verma; Kristan A. Schneider (and 2 more)
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Contributors
Kanika Verma
(Author)
Rini Chaturvedi
(Author)
Ayush K. Lahariya
(Author)
Anil K. Verma
(Author)
Kristan A. Schneider
(Author)
Anup R. Anvikar
(Author)
Praveen K. Bharti
(Author)
[ORCID: 0000-0003-4675-6869]
External identifiers
Abstract
AbstractDihydrofolate reductase (DHFR) is a ubiquitous enzyme that regulates the biosynthesis of tetrahydrofolate among various species of Plasmodium parasite. It is a validated target of the antifolate drug pyrimethamine (Pyr) in Plasmodium falciparum (Pf), but its clinical efficacy has been hampered due to the emergence of drug resistance. This has made the attempt to screen Food & Drug Administration‐approved drugs against wild‐ and mutant PfDHFR by employing an in‐silico pipeline to identify potent candidates. The current study has followed a virtual screening approach for identifying potential DHFR inhibitors from DrugBank database, based on a structure similarity search of candidates, followed by absorption, distribution, metabolism, and excretion estimation. The screened drugs were subjected to various parameters like docking, molecular mechanics with generalized born and surface area solvation calculations, and molecular simulations. We have thus identified two potential drug candidates, duloxetine and guanethidine, which can be repurposed to be tested for their efficacy against wild type and drug resistant falciparum malaria.
Added
2024-05-07
Last modified
2024-05-07
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Kristan Schneider
Kristan Schneider
Antimicrobial stewardship capacity and antibiotic utilisation practices in the Cape Coast Teaching Hospital, Ghana: A point prevalence survey study
PLOS ONE
2024-01-25 | Journal article
Contributors:
Elizabeth Agyare; Joseph Elikem Efui Acolatse; Mavis Puopelle Dakorah; George Akafity; Victoria J. Chalker (and 10 more)
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Contributors
Elizabeth Agyare
(Author)
Joseph Elikem Efui Acolatse
(Author)
[ORCID: 0000-0001-6556-3208]
Mavis Puopelle Dakorah
(Author)
George Akafity
(Author)
Victoria J. Chalker
(Author)
Owen B. Spiller
(Author)
Kristan Alexander Schneider
(Author)
Saviour Yevutsey
(Author)
Nana Benyin Aidoo
(Author)
Sophia Blankson
(Author)
Frederick Mensah-Acheampong
(Author)
Robert Incoom
(Author)
Amanj Kurdi
(Author)
[ORCID: 0000-0001-5036-1988]
Brian Godman
(Author)
[ORCID: 0000-0001-6539-6972]
Eric Kofi Ngyedu
(Author)
External identifiers
ISSN:
1932-6203
Abstract
Introduction
Antimicrobial resistance (AMR) is a global threat that necessitates coordinated strategies to improve antibiotic prescribing and reduce AMR. A key activity is ascertaining current prescribing patterns in hospitals to identify targets for quality improvement programmes.
Methods
The World Health Organisation point prevalence survey methodology was used to assess antibiotic prescribing in the Cape Coast Teaching Hospital. All core variables identified by the methodology were recorded.
Results
A total of 78.8% (82/104) patients were prescribed at least one antibiotic, with the majority from adult surgical wards (52.14%). Significantly longer hospital stays were associated with patients who underwent surgery (p = 0.0423). “Access” antibiotics dominated total prescriptions (63.8%, 132/207) with ceftriaxone, cefuroxime, and ciprofloxacin being the most prescribed “Watch” antibiotics. The most common indications were for medical prophylaxis (59.8%, 49/82) and surgical prophylaxis (46.3%, 38/82). Over one-third of surgical prophylaxis (34.2%, 13/38) indications extended beyond one day. There was moderate documentation of reasons for antibiotic treatment in patient notes (65.9%, 54/82), and targeted therapy after samples were taken for antimicrobial susceptibility testing (41.7%, 10/24). Guideline compliance was low (25%) where available.
Conclusions
There was high use of antibiotics within the hospital which needs addressing. Identified quality targets include developing surgical prophylaxis guidelines, reviewing “Watch” antibiotic prescribing, and assessing antibiotic durations for patients on two or more antibiotics. Organizational-level deficiencies were also identified that need addressing to help instigate ASPs. These can be addressed by developing local prescribing protocols and antibiotic stewardship policies in this hospital and wider in Ghana and across Africa.
Added
2024-05-07
Last modified
2024-05-07
Source:
Kristan Schneider
Kristan Schneider
Low Prevalence of Antimalarial Resistance Mutations in India During 2014–2015: Impact of Combining First-line Therapy With Primaquine
The Journal of Infectious Diseases
2023-12-02 | Journal article
Contributors:
Nazia A Ali; Shrikant Nema; Kristan A Schneider; Sri Krishna; Anil Kumar Verma (and 2 more)
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Nazia A Ali
(Author)
Shrikant Nema
(Author)
[ORCID: 0000-0003-0296-8296]
Kristan A Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
Sri Krishna
(Author)
Anil Kumar Verma
(Author)
[ORCID: 0000-0002-3105-4138]
Aparup Das
(Author)
[ORCID: 0000-0002-4081-5816]
Praveen Kumar Bharti
(Author)
[ORCID: 0000-0003-2548-4884]
External identifiers
Abstract
Abstract
Background
Antimalarial drug resistance surveillance and containment are crucial for countries aiming to eliminate malaria. Monitoring resistance evolution through studies before and after treatment policy changes is essential.
Methods
A total of 939 Plasmodium falciparum-positive blood samples were collected between 2014 and 2015 across 10 sites in India, categorized into 4 geographic clusters. Polymerase chain reaction-amplified products were sequenced to identify point mutations at drug resistance-conferring genes (Pfdhfr, Pfdhps, Pfmdr1, and Pfk13).
Results
Triple Pfdhfr mutants were found only in northeast India bordering Myanmar, while the wild type (WT) was dominant in central India. Pfdhps WTs were prevalent in all areas, and no double mutants were found. Except in northwest India, Pfmdr1 WT was dominant in all clusters. Nonsynonymous double mutations were only found in northwest India. Only synonymous mutations occurred in Pfk13. These were found in central India at a low frequency. The pattern of linkage disequilibrium and principal component analysis reflects low pressure for drug resistance and heterogeneity between the geographic clusters.
Conclusions
Resistance levels were highest in northeast India, close to the Myanmar border, where resistance is common. Primaquine has been widely used as a gametocidal and schizonticidal drug, likely contributing to maintaining low drug resistance levels and preventing strong selection for resistance.
Background
Antimalarial drug resistance surveillance and containment are crucial for countries aiming to eliminate malaria. Monitoring resistance evolution through studies before and after treatment policy changes is essential.
Methods
A total of 939 Plasmodium falciparum-positive blood samples were collected between 2014 and 2015 across 10 sites in India, categorized into 4 geographic clusters. Polymerase chain reaction-amplified products were sequenced to identify point mutations at drug resistance-conferring genes (Pfdhfr, Pfdhps, Pfmdr1, and Pfk13).
Results
Triple Pfdhfr mutants were found only in northeast India bordering Myanmar, while the wild type (WT) was dominant in central India. Pfdhps WTs were prevalent in all areas, and no double mutants were found. Except in northwest India, Pfmdr1 WT was dominant in all clusters. Nonsynonymous double mutations were only found in northwest India. Only synonymous mutations occurred in Pfk13. These were found in central India at a low frequency. The pattern of linkage disequilibrium and principal component analysis reflects low pressure for drug resistance and heterogeneity between the geographic clusters.
Conclusions
Resistance levels were highest in northeast India, close to the Myanmar border, where resistance is common. Primaquine has been widely used as a gametocidal and schizonticidal drug, likely contributing to maintaining low drug resistance levels and preventing strong selection for resistance.
Added
2024-05-07
Last modified
2024-05-07
Source:
Kristan Schneider
Kristan Schneider
Human NCR3 gene variants rs2736191 and rs11575837 alter longitudinal risk for development of pediatric malaria episodes and severe malarial anemia
BMC Genomics
2023-09-13 | Journal article
Contributors:
Clinton O. Onyango; Qiuying Cheng; Elly O. Munde; Evans Raballah; Samuel B. Anyona (and 6 more)
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Contributors
Clinton O. Onyango
(Author)
Qiuying Cheng
(Author)
Elly O. Munde
(Author)
Evans Raballah
(Author)
Samuel B. Anyona
(Author)
Benjamin H. McMahon
(Author)
Christophe G. Lambert
(Author)
Patrick O. Onyango
(Author)
Kristan A. Schneider
(Author)
Douglas J. Perkins
(Author)
Collins Ouma
(Author)
External identifiers
ISSN:
1471-2164
Abstract
Abstract
Background
Plasmodium falciparum malaria is a leading cause of pediatric morbidity and mortality in holoendemic transmission areas. Severe malarial anemia [SMA, hemoglobin (Hb) G and rs11575837:C > T) and their haplotypes. The prospective observational study was conducted over a 36 mos. follow-up period in a cohort of children (n = 1,515, aged 1.9–40 mos.) residing in a holoendemic P. falciparum transmission region, Siaya, Kenya.
Results
Poisson regression modeling, controlling for anemia-promoting covariates, revealed a significantly increased risk of malaria in carriers of the homozygous mutant allele genotype (TT) for rs11575837 after multiple test correction [Incidence rate ratio (IRR) = 1.540, 95% CI = 1.114–2.129, P = 0.009]. Increased risk of SMA was observed for rs2736191 in children who inherited the CG genotype (IRR = 1.269, 95% CI = 1.009–1.597, P = 0.041) and in the additive model (presence of 1 or 2 copies) (IRR = 1.198, 95% CI = 1.030–1.393, P = 0.019), but was not significant after multiple test correction. Modeling of the haplotypes revealed that the CC haplotype had a significant additive effect for protection against SMA (i.e., reduced risk for development of SMA) after multiple test correction (IRR = 0.823, 95% CI = 0.711–0.952, P = 0.009). Although increased susceptibility to SMA was present in carriers of the GC haplotype (IRR = 1.276, 95% CI = 1.030–1.581, P = 0.026) with an additive effect (IRR = 1.182, 95% CI = 1.018–1.372, P = 0.029), the results did not remain significant after multiple test correction. None of the NCR3 genotypes or haplotypes were associated with all-cause mortality.
Conclusions
Variation in NCR3 alters susceptibility to malaria and SMA during the acquisition of naturally-acquired malarial immunity. These results highlight the importance of NK cells in the innate immune response to malaria.
Background
Plasmodium falciparum malaria is a leading cause of pediatric morbidity and mortality in holoendemic transmission areas. Severe malarial anemia [SMA, hemoglobin (Hb) G and rs11575837:C > T) and their haplotypes. The prospective observational study was conducted over a 36 mos. follow-up period in a cohort of children (n = 1,515, aged 1.9–40 mos.) residing in a holoendemic P. falciparum transmission region, Siaya, Kenya.
Results
Poisson regression modeling, controlling for anemia-promoting covariates, revealed a significantly increased risk of malaria in carriers of the homozygous mutant allele genotype (TT) for rs11575837 after multiple test correction [Incidence rate ratio (IRR) = 1.540, 95% CI = 1.114–2.129, P = 0.009]. Increased risk of SMA was observed for rs2736191 in children who inherited the CG genotype (IRR = 1.269, 95% CI = 1.009–1.597, P = 0.041) and in the additive model (presence of 1 or 2 copies) (IRR = 1.198, 95% CI = 1.030–1.393, P = 0.019), but was not significant after multiple test correction. Modeling of the haplotypes revealed that the CC haplotype had a significant additive effect for protection against SMA (i.e., reduced risk for development of SMA) after multiple test correction (IRR = 0.823, 95% CI = 0.711–0.952, P = 0.009). Although increased susceptibility to SMA was present in carriers of the GC haplotype (IRR = 1.276, 95% CI = 1.030–1.581, P = 0.026) with an additive effect (IRR = 1.182, 95% CI = 1.018–1.372, P = 0.029), the results did not remain significant after multiple test correction. None of the NCR3 genotypes or haplotypes were associated with all-cause mortality.
Conclusions
Variation in NCR3 alters susceptibility to malaria and SMA during the acquisition of naturally-acquired malarial immunity. These results highlight the importance of NK cells in the innate immune response to malaria.
Added
2024-05-07
Last modified
2024-05-07
Source:
Kristan Schneider
Kristan Schneider
Estimating multiplicity of infection, haplotype frequencies, and linkage disequilibria from multi-allelic markers for molecular disease surveillance
2023-08-30 | Preprint
Contributors:
Henri Christian Junior Tsoungui Obama; Kristan Alexander Schneider
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Henri Christian Junior Tsoungui Obama
(Author)
Kristan Alexander Schneider
(Author)
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Added
2023-08-30
Last modified
2023-08-30
Source:
Crossref
Crossref
Disproportionate impact of COVID-19 severity and mortality on hospitalized American Indian/Alaska Native patients
PNAS Nexus
2023-08-01 | Journal article
Contributors:
Ivy Hurwitz; Alexandra V Yingling; Teah Amirkabirian; Amber Castillo; Jehanzaeb J Khan (and 18 more)
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Contributors
Ivy Hurwitz
(Author)
[ORCID: 0000-0003-1566-1111]
Alexandra V Yingling
(Author)
Teah Amirkabirian
(Author)
Amber Castillo
(Author)
[ORCID: 0000-0002-9037-9215]
Jehanzaeb J Khan
(Author)
Alexandra Do
(Author)
[ORCID: 0009-0009-7365-7306]
Dominic K Lundquist
(Author)
October Barnes
(Author)
Christophe G Lambert
(Author)
[ORCID: 0000-0003-1994-2893]
Annabeth Fieck
(Author)
Gregory Mertz
(Author)
Clinton Onyango
(Author)
Samuel B Anyona
(Author)
[ORCID: 0000-0001-5813-4018]
J Pedro Teixeira
(Author)
[ORCID: 0000-0002-2466-9644]
Michelle Harkins
(Author)
[ORCID: 0000-0002-9679-2553]
Mark Unruh
(Author)
[ORCID: 0000-0001-7103-656X]
Qiuying Cheng
(Author)
[ORCID: 0000-0002-1343-1171]
Shuguang Leng
(Author)
[ORCID: 0000-0002-9860-8158]
Philip Seidenberg
(Author)
Anthony Worsham
(Author)
[ORCID: 0000-0003-4367-4577]
Jens O Langsjoen
(Author)
Kristan A Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
Douglas J Perkins
(Author)
[ORCID: 0000-0001-9390-6255]
External identifiers
ISSN:
2752-6542
Abstract
Abstract
Epidemiological data across the United States of America illustrate health disparities in COVID-19 infection, hospitalization, and mortality by race/ethnicity. However, limited information is available from prospective observational studies in hospitalized patients, particularly for American Indian or Alaska Native (AI/AN) populations. Here, we present risk factors associated with severe COVID-19 and mortality in patients (4/2020–12/2021, n = 475) at the University of New Mexico Hospital. Data were collected on patient demographics, infection duration, laboratory measures, comorbidities, treatment(s), major clinical events, and in-hospital mortality. Severe disease was defined by COVID-related intensive care unit requirements and/or death. The cohort was stratified by self-reported race/ethnicity: AI/AN (30.7%), Hispanic (47.0%), non-Hispanic White (NHW, 18.5%), and Other (4.0%, not included in statistical comparisons). Despite similar timing of infection and comparable comorbidities, admission characteristics for AI/AN patients included younger age (P = 0.02), higher invasive mechanical ventilation requirements (P = 0.0001), and laboratory values indicative of more severe disease. Throughout hospitalization, the AI/AN group also experienced elevated invasive mechanical ventilation (P < 0.0001), shock (P = 0.01), encephalopathy (P = 0.02), and severe COVID-19 (P = 0.0002), consistent with longer hospitalization (P < 0.0001). Self-reported AI/AN race/ethnicity emerged as the highest risk factor for severe COVID-19 (OR = 3.19; 95% CI = 1.70–6.01; P = 0.0003) and was a predictor of in-hospital mortality (OR = 2.35; 95% CI = 1.12–4.92; P = 0.02). Results from this study highlight the disproportionate impact of COVID-19 on hospitalized AI/AN patients, who experienced more severe illness and associated mortality, compared to Hispanic and NHW patients, even when accounting for symptom onset and comorbid conditions. These findings underscore the need for interventions and resources to address health disparities in the COVID-19 pandemic.
Epidemiological data across the United States of America illustrate health disparities in COVID-19 infection, hospitalization, and mortality by race/ethnicity. However, limited information is available from prospective observational studies in hospitalized patients, particularly for American Indian or Alaska Native (AI/AN) populations. Here, we present risk factors associated with severe COVID-19 and mortality in patients (4/2020–12/2021, n = 475) at the University of New Mexico Hospital. Data were collected on patient demographics, infection duration, laboratory measures, comorbidities, treatment(s), major clinical events, and in-hospital mortality. Severe disease was defined by COVID-related intensive care unit requirements and/or death. The cohort was stratified by self-reported race/ethnicity: AI/AN (30.7%), Hispanic (47.0%), non-Hispanic White (NHW, 18.5%), and Other (4.0%, not included in statistical comparisons). Despite similar timing of infection and comparable comorbidities, admission characteristics for AI/AN patients included younger age (P = 0.02), higher invasive mechanical ventilation requirements (P = 0.0001), and laboratory values indicative of more severe disease. Throughout hospitalization, the AI/AN group also experienced elevated invasive mechanical ventilation (P < 0.0001), shock (P = 0.01), encephalopathy (P = 0.02), and severe COVID-19 (P = 0.0002), consistent with longer hospitalization (P < 0.0001). Self-reported AI/AN race/ethnicity emerged as the highest risk factor for severe COVID-19 (OR = 3.19; 95% CI = 1.70–6.01; P = 0.0003) and was a predictor of in-hospital mortality (OR = 2.35; 95% CI = 1.12–4.92; P = 0.02). Results from this study highlight the disproportionate impact of COVID-19 on hospitalized AI/AN patients, who experienced more severe illness and associated mortality, compared to Hispanic and NHW patients, even when accounting for symptom onset and comorbid conditions. These findings underscore the need for interventions and resources to address health disparities in the COVID-19 pandemic.
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2024-05-07
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2024-05-07
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Kristan Schneider
Kristan Schneider
Estimating multiplicity of infection, allele frequencies, and prevalences accounting for incomplete data
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Meraj Hashemi
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Kristan A. Schneider
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2023-06-03
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2023-06-06
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India-EMBO Lecture Course: understanding malaria from molecular epidemiology, population genetics, and evolutionary perspectives
Trends in Parasitology
2023-05 | Journal article
Contributors:
Abhinav Sinha; Sonalika Kar; Nimita Deora; Manoswini Dash; Aparna Tiwari (and 3 more)
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Abhinav Sinha
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Sonalika Kar
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Nimita Deora
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Manoswini Dash
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Aparna Tiwari
(Author)
Lokesh Kori
(Author)
Kristan Schneider
(Author)
Lisa Ranford-Cartwright
(Author)
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2023-03-16
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2023-04-12
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A flexible age-dependent, spatially-stratified predictive model for the spread of COVID-19, accounting for multiple viral variants and vaccines
PLOS ONE
2023-01-20 | Journal article
Contributors:
Kristan Alexander Schneider; Mohammad-Reza Malekpour; Henri Christian Junior Tsoungui Obama; Nessma Adil Mahmoud Yousif
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Kristan Alexander Schneider
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Mohammad-Reza Malekpour
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Henri Christian Junior Tsoungui Obama
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Nessma Adil Mahmoud Yousif
(Author)
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2023-01-20
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2023-01-20
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Predicting the combined effects of case isolation, safe funeral practices, and contact tracing during Ebola virus disease outbreaks
PLOS ONE
2023-01-17 | Journal article
Contributors:
Aliou Bouba; Jan Rychtář; Kristina Barbara Helle; Kristan Alexander Schneider
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Aliou Bouba
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Jan Rychtář
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Kristina Barbara Helle
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Kristan Alexander Schneider
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2023-01-17
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2023-01-17
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Referee report. For: Optimal control model of human-to-human transmission of monkeypox virus [version 2; peer review: 2 approved with reservations, 1 not approved]
F1000 Research Limited
2023 | Journal article
Contributors:
Kristan Alexander Schneider; author; Martin Eichner
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Kristan Alexander Schneider
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Martin Eichner
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2024-05-07
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2024-05-07
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Kristan Schneider
Kristan Schneider
Genetic variation in CSF2 (5q31.1) is associated with longitudinal susceptibility to pediatric malaria, severe malarial anemia, and all-cause mortality in a high-burden malaria and HIV region of Kenya
Tropical Medicine and Health
2022-12 | Journal article
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Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1349-4147
Abstract
AbstractPlasmodium falciparum infections remain among the leading causes of morbidity and mortality in holoendemic transmission areas. Located within region 5q31.1, the colony-stimulating factor 2 gene (CSF2) encodes granulocyte–macrophage colony-stimulating factor (GM-CSF), a hematopoietic growth factor that mediates host immune responses. Since the effect of CSF2 variation on malaria pathogenesis remains unreported, we investigated the impact of two genetic variants in the 5q31.1 gene region flanking CSF2:g-7032 G > A (rs168681:G > A) and CSF2:g.64544T > C (rs246835:T > C) on the rate and timing of malaria and severe malarial anemia (SMA, Hb
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Screening of potential antiplasmodial agents targeting cysteine protease-Falcipain 2: a computational pipeline
Journal of Biomolecular Structure and Dynamics
2022-10-11 | Journal article
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Kristan Schneider
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Kristan Schneider
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Predicting the combined effects of case isolation, safe funeral practices, and contact tracing during Ebola virus disease outbreaks
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Kristan Schneider
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AbstractBackgroundThe recent outbreaks of Ebola virus disease (EVD) in Uganda and the Marburg virus disease in Ghana reflect a persisting threat of Filoviridae to the global health community. Characteristic of Filoviridae are not just their high case fatality rates, but also that corpses are highly contagious and prone to cause infections in the absence of appropriate precautions. Vaccines against the most virulent Ebolavirus species, the Zaire ebolavirus (ZEBOV) are approved. However, there exists no approved vaccine or treatment against the Sudan ebolavirus (SUDV) which causes the current outbreak of EVD. Hence, the control of the outbreak relies on case isolation, safe funeral practices, and contact tracing. So far, the effectiveness of these control measures was studied only separately by epidemiological models, while the impact of their interaction is unclear.Methods and findingsTo sustain decision making in public health-emergency management, we introduce a predictive model to study the interaction of case isolation, safe funeral practices, and contact tracing. The model is a complex extension of an SEIR-type model, and serves as an epidemic preparedness tool. The model considers different phases of the EVD infections, the possibility of infections being treated in isolation (if appropriately diagnosed), in hospital (if not properly diagnosed), or at home (if the infected do not present to hospital for whatever reason). It is assumed that the corpses of those who died in isolation are buried with proper safety measures, while those who die outside isolation might be buried unsafely, such that transmission can occur during the funeral. Furthermore, the contacts of individuals in isolation will be traced. Based on parameter estimates from the scientific literature, the model suggests that proper diagnosis and hence isolation of cases has the highest impact in reducing the size of the outbreak. However, the combination of case isolation and safe funeral practices alone are insufficient to fully contain the epidemic under plausible parameters. This changes if these measures are combined with contact tracing. In addition, shortening the time to successfully trace back contacts contribute substantially to contain the outbreak.ConclusionsIn the absence of an approved vaccine and treatment, EVD management by proper and fast diagnostics in combination with epidemic awareness are fundamental. Awareness will particularly facilitate contact tracing and safe funeral practices. Moreover, proper and fast diagnostics are a major determinant of case isolation. The model introduced here is not just applicable to EVD, but also to other hemorrhagic diseases such as the MVD or the Lassa fever.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
The many definitions of multiplicity of infection
Frontiers in Epidemiology
2022-10-05 | Journal article
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
2674-1199
Abstract
The presence of multiple genetically different pathogenic variants within the same individual host is common in infectious diseases. Although this is neglected in some diseases, it is well recognized in others like malaria, where it is typically referred to as multiplicity of infection (MOI) or complexity of infection (COI). In malaria, with the advent of molecular surveillance, data is increasingly being available with enough resolution to capture MOI and integrate it into molecular surveillance strategies. The distribution of MOI on the population level scales with transmission intensities, while MOI on the individual level is a confounding factor when monitoring haplotypes of particular interests, e.g., those associated with drug-resistance. Particularly, in high-transmission areas, MOI leads to a discrepancy between the likelihood of a haplotype being observed in an infection (prevalence) and its abundance in the pathogen population (frequency). Despite its importance, MOI is not universally defined. Competing definitions vary from verbal ones to those based on concise statistical frameworks. Heuristic approaches to MOI are popular, although they do not mine the full potential of available data and are typically biased, potentially leading to misinferences. We introduce a formal statistical framework and suggest a concise definition of MOI and its distribution on the host-population level. We show how it relates to alternative definitions such as the number of distinct haplotypes within an infection or the maximum number of alleles detectable across a set of genetic markers. It is shown how alternatives can be derived from the general framework. Different statistical methods to estimate the distribution of MOI and pathogenic variants at the population level are discussed. The estimates can be used as plug-ins to reconstruct the most probable MOI of an infection and set of infecting haplotypes in individual infections. Furthermore, the relation between prevalence of pathogenic variants and their frequency (relative abundance) in the pathogen population in the context of MOI is clarified, with particular regard to seasonality in transmission intensities. The framework introduced here helps to guide the correct interpretation of results emerging from different definitions of MOI. Especially, it excels comparisons between studies based on different analytical methods.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Yes, it matters who is spreading monkeypox – Authors' reply
The Lancet Infectious Diseases
2022-10 | Journal article
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1473-3099
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Gametocytogenesis-enhancing drug combinations can facilitate artemisinin resistance despite better clinical outcomes
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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Abstract
Background: Malaria eradication goals are threatened by the spread of artemisinin resistance, which is an evolutionary process. The selective advantage of mutations in Plasmodium falciparum conferring tolerance or even resistance is determined as the probability of their successful transmission. The drug’s efficacy in clearing merozoites is the main determinant for the clinical pathogenesis, but only one of many factors determining successful transmission. The actual steps in the transmission cycles contribute as “fitness components”. The abundance of gametocytes is crucial in mediating how the selective advantage at the merozoite level is translated into evolutionary fitness. In this context it is important to recognize that some drugs are associated with higher gametocytaemia.
Method: A mechanistic model, which quantitatively describes how evolutionary fitness is determined by the parasite's life history in interaction with antimalarial drugs is formulated. The hypothetical effect of a gametocytogenesis-enhancing drug action on the evolutionary fitness is included. Once fitness is determined, an evolutionary-genetic model is used to describe the resulting trajectory of drug resistance evolution.
Results: Assuming intuitive model parameters, the evolutionary fitness of two alternative drug treatments with the same effectiveness on asexual parasites, with and without a gametocytogenesis-enhancing effect are contrasted. The gametocytogenesis-enhancing effect leads to a substantially faster spread of drug resistance. This result changes quantitatively, but not qualitatively, if a threshold gametocytaemia is assumed for successful malaria transmission. Isolating infections in quarantine in order to prevent transmission, can substantially accelerate the dispersion of resistance if antimalarials delay gametocyte development.
Conclusions: Gametocytogenesis-enhancing drug treatments can excel the spread of resistance. Initially it might appear that such a treatment leads to improved clinical outcomes, because drug resistance is difficult to detect on a population-level as long as resistance-conferring mutations have low prevalence. Hence, partnering artemisinin with drugs such as sulfadoxine-pyrimethamine of amodiaquine, which have been associated with higher gametocytaemia, might facilitate the spread of resistance.
Background: Malaria eradication goals are threatened by the spread of artemisinin resistance, which is an evolutionary process. The selective advantage of mutations in Plasmodium falciparum conferring tolerance or even resistance is determined as the probability of their successful transmission. The drug’s efficacy in clearing merozoites is the main determinant for the clinical pathogenesis, but only one of many factors determining successful transmission. The actual steps in the transmission cycles contribute as “fitness components”. The abundance of gametocytes is crucial in mediating how the selective advantage at the merozoite level is translated into evolutionary fitness. In this context it is important to recognize that some drugs are associated with higher gametocytaemia.
Method: A mechanistic model, which quantitatively describes how evolutionary fitness is determined by the parasite's life history in interaction with antimalarial drugs is formulated. The hypothetical effect of a gametocytogenesis-enhancing drug action on the evolutionary fitness is included. Once fitness is determined, an evolutionary-genetic model is used to describe the resulting trajectory of drug resistance evolution.
Results: Assuming intuitive model parameters, the evolutionary fitness of two alternative drug treatments with the same effectiveness on asexual parasites, with and without a gametocytogenesis-enhancing effect are contrasted. The gametocytogenesis-enhancing effect leads to a substantially faster spread of drug resistance. This result changes quantitatively, but not qualitatively, if a threshold gametocytaemia is assumed for successful malaria transmission. Isolating infections in quarantine in order to prevent transmission, can substantially accelerate the dispersion of resistance if antimalarials delay gametocyte development.
Conclusions: Gametocytogenesis-enhancing drug treatments can excel the spread of resistance. Initially it might appear that such a treatment leads to improved clinical outcomes, because drug resistance is difficult to detect on a population-level as long as resistance-conferring mutations have low prevalence. Hence, partnering artemisinin with drugs such as sulfadoxine-pyrimethamine of amodiaquine, which have been associated with higher gametocytaemia, might facilitate the spread of resistance.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
A maximum-likelihood method to estimate haplotype frequencies and prevalence alongside multiplicity of infection from SNP data
Frontiers in Epidemiology
2022-09-23 | Journal article
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
2674-1199
Abstract
The introduction of genomic methods facilitated standardized molecular disease surveillance. For instance, SNP barcodes in Plasmodium vivax and Plasmodium falciparum malaria allows the characterization of haplotypes, their frequencies and prevalence to reveal temporal and spatial transmission patterns. A confounding factor is the presence of multiple genetically distinct pathogen variants within the same infection, known as multiplicity of infection (MOI). Disregarding ambiguous information, as usually done in ad-hoc approaches, leads to less confident and biased estimates. We introduce a statistical framework to obtain maximum-likelihood estimates (MLE) of haplotype frequencies and prevalence alongside MOI from malaria SNP data, i.e., multiple biallelic marker loci. The number of model parameters increases geometrically with the number of genetic markers considered and no closed-form solution exists for the MLE. Therefore, the MLE needs to be derived numerically. We use the Expectation-Maximization (EM) algorithm to derive the maximum-likelihood estimates, an efficient and easy-to-implement algorithm that yields a numerically stable solution. We also derive expressions for haplotype prevalence based on either all or just the unambiguous genetic information and compare both approaches. The latter corresponds to a biased ad-hoc estimate of prevalence. We assess the performance of our estimator by systematic numerical simulations assuming realistic sample sizes and various scenarios of transmission intensity. For reasonable sample sizes, and number of loci, the method has little bias. As an example, we apply the method to a dataset from Cameroon on sulfadoxine-pyrimethamine resistance in P. falciparum malaria. The method is not confined to malaria and can be applied to any infectious disease with similar transmission behavior. An easy-to-use implementation of the method as an R-script is provided.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Nonsynonymous amino acid changes in the α-chain of complement component 5 influence longitudinal susceptibility to Plasmodium falciparum infections and severe malarial anemia in kenyan children
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1664-8021
Abstract
Background: Severe malarial anemia (SMA; Hb < 5.0 g/dl) is a leading cause of childhood morbidity and mortality in holoendemic Plasmodium falciparum transmission regions such as western Kenya.Methods: We investigated the relationship between two novel complement component 5 (C5) missense mutations [rs17216529:C>T, p(Val145Ile) and rs17610:C>T, p(Ser1310Asn)] and longitudinal outcomes of malaria in a cohort of Kenyan children (under 60 mos, n = 1,546). Molecular modeling was used to investigate the impact of the amino acid transitions on the C5 protein structure.Results: Prediction of the wild-type and mutant C5 protein structures did not reveal major changes to the overall structure. However, based on the position of the variants, subtle differences could impact on the stability of C5b. The influence of the C5 genotypes/haplotypes on the number of malaria and SMA episodes over 36 months was determined by Poisson regression modeling. Genotypic analyses revealed that inheritance of the homozygous mutant (TT) for rs17216529:C>T enhanced the risk for both malaria (incidence rate ratio, IRR = 1.144, 95%CI: 1.059–1.236, p = 0.001) and SMA (IRR = 1.627, 95%CI: 1.201–2.204, p = 0.002). In the haplotypic model, carriers of TC had increased risk of malaria (IRR = 1.068, 95%CI: 1.017–1.122, p = 0.009), while carriers of both wild-type alleles (CC) were protected against SMA (IRR = 0.679, 95%CI: 0.542–0.850, p = 0.001).Conclusion: Collectively, these findings show that the selected C5 missense mutations influence the longitudinal risk of malaria and SMA in immune-naïve children exposed to holoendemic P. falciparum transmission through a mechanism that remains to be defined.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Does it matter who is spreading monkeypox?
The Lancet Infectious Diseases
2022-09 | Journal article
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1473-3099
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Reconsidering the incubation period of Marburg virus disease
The Lancet Infectious Diseases
2022-09 | Journal article
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1473-3099
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Investigating the impact of multiple feeding attempts on mosquito dynamics via mathematical models
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
0025-5564
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Elevated SARS-CoV-2 in peripheral blood and increased COVID-19 severity in American Indians/Alaska Natives
Experimental Biology and Medicine
2022-07 | Journal article
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Kristan Schneider
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Kristan Schneider
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Abstract
Epidemiological data across the United States show health disparities in COVID-19 infection, hospitalization, and mortality by race/ethnicity. While the association between elevated SARS-CoV-2 viral loads (VLs) (i.e. upper respiratory tract (URT) and peripheral blood (PB)) and increased COVID-19 severity has been reported, data remain largely unavailable for some disproportionately impacted racial/ethnic groups, particularly for American Indian or Alaska Native (AI/AN) populations. As such, we determined the relationship between SARS-CoV-2 VL dynamics and disease severity in a diverse cohort of hospitalized patients. Results presented here are for study participants ( n = 94, ages 21–88 years) enrolled in a prospective observational study between May and October 2020 who had SARS-CoV-2 viral clades 20A, C, and G. Based on self-reported race/ethnicity and sample size distribution, the cohort was stratified into two groups: (AI/AN, n = 43) and all other races/ethnicities combined (non-AI/AN, n = 51). SARS-CoV-2 VLs were quantified in the URT and PB on days 0–3, 6, 9, and 14. The strongest predictor of severe COVID-19 in the study population was the mean VL in PB (OR = 3.34; P = 2.00 × 10−4). The AI/AN group had the following: (1) comparable co-morbidities and admission laboratory values, yet more severe COVID-19 (OR = 4.81; P = 0.014); (2) a 2.1 longer duration of hospital stay ( P = 0.023); and (3) higher initial and cumulative PB VLs during severe disease ( P = 0.025). Moreover, self-reported race/ethnicity as AI/AN was the strongest predictor of elevated PB VLs ( β = 1.08; P = 6.00 × 10−4) and detection of SARS-CoV-2 in PB (hazard ratio = 3.58; P = 0.004). The findings presented here suggest a strong relationship between PB VL (magnitude and frequency) and severe COVID-19, particularly for the AI/AN group.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Complement component 3 mutations alter the longitudinal risk of pediatric malaria and severe malarial anemia
Experimental Biology and Medicine
2022-04 | Journal article
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Kristan Schneider
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Kristan Schneider
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Severe malarial anemia (SMA) is a leading cause of childhood morbidity and mortality in holoendemic Plasmodium falciparum transmission regions. To gain enhanced understanding of predisposing factors for SMA, we explored the relationship between complement component 3 (C3) missense mutations [rs2230199 (2307C>G, Arg>Gly102) and rs11569534 (34420G>A, Gly>Asp1224)], malaria, and SMA in a cohort of children (n = 1617 children) over 36 months of follow-up. Variants were selected based on their ability to impart amino acid substitutions that can alter the structure and function of C3. The 2307C>G mutation results in a basic to a polar residue change (Arg to Gly) at position 102 (β-chain) in the macroglobulin-1 (MG1) domain, while 34420G>A elicits a polar to acidic residue change (Gly to Asp) at position 1224 (α-chain) in the thioester-containing domain. After adjusting for multiple comparisons, longitudinal analyses revealed that inheritance of the homozygous mutant (GG) at 2307 enhanced the risk of SMA (RR = 2.142, 95%CI: 1.229–3.735, P = 0.007). The haplotype containing both wild-type alleles (CG) decreased the incident risk ratio of both malaria (RR = 0.897, 95%CI: 0.828–0.972, P = 0.008) and SMA (RR = 0.617, 95%CI: 0.448–0.848, P = 0.003). Malaria incident risk ratio was also reduced in carriers of the GG (Gly102Gly1224) haplotype (RR = 0.941, 95%CI: 0.888–0.997, P = 0.040). Collectively, inheritance of the missense mutations in MG1 and thioester-containing domain influence the longitudinal risk of malaria and SMA in children exposed to intense Plasmodium falciparum transmission.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Predicting the impact of COVID-19 vaccination campaigns – a flexible age-dependent, spatially-stratified predictive model, accounting for multiple viral variants and vaccines
2022-01-01 | Preprint
Contributors:
Kristan Alexander Schneider; Henri Christian Junior Tsoungui Obama; Nessma Adil Mahmoud Yousif; Pierre Marie Ngougoue Ngougoue
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Kristan Alexander Schneider
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Henri Christian Junior Tsoungui Obama
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Nessma Adil Mahmoud Yousif
(Author)
Pierre Marie Ngougoue Ngougoue
(Author)
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2022-01-02
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2022-06-02
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Bias-corrected maximum-likelihood estimation of multiplicity of infection and lineage frequencies
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1932-6203
Abstract
Background
The UN’s Sustainable Development Goals are devoted to eradicate a range of infectious diseases to achieve global well-being. These efforts require monitoring disease transmission at a level that differentiates between pathogen variants at the genetic/molecular level. In fact, the advantages of genetic (molecular) measures like multiplicity of infection (MOI) over traditional metrics, e.g., R0, are being increasingly recognized. MOI refers to the presence of multiple pathogen variants within an infection due to multiple infective contacts. Maximum-likelihood (ML) methods have been proposed to derive MOI and pathogen-lineage frequencies from molecular data. However, these methods are biased.
Methods and findings
Based on a single molecular marker, we derive a bias-corrected ML estimator for MOI and pathogen-lineage frequencies. We further improve these estimators by heuristical adjustments that compensate shortcomings in the derivation of the bias correction, which implicitly assumes that data lies in the interior of the observational space. The finite sample properties of the different variants of the bias-corrected estimators are investigated by a systematic simulation study. In particular, we investigate the performance of the estimator in terms of bias, variance, and robustness against model violations. The corrections successfully remove bias except for extreme parameters that likely yield uninformative data, which cannot sustain accurate parameter estimation. Heuristic adjustments further improve the bias correction, particularly for small sample sizes. The bias corrections also reduce the estimators’ variances, which coincide with the Cramér-Rao lower bound. The estimators are reasonably robust against model violations.
Conclusions
Applying bias corrections can substantially improve the quality of MOI estimates, particularly in areas of low as well as areas of high transmission—in both cases estimates tend to be biased. The bias-corrected estimators are (almost) unbiased and their variance coincides with the Cramér-Rao lower bound, suggesting that no further improvements are possible unless additional information is provided. Additional information can be obtained by combining data from several molecular markers, or by including information that allows stratifying the data into heterogeneous groups.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Differential Gene Expression in Host Ubiquitination Processes in Childhood Malarial Anemia
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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ISSN:
1664-8021
Abstract
Background: Malaria remains one of the leading global causes of childhood morbidity and mortality. In holoendemic Plasmodium falciparum transmission regions, such as western Kenya, severe malarial anemia [SMA, hemoglobin (Hb) < 6.0 g/dl] is the primary form of severe disease. Ubiquitination is essential for regulating intracellular processes involved in innate and adaptive immunity. Although dysregulation in ubiquitin molecular processes is central to the pathogenesis of multiple human diseases, the expression patterns of ubiquitination genes in SMA remain unexplored.Methods: To examine the role of the ubiquitination processes in pathogenesis of SMA, differential gene expression profiles were determined in Kenyan children (n = 44, aged <48 mos) with either mild malarial anemia (MlMA; Hb ≥9.0 g/dl; n = 23) or SMA (Hb <6.0 g/dl; n = 21) using the Qiagen Human Ubiquitination Pathway RT2 Profiler PCR Array containing a set of 84 human ubiquitination genes.Results: In children with SMA, 10 genes were down-regulated (BRCC3, FBXO3, MARCH5, RFWD2, SMURF2, UBA6, UBE2A, UBE2D1, UBE2L3, UBR1), and five genes were up-regulated (MDM2, PARK2, STUB1, UBE2E3, UBE2M). Enrichment analyses revealed Ubiquitin-Proteasomal Proteolysis as the top disrupted process, along with altered sub-networks involved in proteasomal, protein, and ubiquitin-dependent catabolic processes.Conclusion: Collectively, these novel results show that protein coding genes of the ubiquitination processes are involved in the pathogenesis of SMA.
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
An integrated virtual screening and drug repurposing strategy for the discovery of new antimalarial drugs against <i>Plasmodium falciparum</i> phosphatidylinositol 3‐kinase
Journal of Cellular Biochemistry
2021-10 | Journal article
DOI:
10.1002/jcb.29954
Contributors:
Kristan Schneider
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Kristan Schneider
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[ORCID: 0000-0003-4138-1180]
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2022-10-15
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2022-10-15
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Kristan Schneider
Kristan Schneider
Is increased mortality by multiple exposures to COVID-19 an overseen factor when aiming for herd immunity?
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Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1932-6203
Abstract
Background
Governments across the globe responded with different strategies to the COVID-19 pandemic. While some countries adopted measures, which have been perceived controversial, others pursued a strategy aiming for herd immunity. The latter is even more controversial and has been called unethical by the WHO Director-General. Inevitably, without proper control measures, viral diversity increases and multiple infectious exposures become common, when the pandemic reaches its maximum. This harbors not only a potential threat overseen by simplified theoretical arguments in support of herd immunity, but also deserves attention when assessing response measures to increasing numbers of infection.
Methods and findings
We extend the simulation model underlying the pandemic preparedness web interface CovidSim 1.1 (http://covidsim.eu/) to study the hypothetical effect of increased morbidity and mortality due to ‘multi-infections’, either acquired at by successive infective contacts during the course of one infection or by a single infective contact with a multi-infected individual. The simulations are adjusted to reflect roughly the situation in the USA. We assume a phase of general contact reduction (“lockdown”) at the beginning of the epidemic and additional case-isolation measures. We study the hypothetical effects of varying enhancements in morbidity and mortality, different likelihoods of multi-infected individuals to spread multi-infections and different susceptibility to multi-infections in different disease phases. It is demonstrated that multi-infections lead to a slight reduction in the number of infections, as these are more likely to get isolated due to their higher morbidity. However, the latter substantially increases the number of deaths. Furthermore, simulations indicate that a potential second lockdown can substantially decrease the epidemic peak, the number of multi-infections and deaths.
Conclusions
Enhanced morbidity and mortality due to multiple disease exposure is a potential threat in the COVID-19 pandemic that deserves more attention. Particularly it underlines another facet questioning disease management strategies aiming for herd immunity.
Added
2022-10-15
Last modified
2022-10-15
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Kristan Schneider
Kristan Schneider
Preventing COVID-19 spread in closed facilities by regular testing of employees—An efficient intervention in long-term care facilities and prisons?
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Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1932-6203
Abstract
Background
Different levels of control measures were introduced to contain the global COVID-19 pandemic, many of which have been controversial, particularly the comprehensive use of diagnostic tests. Regular testing of high-risk individuals (pre-existing conditions, older than 60 years of age) has been suggested by public health authorities. The WHO suggested the use of routine screening of residents, employees, and visitors of long-term care facilities (LTCF) to protect the resident risk group. Similar suggestions have been made by the WHO for other closed facilities including incarceration facilities (e.g., prisons or jails), wherein parts of the U.S., accelerated release of approved inmates is taken as a measure to mitigate COVID-19.
Methods and findings
Here, the simulation model underlying the pandemic preparedness tool CovidSim 1.1 (http://covidsim.eu/) is extended to investigate the effect of regularly testing of employees to protect immobile resident risk groups in closed facilities. The reduction in the number of infections and deaths within the risk group is investigated. Our simulations are adjusted to reflect the situation of LTCFs in Germany, and incarceration facilities in the U.S.
COVID-19 spreads in closed facilities due to contact with infected employees even under strict confinement of visitors in a pandemic scenario without targeted protective measures. Testing is only effective in conjunction with targeted contact reduction between the closed facility and the outside world—and will be most inefficient under strategies aiming for herd immunity. The frequency of testing, the quality of tests, and the waiting time for obtaining test results have noticeable effects. The exact reduction in the number of cases depends on disease prevalence in the population and the levels of contact reductions. Testing every 5 days with a good quality test and a processing time of 24 hours can lead up to a 40% reduction in the number of infections. However, the effects of testing vary substantially among types of closed facilities and can even be counterproductive in U.S. IFs.
Conclusions
The introduction of COVID-19 in closed facilities is unavoidable without a thorough screening of persons that can introduce the disease into the facility. Regular testing of employees in closed facilities can contribute to reducing the number of infections there, but is only meaningful as an accompanying measure, whose economic benefit needs to be assessed carefully.
Added
2022-10-15
Last modified
2022-10-15
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Kristan Schneider
Kristan Schneider
The impact of COVID-19 vaccination campaigns accounting for antibody-dependent enhancement
Homepage URL
Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1932-6203
Abstract
Background
COVID-19 vaccines are approved, vaccination campaigns are launched, and worldwide return to normality seems within close reach. Nevertheless, concerns about the safety of COVID-19 vaccines arose, due to their fast emergency approval. In fact, the problem of antibody-dependent enhancement was raised in the context of COVID-19 vaccines.
Methods and findings
We introduce a complex extension of the model underlying the pandemic preparedness tool CovidSim 1.1 (http://covidsim.eu/) to optimize vaccination strategies with regard to the onset of campaigns, vaccination coverage, vaccination schedules, vaccination rates, and efficiency of vaccines. Vaccines are not assumed to immunize perfectly. Some individuals fail to immunize, some reach only partial immunity, and—importantly—some develop antibody-dependent enhancement, which increases the likelihood of developing symptomatic and severe episodes (associated with higher case fatality) upon infection. Only a fraction of the population will be vaccinated, reflecting vaccination hesitancy or contraindications. The model is intended to facilitate decision making by exploring ranges of parameters rather than to be fitted by empirical data. We parameterized the model to reflect the situation in Germany and predict increasing incidence (and prevalence) in early 2021 followed by a decline by summer. Assuming contact reductions (curfews, social distancing, etc.) to be lifted in summer, disease incidence will peak again. Fast vaccine deployment contributes to reduce disease incidence in the first quarter of 2021, and delay the epidemic outbreak after the summer season. Higher vaccination coverage results in a delayed and reduced epidemic peak. A coverage of 75%–80% is necessary to prevent an epidemic peak without further drastic contact reductions.
Conclusions
With the vaccine becoming available, compliance with contact reductions is likely to fade. To prevent further economic damage from COVID-19, high levels of immunization need to be reached before next year’s flu season, and vaccination strategies and disease management need to be flexibly adjusted. The predictive model can serve as a refined decision support tool for COVID-19 management.
Added
2022-10-15
Last modified
2022-10-15
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Kristan Schneider
Kristan Schneider
Changes in the frequencies of Plasmodium falciparum dhps and dhfr drug-resistant mutations in children from Western Kenya from 2005 to 2018: the rise of Pfdhps S436H
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Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1475-2875
Abstract
Abstract
Background
Sulfadoxine-pyrimethamine (SP) is the only anti-malarial drug formulation approved for intermittent preventive treatment in pregnancy (IPTp). However, mutations in the Plasmodium falciparum dhfr (Pfdhfr) and dhps (Pfdhps) genes confer resistance to pyrimethamine and sulfadoxine, respectively. Here, the frequencies of SP resistance-associated mutations from 2005 to 2018 were compared in samples from Kenyan children with malaria residing in a holoendemic transmission region.
Methods
Partial sequences of the Pfdhfr and Pfdhps genes were amplified and sequenced from samples collected in 2005 (n = 81), 2010 (n = 95), 2017 (n = 43), and 2018 (n = 55). The frequency of known mutations conferring resistance to pyrimethamine and sulfadoxine were estimated and compared. Since artemisinin-based combination therapy (ACT) is the current first-line treatment for malaria, the presence of mutations in the propeller domain of P. falciparum kelch13 gene (Pfk13) linked to ACT-delayed parasite clearance was studied in the 2017/18 samples.
Results
Among other changes, the point mutation of Pfdhps S436H increased in frequency from undetectable in 2005 to 28% in 2017/18. Triple Pfdhfr mutant allele (CIRNI) increased in frequency from 84% in 2005 to 95% in 2017/18, while the frequency of Pfdhfr double mutant alleles declined (allele CICNI from 29% in 2005 to 6% in 2017/18, and CNRNI from 9% in 2005 to undetectable in 2010 and 2017/18). Thus, a multilocus Pfdhfr/Pfdhps genotype with six mutations (HGEAA/CIRNI), including Pfdhps S436H, increased in frequency from 2010 to 2017/18. Although none of the mutations associated with ACT-delayed parasite clearance was observed, the Pfk13 mutation A578S, the most widespread Pfk13 SNP found in Africa, was detected in low frequency (2.04%).
Conclusions
There were changes in SP resistance mutant allele frequencies, including an increase in the Pfdhps S436H. Although these patterns seem consistent with directional selection due to drug pressure, there is a lack of information to determine the actual cause of such changes. These results suggest incorporating molecular surveillance of Pfdhfr/Pfdhps mutations in the context of SP efficacy studies for intermittent preventive treatment in pregnancy (IPTp).
Background
Sulfadoxine-pyrimethamine (SP) is the only anti-malarial drug formulation approved for intermittent preventive treatment in pregnancy (IPTp). However, mutations in the Plasmodium falciparum dhfr (Pfdhfr) and dhps (Pfdhps) genes confer resistance to pyrimethamine and sulfadoxine, respectively. Here, the frequencies of SP resistance-associated mutations from 2005 to 2018 were compared in samples from Kenyan children with malaria residing in a holoendemic transmission region.
Methods
Partial sequences of the Pfdhfr and Pfdhps genes were amplified and sequenced from samples collected in 2005 (n = 81), 2010 (n = 95), 2017 (n = 43), and 2018 (n = 55). The frequency of known mutations conferring resistance to pyrimethamine and sulfadoxine were estimated and compared. Since artemisinin-based combination therapy (ACT) is the current first-line treatment for malaria, the presence of mutations in the propeller domain of P. falciparum kelch13 gene (Pfk13) linked to ACT-delayed parasite clearance was studied in the 2017/18 samples.
Results
Among other changes, the point mutation of Pfdhps S436H increased in frequency from undetectable in 2005 to 28% in 2017/18. Triple Pfdhfr mutant allele (CIRNI) increased in frequency from 84% in 2005 to 95% in 2017/18, while the frequency of Pfdhfr double mutant alleles declined (allele CICNI from 29% in 2005 to 6% in 2017/18, and CNRNI from 9% in 2005 to undetectable in 2010 and 2017/18). Thus, a multilocus Pfdhfr/Pfdhps genotype with six mutations (HGEAA/CIRNI), including Pfdhps S436H, increased in frequency from 2010 to 2017/18. Although none of the mutations associated with ACT-delayed parasite clearance was observed, the Pfk13 mutation A578S, the most widespread Pfk13 SNP found in Africa, was detected in low frequency (2.04%).
Conclusions
There were changes in SP resistance mutant allele frequencies, including an increase in the Pfdhps S436H. Although these patterns seem consistent with directional selection due to drug pressure, there is a lack of information to determine the actual cause of such changes. These results suggest incorporating molecular surveillance of Pfdhfr/Pfdhps mutations in the context of SP efficacy studies for intermittent preventive treatment in pregnancy (IPTp).
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
Kristan Schneider
Malaria in Venezuela: changes in the complexity of infection reflects the increment in transmission intensity
Homepage URL
Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1475-2875
Abstract
Abstract
Background
Malaria incidence has reached staggering numbers in Venezuela. Commonly, Bolívar State accounted for approximately 70% of the country cases every year. Most cases cluster in the Sifontes municipality, a region characterized by an extractive economy, including gold mining. An increase in migration to Sifontes, driven by gold mining, fueled a malaria spillover to the rest of the country and the region. Here samples collected in 2018 were compared with a previous study of 2003/2004 to describe changes in the parasites population structures and the frequency of point mutations linked to anti-malarial drugs.
Methods
A total of 88 Plasmodium falciparum and 94 Plasmodium vivax isolates were collected in 2018 and compared with samples from 2003/2004 (106 P. falciparum and 104 P. vivax). For P. falciparum, mutations linked to drug resistance (Pfdhfr, Pfdhps, and Pfcrt) and the Pfk13 gene associated with artemisinin delayed parasite clearance, were analysed. To estimate the multiplicity of infection (MOI), and perform P. falciparum and P. vivax population genetic analyses, the parasites were genotyped by using eight standardized microsatellite loci.
Results
The P. falciparum parasites are still harbouring drug-resistant mutations in Pfdhfr, Pfdhps, and Pfcrt. However, there was a decrease in the frequency of highly resistant Pfdhps alleles. Mutations associated with artemisinin delayed parasite clearance in the Pfk13 gene were not found. Consistent with the increase in transmission, polyclonal infections raised from 1.9% in 2003/2004 to 39% in 2018 in P. falciparum and from 16.3 to 68% in P. vivax. There is also a decrease in linkage disequilibrium. Bayesian clustering yields two populations linked to the time of sampling, showing that the parasite populations temporarily changed. However, the samples from 2003/2004 and 2018 have several alleles per locus in common without sharing multi-locus genotypes.
Conclusions
The frequency of mutations linked with drug resistance in P. falciparum shows only changes in Pfdhps. Observations presented here are consistent with an increase in transmission from the previously circulating parasites. Following populations longitudinally, using molecular surveillance, provides valuable information in cases such as Venezuela with a fluid malaria situation that is affecting the regional goals toward elimination.
Background
Malaria incidence has reached staggering numbers in Venezuela. Commonly, Bolívar State accounted for approximately 70% of the country cases every year. Most cases cluster in the Sifontes municipality, a region characterized by an extractive economy, including gold mining. An increase in migration to Sifontes, driven by gold mining, fueled a malaria spillover to the rest of the country and the region. Here samples collected in 2018 were compared with a previous study of 2003/2004 to describe changes in the parasites population structures and the frequency of point mutations linked to anti-malarial drugs.
Methods
A total of 88 Plasmodium falciparum and 94 Plasmodium vivax isolates were collected in 2018 and compared with samples from 2003/2004 (106 P. falciparum and 104 P. vivax). For P. falciparum, mutations linked to drug resistance (Pfdhfr, Pfdhps, and Pfcrt) and the Pfk13 gene associated with artemisinin delayed parasite clearance, were analysed. To estimate the multiplicity of infection (MOI), and perform P. falciparum and P. vivax population genetic analyses, the parasites were genotyped by using eight standardized microsatellite loci.
Results
The P. falciparum parasites are still harbouring drug-resistant mutations in Pfdhfr, Pfdhps, and Pfcrt. However, there was a decrease in the frequency of highly resistant Pfdhps alleles. Mutations associated with artemisinin delayed parasite clearance in the Pfk13 gene were not found. Consistent with the increase in transmission, polyclonal infections raised from 1.9% in 2003/2004 to 39% in 2018 in P. falciparum and from 16.3 to 68% in P. vivax. There is also a decrease in linkage disequilibrium. Bayesian clustering yields two populations linked to the time of sampling, showing that the parasite populations temporarily changed. However, the samples from 2003/2004 and 2018 have several alleles per locus in common without sharing multi-locus genotypes.
Conclusions
The frequency of mutations linked with drug resistance in P. falciparum shows only changes in Pfdhps. Observations presented here are consistent with an increase in transmission from the previously circulating parasites. Following populations longitudinally, using molecular surveillance, provides valuable information in cases such as Venezuela with a fluid malaria situation that is affecting the regional goals toward elimination.
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
Kristan Schneider
The COVID-19 pandemic preparedness simulation tool: CovidSIM
Homepage URL
Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1471-2334
Abstract
Abstract
Background
Efficient control and management in the ongoing COVID-19 pandemic needs to carefully balance economical and realizable interventions. Simulation models can play a cardinal role in forecasting possible scenarios to sustain decision support.
Methods
We present a sophisticated extension of a classical SEIR model. The simulation tool CovidSIM Version 1.0 is an openly accessible web interface to interactively conduct simulations of this model. The simulation tool is used to assess the effects of various interventions, assuming parameters that reflect the situation in Austria as an example.
Results
Strict contact reduction including isolation of infected persons in quarantine wards and at home can substantially delay the peak of the epidemic. Home isolation of infected individuals effectively reduces the height of the peak. Contact reduction by social distancing, e.g., by curfews, sanitary behavior, etc. are also effective in delaying the epidemic peak.
Conclusions
Contact-reducing mechanisms are efficient to delay the peak of the epidemic. They might also be effective in decreasing the peak number of infections depending on seasonal fluctuations in the transmissibility of the disease.
Background
Efficient control and management in the ongoing COVID-19 pandemic needs to carefully balance economical and realizable interventions. Simulation models can play a cardinal role in forecasting possible scenarios to sustain decision support.
Methods
We present a sophisticated extension of a classical SEIR model. The simulation tool CovidSIM Version 1.0 is an openly accessible web interface to interactively conduct simulations of this model. The simulation tool is used to assess the effects of various interventions, assuming parameters that reflect the situation in Austria as an example.
Results
Strict contact reduction including isolation of infected persons in quarantine wards and at home can substantially delay the peak of the epidemic. Home isolation of infected individuals effectively reduces the height of the peak. Contact reduction by social distancing, e.g., by curfews, sanitary behavior, etc. are also effective in delaying the epidemic peak.
Conclusions
Contact-reducing mechanisms are efficient to delay the peak of the epidemic. They might also be effective in decreasing the peak number of infections depending on seasonal fluctuations in the transmissibility of the disease.
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
Kristan Schneider
Preventing COVID-19 spread in closed facilities by regular testing of employees – an efficient intervention in long-term care facilities and prisons?
2020-10-14 | Other
Contributors:
H. Christian Tsoungui Obama, Jr.; M. Y. Nessma Adil; N. Looli Alawam; Pierre M. Ngougoue N.; Gideon A. Ngwa (and 2 more)
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H. Christian Tsoungui Obama, Jr.
(Author)
M. Y. Nessma Adil
(Author)
N. Looli Alawam
(Author)
Pierre M. Ngougoue N.
(Author)
Gideon A. Ngwa
(Author)
Miranda Teboh-Ewungkem
(Author)
Kristan A. Schneider
(Author)
External identifiers
Added
2021-03-17
Last modified
2022-06-01
Source:
Crossref
Crossref
Limited differentiation among Plasmodium vivax populations from the northwest and to the south Pacific Coast of Colombia: A malaria corridor?
PLOS Neglected Tropical Diseases
2019-03-28 | Journal article
Contributors:
Kristan Schneider
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Contributors
Kristan Schneider
(Author)
[ORCID: 0000-0003-4138-1180]
External identifiers
ISSN:
1935-2735
Added
2022-10-15
Last modified
2022-10-15
Source:
Kristan Schneider
Kristan Schneider
Large and finite sample properties of a maximum-likelihood estimator for multiplicity of infection
PLOS ONE
2018-04-09 | Journal article
Contributors:
Kristan Alexander Schneider; Ryan E. Wiegand
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Contributors
Kristan Alexander Schneider
(Author)
Ryan E. Wiegand
(Editor)
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Added
2018-12-14
Last modified
2022-05-27
Source:
Crossref
Crossref
Correction: A Likelihood Approach to Estimate the Number of Co-Infections
PLOS ONE
2018-02-08 | Journal article
Contributors:
Kristan A. Schneider; Ananias A. Escalante
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Kristan A. Schneider
(Author)
Ananias A. Escalante
(Author)
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DOI:
10.1371/journal.pone.0192877
ISSN:
1932-6203
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
Profiles of low complexity regions in Apicomplexa
BMC Evolutionary Biology
2016-02 | Journal article
Contributors:
Fabia U. Battistuzzi; Kristan A. Schneider; Matthew K. Spencer; David Fisher; Sophia Chaudhry (and 1 more)
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Fabia U. Battistuzzi
(Author)
Kristan A. Schneider
(Author)
Matthew K. Spencer
(Author)
David Fisher
(Author)
Sophia Chaudhry
(Author)
Ananias A. Escalante
(Author)
External identifiers
DOI:
10.1186/s12862-016-0625-0
ISSN:
1471-2148
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
Persistence of Sulfadoxine-Pyrimethamine Resistance Despite Reduction of Drug Pressure in Malawi
Journal of Infectious Diseases
2015-02-11 | Journal article
Contributors:
Elena Artimovich; Kristan Schneider; Terrie E. Taylor; James G. Kublin; Fraction K. Dzinjalamala (and 4 more)
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Contributors
Elena Artimovich
(Author)
Kristan Schneider
(Author)
Terrie E. Taylor
(Author)
James G. Kublin
(Author)
Fraction K. Dzinjalamala
(Author)
Ananias A. Escalante
(Author)
Christopher V. Plowe
(Author)
Miriam K. Laufer
(Author)
Shannon Takala-Harrison
(Author)
External identifiers
DOI:
10.1093/infdis/jiv078
ISSN:
0022-1899
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
A Population Genetic Model for the Initial Spread of Partially Resistant Malaria Parasites under Anti-Malarial Combination Therapy and Weak Intrahost Competition
PLoS ONE
2014-07-09 | Journal article
Contributors:
Yuseob Kim; Ananias A. Escalante; Kristan A. Schneider; David J. Sullivan
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Contributors
Yuseob Kim
(Author)
Ananias A. Escalante
(Author)
Kristan A. Schneider
(Author)
David J. Sullivan
(Editor)
External identifiers
DOI:
10.1371/journal.pone.0101601
ISSN:
1932-6203
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
A likelihood approach to estimate the number of co-infections
Contributors
Schneider, K.A.
(Author)
Escalante, A.A.
(Author)
External identifiers
DOI:
10.1371/journal.pone.0097899
EID:
2-s2.0-84903776463
Added
2018-03-13
Last modified
2022-05-26
Source:
Scopus - Elsevier
Scopus - Elsevier
Genetic Hitchhiking under Heterogeneous Spatial Selection Pressures
PLoS ONE
2013-04 | Journal article
Contributors:
Kristan A. Schneider; Yuseob Kim; Stephen R. Proulx
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Contributors
Kristan A. Schneider
(Author)
Yuseob Kim
(Author)
Stephen R. Proulx
(Editor)
External identifiers
DOI:
10.1371/journal.pone.0061742
ISSN:
1932-6203
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
Fitness components and natural selection: why are there different patterns on the emergence of drug resistance in Plasmodium falciparum and Plasmodium vivax?
Malaria Journal
2013 | Journal article
Contributors:
Kristan A Schneider; Ananias A Escalante
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Contributors
Kristan A Schneider
(Author)
Ananias A Escalante
(Author)
External identifiers
DOI:
10.1186/1475-2875-12-15
ISSN:
1475-2875
Added
2018-03-13
Last modified
2022-05-26
Source:
Crossref Metadata Search
Crossref Metadata Search
The Hitchhiking Effect of a Strongly Selected Substitution in Male Germline on Neutral Polymorphism in a Monogamy Population
Contributors
Li, J.
(Author)
Schneider, K.A.
(Author)
Li, H.
(Author)
External identifiers
DOI:
10.1371/journal.pone.0071497
EID:
2-s2.0-84883183868
Added
2018-03-13
Last modified
2022-05-26
Source:
Scopus - Elsevier
Scopus - Elsevier