@article{Partey2025,

title = {Functional antibody responses to SARS-CoV-2 variants before and after booster vaccination among adults in Ghana},

author = {F. D. Partey and A. N. A. Pobee and I. K. Damptey and F. Osei and M. M. A. K. Owusu-Amponsah and Y. A. A. Ansah and C. Ye and S. Bradfute and I. Hurwitz and P. K. Quashie and M. F. Ofori and A. K. Kusi and D. J. Perkins and G. A. Awandare},

doi = {10.3389/ebm.2025.10440},

issn = {1535-3699},

year  = {2025},

date = {2025-07-21},

urldate = {2025-07-21},

journal = {Exp. Biol. Med.},

volume = {250},

publisher = {Frontiers Media SA},

abstract = {\<jats:p\>COVID-19 booster vaccinations are needed to enhance waning immunity and the emergence of new variants. In Africa, where COVID-19 vaccine coverage is low, there is a paucity of data on COVID-19 vaccine-induced immunity, particularly in the post-omicron era. This study examined the functional activity of vaccine-induced antibody responses against different variants before and after booster vaccinations in adults in Ghana, between November 2022 and February 2023. SARS-CoV-2 nucleocapsid protein and spike receptor binding domain (RBD) antigen-specific IgG levels against different viral variants were determined in plasma. Plasma was tested for the ability to inhibit ACE-2 binding to RBD variants. N antigen-specific antibody levels were comparable between vaccinated and previously infected, but unvaccinated individuals. However, RBD IgG levels before booster vaccinations were significantly higher in vaccinated participants than in exposed, unvaccinated individuals, except for Omicron. RBD IgG levels remained unchanged after the booster in participants with three prior vaccine doses but were significantly higher than in those with only primary vaccinations (Wild type p = 0.0315, Alpha p = 0.0090, Beta p = 0.0020, Delta p = 0.0040) except Omicron (p = 0.09). Participants who received the Pfizer-BioNTech vaccine showed a significant increase (p \< 0.05) in RBD IgG levels against all tested variants from baseline to 3 months. In contrast, participants who received the J\&J vaccine only showed a significant increase in RBD IgG to Wildtype (p = 0.04), Alpha (p \< 0.0001), and Beta (p \< 0.0001), but not Delta and Omicron. The inhibition of ACE-2 binding and live virus neutralization titers were significantly higher in vaccinated individuals than in unvaccinated individuals before the booster (p \< 0.001). Virus neutralization titers against Wildtype were significantly high 3 months after booster (p \< 0.001), but neutralization titers against Omicron remained stable from baseline to 3 months after booster. Extended interval between vaccinations may enhance vaccine-induced antibody responses.\</jats:p\>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wasena2025,

title = {Diagnostic accuracy of PfHRP2-based malaria rapid diagnostic tests and antigenemia persistence in Kenyan children from a holoendemic region: implications for case management and surveillance},

author = {Sharley A. Wasena and Clinton O. Onyango and Shamim W. Osata and Samuel B. Anyona and Evans Raballah and Ivy Hurwitz and Philip D. Seidenberg and Collins Ouma and Qiuying Cheng and Kristan A. Schneider and Douglas J. Perkins},

doi = {10.3389/ebm.2025.10585},

issn = {1535-3699},

year  = {2025},

date = {2025-05-22},

journal = {Exp. Biol. Med.},

volume = {250},

publisher = {Frontiers Media SA},

abstract = {Malaria remains a significant cause of childhood morbidity and mortality, with Plasmodium falciparum Histidine-Rich Protein 2 (PfHRP2)-based malaria rapid diagnostic tests (mRDTs) widely used in endemic regions where microscopy is sometimes not feasible. While these tests offer high sensitivity, persistent PfHRP2 antigenemia and gene deletions can cause false-positive and false-negative results, compromising their accuracy for malaria case management and surveillance. This study evaluated the diagnostic performance and antigen persistence of PfHRP2-mRDTs using data from a longitudinal birth cohort of 750 children followed monthly from birth to 36 months in a holoendemic region of Kenya. Malaria diagnosis was performed using both microscopy and mRDTs, with a total of 15,006 clinical events recorded from 573 children between 2017 and 2023. Data from an independent acute febrile cohort of 937 children (\<5 years) followed for 14 days was analyzed to validate the findings. The mRDT showed a high sensitivity of 97.27% but a moderate specificity of 65.00% in acute febrile illness, indicating frequent false-positive results. The positive predictive value was low (35.10%), suggesting that confirmatory testing is needed, while the negative predictive value was high (98.89%), reinforcing the reliability of mRDTs in ruling out malaria. Persistent PfHRP2 antigenemia was observed, with a median antigen clearance time of 51.14 days, respectively. Higher initial parasite densities (\>50,000/μL) were associated with a slower antigen decay rate (p = 0.001), highlighting the challenge of interpreting positive mRDT results after treatment. Validation using the acute febrile cohort showed that mRDT specificity exceeded 95% at initial diagnosis and follow-up. Overall, PfHRP2-based mRDTs remain valuable for frontline malaria diagnosis but are limited by antigen persistence, leading to false positives in follow-up testing. Where feasible, integration of confirmatory diagnostic methods, such as microscopy or molecular assays, could improve the performance of malaria case management and clinical decision making, particularly in high-transmission settings.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40234522,

title = {Impact of age, HIV1, sickle-cell genotypes, and interferon-gamma gene upstream variants on malaria disease outcomes in a longitudinal pediatric cohort},

author = {Evans Raballah and Samuel B Anyona and Shamim W Osata and Sharley A Wasena and Clinton Onyango and Ivy Hurwitz and Qiuying Cheng and Philip D Seidenberg and Benjamin H McMahon and Collins Ouma and John M Ong'echa and Kristan A Schneider and Douglas J Perkins},

doi = {10.1038/s41598-025-97267-x},

issn = {2045-2322},

year  = {2025},

date = {2025-04-01},

urldate = {2025-04-01},

journal = {Sci Rep},

volume = {15},

number = {1},

pages = {13043},

abstract = {This prospective cohort study explored the association between two upstream IFN-γ variants (rs2069709: G > T and rs2069705: A > G) and hazard factors for malaria outcomes in a longitudinal cohort of children (n = 941, 3-36 mos.), followed for three years. The impact of age, sex, previous malaria exposure, HIV1 infection, and sickle-cell genotypes (HbAA, HbAS, and HbSS) was also investigated. Reduced malaria episodes were associated with older age at enrollment [HR = 0.957 (95% CI = 0.953-0.961) per month, P < 2.2e-16], HIV1 infection [0.687 (0.545-0.866), P = 0.001], being female [0.910 (0.859-0.964), P = 0.040], and HbAS [0.823 (0.754-0.898), P = 0.005]. The GA/TA diplotype [0.376 (0.230-0.614), P = 0.002] also reduced the hazard of malaria, while TA haplotype increased susceptibility [1.749 (1.159-2.640), P = 0.029]. Factors protecting against the development of SMA [Hemoglobin (Hb < 6.0 g/dL)] included older age [0.927 (0.913-0.942) per month, P < 2.2e-16], previous malaria episodes [0.576 (0.542-0.614, P = 9.5e-32)], HbAS [0.553 (0.400-0.766), P = 0.015]. The rs2069705AG genotype increased the hazard of SMA [1.697 (1.002-2.875), P = 0.042]. Reduced hazard of mortality was observed for older children [0.898 (0.857-0.941), P < 2.2e-16], while a higher hazard was present in HIV-infected children [12.475 (6.380-24.392), P < 2.2e-16], and in those with HbSS [6.341 (1.944-20.686), P = 0.007]. The GG haplotype increased the mortality hazard [1.817 (0.936-3.527), P = 0.078]. The results here highlight critical factors influencing the hazard of malaria, SMA, and mortality.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40030473,

title = {Detecting Opioid Use Disorder in Health Claims Data With Positive Unlabeled Learning},

author = {Praveen Kumar and Fariha Moomtaheen and Scott A Malec and Jeremy J Yang and Cristian G Bologa and Kristan A Schneider and Yiliang Zhu and Mauricio Tohen and Gerardo Villarreal and Douglas J Perkins and Elliot M Fielstein and Sharon E Davis and Michael E Matheny and Christophe G Lambert},

doi = {10.1109/JBHI.2024.3515805},

issn = {2168-2208},

year  = {2025},

date = {2025-02-01},

journal = {IEEE J Biomed Health Inform},

volume = {29},

number = {2},

pages = {750--757},

abstract = {Accurate detection and prevalence estimation of behavioral health conditions, such as opioid use disorder (OUD), are crucial for identifying at-risk individuals, determining treatment needs, monitoring prevention and intervention efforts, and recruiting treatment-naive participants for clinical trials. The availability of extensive health data, combined with advancements in machine learning (ML) frameworks, has enabled researchers to employ various ML techniques to predict or identify OUD within patient health data. Ideally, we could directly estimate the prevalence, or the proportion of a population with a condition over time. However, underdiagnosis and undercoding of conditions in patient health records make it challenging to determine the true prevalence of these conditions and to identify at-risk patients with less severe conditions who are more likely to be missed. Consequently, patients without diagnoses may comprise positive and negative examples for a given condition. Treating all undiagnosed (uncoded) patients as negative when applying ML methods can introduce bias into models, affecting their predictive power. To address this issue, we employed Positive Unlabeled Learning Selected Not At Random (PULSNAR), a Positive and Unlabeled (PU) learning technique, to estimate the probability of a given patient having OUD during a time window and the overall population prevalence of OUD. In a sample of 3,342,044 commercially insured US patients with at least one opioid prescription filled, PULSNAR estimated that 5.08% of patients have a cumulative prevalence of OUD over a 2-5 a observation period, compared to the 1.35% with a recorded OUD diagnosis, with 73.5% of cases not diagnosed/coded. The prevalence estimates provided by PULSNAR are consistent with those reported in other studies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Sood2025,

title = {Effectiveness of Frequent Point-of-Care Molecular COVID-19 Surveillance in a Rural Workplace: Nonrandomized Controlled Clinical Trial Among Miners},

author = {Akshay Sood and William “Cotton” Jarrell and Xin W Shore and Nestor Sosa and Alisha Parada and Nicholas Edwardson and Alexandra V Yingling and Teah Amirkabirian and Qiuying Cheng and Ivy Hurwitz and Linda S Cook and Shuguang Leng and Orrin B Myers and Douglas J Perkins},

doi = {10.2196/59845},

issn = {2369-2960},

year  = {2025},

date = {2025-01-27},

journal = {JMIR Public Health Surveill},

volume = {11},

pages = {e59845--e59845},

publisher = {JMIR Publications Inc.},

abstract = {Abstract

          

            Background

            Numerous studies have assessed the risk of SARS-CoV-2 exposure and infection among health care workers during the pandemic. However, far fewer studies have investigated the impact of SARS-CoV-2 on essential workers in other sectors. Moreover, guidance for maintaining a safely operating workplace in sectors outside of health care remains limited. Workplace surveillance has been recommended by the Centers for Disease Control and Prevention, but few studies have examined the feasibility or effectiveness of this approach.

          

          

            Objective

            The objective of this study was to investigate the feasibility and effectiveness of using frequent point-of-care molecular workplace surveillance as an intervention strategy to prevent the spread of SARS-CoV-2 at essential rural workplaces (mining sites) where physical distancing, remote work, and flexible schedules are not possible.

          

          

            Methods

            In this nonrandomized controlled clinical trial conducted from February 2021, to March 2022, 169 miners in New Mexico (intervention cohort) and 61 miners in Wyoming (control cohort) were enrolled. Investigators performed point-of-care rapid antigen testing on midnasal swabs (NSs) self-collected by intervention miners. Our first outcome was the intervention acceptance rate in the intervention cohort. Our second outcome was the rate of cumulative postbaseline seropositivity to SARS-CoV-2 nucleocapsid protein, which was analyzed in the intervention cohort and compared to the control cohort between baseline and 12 months. The diagnostic accuracy of detecting SARS-CoV-2 using rapid antigen testing on NSs was compared to laboratory-based reverse transcriptase polymerase chain reaction (RT-PCR) on nasopharyngeal swabs (NPSs) in a subset of 68 samples.

          

          

            Results

            Our intervention had a mean acceptance rate of 96.4% (11,413/11,842). The intervention miners exhibited a lower cumulative postbaseline incident seropositivity at 12 months compared to control miners (14/97, 14% vs 17/45, 38%; P=.002). Analysis of SARS-CoV-2 antigen detection in self-administered NSs revealed 100% sensitivity and specificity compared to laboratory-based RT-PCR testing on NPSs.

          

          

            Conclusions

            Our findings establish frequent point-of-care molecular workplace COVID-19 surveillance as a feasible option for keeping essential rural workplaces open and preventing SARS-CoV-2 spread. These findings extend beyond this study, providing valuable insights for designing interventions to maintain employees’ safety at other essential workplaces during an infectious disease outbreak.

          },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Duran2024,

title = {Calcium signaling from damaged lysosomes induces cytoprotective stress granules},

author = {Jacob Duran and Jay E Salinas and Rui ping Wheaton and Suttinee Poolsup and Lee Allers and Monica Rosas-Lemus and Li Chen and Qiuying Cheng and Jing Pu and Michelle Salemi and Brett Phinney and Pavel Ivanov and Alf Hr{a}kon Lystad and Kiran Bhaskar and Jaya Rajaiya and Douglas J Perkins and Jingyue Jia},

doi = {10.1038/s44318-024-00292-1},

issn = {1460-2075},

year  = {2024},

date = {2024-12-16},

journal = {EMBO J},

volume = {43},

number = {24},

pages = {6410--6443},

publisher = {Springer Science and Business Media LLC},

abstract = {AbstractLysosomal damage induces stress granule (SG) formation. However, the importance of SGs in determining cell fate and the precise mechanisms that mediate SG formation in response to lysosomal damage remain unclear. Here, we describe a novel calcium-dependent pathway controlling SG formation, which promotes cell survival during lysosomal damage. Mechanistically, the calcium-activated protein ALIX transduces lysosomal damage signals to SG formation by controlling eIF2α phosphorylation after sensing calcium leakage. ALIX enhances eIF2α phosphorylation by promoting the association between PKR and its activator PACT, with galectin-3 inhibiting this interaction; these regulatory events occur on damaged lysosomes. We further find that SG formation plays a crucial role in promoting cell survival upon lysosomal damage caused by factors such as SARS-CoV-2ORF3a, adenovirus, malarial pigment, proteopathic tau, or environmental hazards. Collectively, these data provide insights into the mechanism of SG formation upon lysosomal damage and implicate it in diseases associated with damaged lysosomes and SGs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Anyona2024,

title = {Entire expressed peripheral blood transcriptome in pediatric severe malarial anemia},

author = {Samuel B. Anyona and Qiuying Cheng and Sharley A. Wasena and Shamim W. Osata and Yan Guo and Evans Raballah and Ivy Hurwitz and Clinton O. Onyango and Collins Ouma and Philip D. Seidenberg and Benjamin H. McMahon and Christophe G. Lambert and Kristan A. Schneider and Douglas J. Perkins},

doi = {10.1038/s41467-024-48259-4},

issn = {2041-1723},

year  = {2024},

date = {2024-12-00},

journal = {Nat Commun},

volume = {15},

number = {1},

publisher = {Springer Science and Business Media LLC},

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.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Onyango2024,

title = {Transcriptomic and Proteomic Insights into Host Immune Responses in Pediatric Severe Malarial Anemia: Dysregulation in HSP60-70-TLR2/4 Signaling and Altered Glutamine Metabolism},

author = {Clinton O. Onyango and Samuel B. Anyona and Ivy Hurwitz and Evans Raballah and Sharely A. Wasena and Shamim W. Osata and Philip Seidenberg and Benjamin H. McMahon and Christophe G. Lambert and Kristan A. Schneider and Collins Ouma and Qiuying Cheng and Douglas J. Perkins},

doi = {10.3390/pathogens13100867},

issn = {2076-0817},

year  = {2024},

date = {2024-10-00},

journal = {Pathogens},

volume = {13},

number = {10},

publisher = {MDPI AG},

abstract = {Severe malarial anemia (SMA, Hb \< 6.0 g/dL) is a leading cause of childhood morbidity and mortality in holoendemic Plasmodium falciparum transmission zones. This study explored the entire expressed human transcriptome in whole blood from 66 Kenyan children with non-SMA (Hb ≥ 6.0 g/dL, n = 41) and SMA (n = 25), focusing on host immune response networks. RNA-seq analysis revealed 6862 differentially expressed genes, with equally distributed up-and down-regulated genes, indicating a complex host immune response. Deconvolution analyses uncovered leukocytic immune profiles indicative of a diminished antigenic response, reduced immune priming, and polarization toward cellular repair in SMA. Weighted gene co-expression network analysis revealed that immune-regulated processes are central molecular distinctions between non-SMA and SMA. A top dysregulated immune response signaling network in SMA was the HSP60-HSP70-TLR2/4 signaling pathway, indicating altered pathogen recognition, innate immune activation, stress responses, and antigen recognition. Validation with high-throughput gene expression from a separate cohort of Kenyan children (n = 50) with varying severities of malarial anemia (n = 38 non-SMA and n = 12 SMA) confirmed the RNA-seq findings. Proteomic analyses in 35 children with matched transcript and protein abundance (n = 19 non-SMA and n = 16 SMA) confirmed dysregulation in the HSP60-HSP70-TLR2/4 signaling pathway. Additionally, glutamine transporter and glutamine synthetase genes were differentially expressed, indicating altered glutamine metabolism in SMA. This comprehensive analysis underscores complex immune dysregulation and novel pathogenic features in SMA.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Onyango2023,

title = {Human NCR3 gene variants rs2736191 and rs11575837 alter longitudinal risk for development of pediatric malaria episodes and severe malarial anemia},

author = {Clinton O. Onyango and Qiuying Cheng and Elly O. Munde and Evans Raballah and Samuel B. Anyona and Benjamin H. McMahon and Christophe G. Lambert and Patrick O. Onyango and Kristan A. Schneider and Douglas J. Perkins and Collins Ouma},

doi = {10.1186/s12864-023-09565-1},

issn = {1471-2164},

year  = {2023},

date = {2023-12-00},

journal = {BMC Genomics},

volume = {24},

number = {1},

publisher = {Springer Science and Business Media LLC},

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) \< 5.0 g/dL in children] is the most common clinical manifestation of severe malaria in such regions. Although innate immune response genes are known to influence the development of SMA, the role of natural killer (NK) cells in malaria pathogenesis remains largely undefined. As such, we examined the impact of genetic variation in the gene encoding a primary NK cell receptor, natural cytotoxicity-triggering receptor 3 (NCR3), on the occurrence of malaria and SMA episodes over time.

              

                Methods

                Susceptibility to malaria, SMA, and all-cause mortality was determined in carriers of NCR3 genetic variants (i.e., rs2736191:C \> 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\textendash40 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\textendash2.129, 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\textendash1.597, P = 0.041) and in the additive model (presence of 1 or 2 copies) (IRR = 1.198, 95% CI = 1.030\textendash1.393, 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\textendash0.952, P = 0.009). Although increased susceptibility to SMA was present in carriers of the GC haplotype (IRR = 1.276, 95% CI = 1.030\textendash1.581, P = 0.026) with an additive effect (IRR = 1.182, 95% CI = 1.018\textendash1.372, 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.

              },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37649584,

title = {Disproportionate impact of COVID-19 severity and mortality on hospitalized American Indian/Alaska Native patients},

author = {Ivy Hurwitz and Alexandra V Yingling and Teah Amirkabirian and Amber Castillo and Jehanzaeb J Khan and Alexandra Do and Dominic K Lundquist and October Barnes and Christophe G Lambert and Annabeth Fieck and Gregory Mertz and Clinton Onyango and Samuel B Anyona and J Pedro Teixeira and Michelle Harkins and Mark Unruh and Qiuying Cheng and Shuguang Leng and Philip Seidenberg and Anthony Worsham and Jens O Langsjoen and Kristan A Schneider and Douglas J Perkins},

doi = {10.1093/pnasnexus/pgad259},

issn = {2752-6542},

year  = {2023},

date = {2023-08-01},

journal = {PNAS Nexus},

volume = {2},

number = {8},

pages = {pgad259},

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 ( = 0.02), higher invasive mechanical ventilation requirements ( = 0.0001), and laboratory values indicative of more severe disease. Throughout hospitalization, the AI/AN group also experienced elevated invasive mechanical ventilation ( < 0.0001), shock ( = 0.01), encephalopathy ( = 0.02), and severe COVID-19 ( = 0.0002), consistent with longer hospitalization ( < 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;  = 0.0003) and was a predictor of in-hospital mortality (OR = 2.35; 95% CI = 1.12-4.92;  = 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.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37340364,

title = {Hemoglobinopathies, merozoite surface protein-2 gene polymorphisms, and acquisition of Epstein Barr virus among infants in Western Kenya},

author = {Perez K Olewe and Shehu Shagari Awandu and Elly O Munde and Samuel B Anyona and Evans Raballah and Asito S Amolo and Sidney Ogola and Erick Ndenga and Clinton O Onyango and Rosemary Rochford and Douglas J Perkins and Collins Ouma},

doi = {10.1186/s12885-023-11063-2},

issn = {1471-2407},

year  = {2023},

date = {2023-06-01},

journal = {BMC Cancer},

volume = {23},

number = {1},

pages = {566},

abstract = {BACKGROUND: Epstein Barr virus (EBV)-associated endemic Burkitt's Lymphoma pediatric cancer is associated with morbidity and mortality among children resident in holoendemic Plasmodium falciparum regions in western Kenya. P. falciparum exerts strong selection pressure on sickle cell trait (SCT), alpha thalassemia (-α/αα), glucose-6-phosphate dehydrogenase (G6PD), and merozoite surface protein 2 (MSP-2) variants (FC27, 3D7) that confer reduced malarial disease severity. The current study tested the hypothesis that SCT, (-α/αα), G6PD mutation and (MSP-2) variants (FC27, 3D7) are associated with an early age of EBV acquisition.nnMETHODS: Data on infant EBV infection status (< 6 and ≥ 6-12 months of age) was abstracted from a previous longitudinal study. Archived infant DNA (n = 81) and mothers DNA (n = 70) samples were used for genotyping hemoglobinopathies and MSP-2. The presence of MSP-2 genotypes in maternal DNA samples was used to indicate infant in-utero malarial exposure. Genetic variants were determined by TaqMan assays or standard PCR. Group differences were determined by Chi-square or Fisher's analysis. Bivariate regression modeling was used to determine the relationship between the carriage of genetic variants and EBV acquisition.nnRESULTS: EBV acquisition for infants < 6 months was not associated with -α/αα (OR = 1.824, P = 0.354), SCT (OR = 0.897, P = 0.881), or G6PD [Viangchan (871G > A)/Chinese (1024 C > T) (OR = 2.614, P = 0.212)] and [Union (1360 C > T)/Kaiping (1388G > A) (OR = 0.321, P = 0.295)]. There was no relationship between EBV acquisition and in-utero exposure to either FC27 (OR = 0.922, P = 0.914) or 3D7 (OR = 0.933, P = 0.921). In addition, EBV acquisition in infants ≥ 6-12 months also showed no association with -α/αα (OR = 0.681, P = 0.442), SCT (OR = 0.513, P = 0.305), G6PD [(Viangchan (871G > A)/Chinese (1024 C > T) (OR = 0.640, P = 0.677)], [Mahidol (487G > A)/Coimbra (592 C > T) (OR = 0.948, P = 0.940)], [(Union (1360 C > T)/Kaiping (1388G > A) (OR = 1.221, P = 0.768)], African A (OR = 0.278, P = 0.257)], or in utero exposure to either FC27 (OR = 0.780, P = 0.662) or 3D7 (OR = 0.549, P = 0.241).nnCONCLUSION: Although hemoglobinopathies (-α/αα, SCT, and G6PD mutations) and in-utero exposure to MSP-2 were not associated with EBV acquisition in infants 0-12 months, novel G6PD variants were discovered in the population from western Kenya. To establish that the known and novel hemoglobinopathies, and in utero MSP-2 exposure do not confer susceptibility to EBV, future studies with larger sample sizes from multiple sites adopting genome-wide analysis are required.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Kisia2022,

title = {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},

author = {Lily E. Kisia and Qiuying Cheng and Evans Raballah and Elly O. Munde and Benjamin H. McMahon and Nick W. Hengartner and John M. Ong’echa and Kiprotich Chelimo and Christophe G. Lambert and Collins Ouma and Prakasha Kempaiah and Douglas J. Perkins and Kristan A. Schneider and Samuel B. Anyona},

doi = {10.1186/s41182-022-00432-5},

issn = {1349-4147},

year  = {2022},

date = {2022-12-00},

journal = {Trop Med Health},

volume = {50},

number = {1},

publisher = {Springer Science and Business Media LLC},

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\textendashmacrophage 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 \< 5.0 g/dL) episodes over 36 months of follow-up. Children (n = 1654, aged 2\textendash70 months) were recruited from a holoendemic P. falciparum transmission area of western Kenya. Decreased incidence rate ratio (IRR) for malaria was conferred by inheritance of the CSF2:g.64544 TC genotype (P = 0.0277) and CSF2 AC/GC diplotype (P = 0.0015). Increased IRR for malaria was observed in carriers of the CSF2 AT/GC diplotype (P = 0.0237), while the inheritance of the CSF2 AT haplotype increased the IRR for SMA (P = 0.0166). A model estimating the longitudinal risk of malaria showed decreased hazard rates among CSF2 AC haplotype carriers (P = 0.0045). Investigation of all-cause mortality revealed that inheritance of the GA genotype at CSF2:g-7032 increased the risk of mortality (P = 0.0315). Higher risk of SMA and all-cause mortality were observed in younger children (P \< 0.0001 and P = 0.0015), HIV-1(+) individuals (P \< 0.0001 and P \< 0.0001), and carriers of HbSS (P = 0.0342 and P = 0.0019). Results from this holoendemic P. falciparum area show that variation in gene region 5q31.1 influences susceptibility to malaria, SMA, and mortality, as does age, HIV-1 status, and inheritance of HbSS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Murata2022,

title = {Effect of vaccination on the case fatality rate for COVID-19 infections 2020\textendash2021: multivariate modelling of data from the US Department of Veterans Affairs},

author = {Glen H Murata and Allison E Murata and Douglas J Perkins and Heather M Campbell and Jenny T Mao and Brent Wagner and Benjamin H McMahon and Curt H Hagedorn},

doi = {10.1136/bmjopen-2022-064135},

issn = {2044-6055},

year  = {2022},

date = {2022-12-00},

journal = {BMJ Open},

volume = {12},

number = {12},

publisher = {BMJ},

abstract = {ObjectivesTo evaluate the benefits of vaccination on the case fatality rate (CFR) for COVID-19 infections.Design, setting and participantsThe US Department of Veterans Affairs has 130 medical centres. We created multivariate models from these data\textemdash339 772 patients with COVID-19\textemdashas of 30 September 2021.Outcome measuresThe primary outcome for all models was death within 60 days of the diagnosis. Logistic regression was used to derive adjusted ORs for vaccination and infection with Delta versus earlier variants. Models were adjusted for confounding factors, including demographics, comorbidity indices and novel parameters representing prior diagnoses, vital signs/baseline laboratory tests and outpatient treatments. Patients with a Delta infection were divided into eight cohorts based on the time from vaccination to diagnosis. A common model was used to estimate the odds of death associated with vaccination for each cohort relative to that of unvaccinated patients.Results9.1% of subjects were vaccinated. 21.5% had the Delta variant. 18 120 patients (5.33%) died within 60 days of their diagnoses. The adjusted OR for a Delta infection was 1.87±0.05, which corresponds to a relative risk (RR) of 1.78. The overall adjusted OR for prior vaccination was 0.280±0.011 corresponding to an RR of 0.291. Raw CFR rose steadily after 10\textendash14 weeks. The OR for vaccination remained stable for 10\textendash34 weeks.ConclusionsOur CFR model controls for the severity of confounding factors and priority of vaccination, rather than solely using the presence of comorbidities. Our results confirm that Delta was more lethal than earlier variants and that vaccination is an effective means of preventing death. After adjusting for major selection biases, we found no evidence that the benefits of vaccination on CFR declined over 34 weeks. We suggest that this model can be used to evaluate vaccines designed for emerging variants.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Raballah2022,

title = {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},

author = {Evans Raballah and Kristen Wilding and Samuel B. Anyona and Elly O. Munde and Ivy Hurwitz and Clinton O. Onyango and Cyrus Ayieko and Christophe G. Lambert and Kristan A. Schneider and Philip D. Seidenberg and Collins Ouma and Benjamin H. McMahon and Qiuying Cheng and Douglas J. Perkins},

doi = {10.3389/fgene.2022.977810},

issn = {1664-8021},

year  = {2022},

date = {2022-09-14},

journal = {Front. Genet.},

volume = {13},

publisher = {Frontiers Media SA},

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\textendash1.236, p = 0.001) and SMA (IRR = 1.627, 95%CI: 1.201\textendash2.204, p = 0.002). In the haplotypic model, carriers of TC had increased risk of malaria (IRR = 1.068, 95%CI: 1.017\textendash1.122, p = 0.009), while carriers of both wild-type alleles (CC) were protected against SMA (IRR = 0.679, 95%CI: 0.542\textendash0.850, p = 0.001).Conclusion: Collectively, these findings show that the selected C5 missense mutations influence the longitudinal risk of malaria and SMA in immune-na\"{i}ve children exposed to holoendemic P. falciparum transmission through a mechanism that remains to be defined.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Perkins2022b,

title = {Elevated SARS-CoV-2 in peripheral blood and increased COVID-19 severity in American Indians/Alaska Natives},

author = {Douglas J Perkins and Alexandra V Yingling and Qiuying Cheng and Amber Castillo and Janae Martinez and Steven B Bradfute and Shuguang Leng and Jeremy Edwards and Yan Guo and Gregory Mertz and Michelle Harkins and Mark Unruh and Anthony Worsham and Christophe G Lambert and J Pedro Teixeira and Phillip Seidenberg and Jens Langsjoen and Kristan Schneider and Ivy Hurwitz},

doi = {10.1177/15353702221091180},

issn = {1535-3699},

year  = {2022},

date = {2022-07-00},

journal = {Exp Biol Med (Maywood)},

volume = {247},

number = {14},

pages = {1253--1263},

publisher = {Frontiers Media SA},

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\textendash88 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\textendash3, 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. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Raballah2021,

title = {Complement component 3 mutations alter the longitudinal risk of pediatric malaria and severe malarial anemia},

author = {Evans Raballah and Samuel B Anyona and Qiuying Cheng and Elly O Munde and Ivy-Foo Hurwitz and Clinton Onyango and Caroline Ndege and Nicolas W Hengartner and Maria Andre\'{i}na Pacheco and Ananias A Escalante and Christophe G Lambert and Collins Ouma and Henri C Jr T Obama and Kristan A Schneider and Philip D Seidenberg and Benjamin H McMahon and Douglas J Perkins},

doi = {10.1177/15353702211056272},

issn = {1535-3699},

year  = {2022},

date = {2022-04-00},

journal = {Exp Biol Med (Maywood)},

volume = {247},

number = {8},

pages = {672--682},

publisher = {Frontiers Media SA},

abstract = { 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\textendash3.735, 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\textendash0.972, P =  0.008) and SMA (RR = 0.617, 95%CI: 0.448\textendash0.848, P =  0.003). Malaria incident risk ratio was also reduced in carriers of the GG (Gly102Gly1224) haplotype (RR = 0.941, 95%CI: 0.888\textendash0.997, 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. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35071802,

title = {Ingestion of hemozoin by peripheral blood mononuclear cells alters temporal gene expression of ubiquitination processes},

author = {Samuel B Anyona and Qiuying Cheng and Evans Raballah and Ivy Hurwitz and Christophe G Lambert and Benjamin H McMahon and Collins Ouma and Douglas J Perkins},

doi = {10.1016/j.bbrep.2022.101207},

issn = {2405-5808},

year  = {2022},

date = {2022-03-01},

journal = {Biochem Biophys Rep},

volume = {29},

pages = {101207},

abstract = { malaria is among the leading causes of childhood morbidity and mortality worldwide. During a natural infection, ingestion of the malarial parasite product, hemozoin (Hz), by circulating phagocytic cells induces dysregulation in innate immunity and enhances malaria pathogenesis. Treatment of cultured peripheral blood mononuclear cells (PBMCs) from healthy, malaria-na\"{i}ve donors with physiological concentrations of Hz can serve as an  model to investigate cellular processes. Although disruptions in host ubiquitination processes are central to the pathogenesis of many diseases, this system remains unexplored in malaria. As such, we investigated the impact of Hz on the temporal expression patterns of 84 genes involved in ubiquitination processes. Donor PBMCs were cultured in the absence or presence of Hz for 3-, 9-, and 24 h. Stimulation with Hz for 3 h did not significantly alter gene expression. Incubation for 9 h, however, elicited significant changes for 6 genes: 4 were down-regulated (, ,  and ) and 2 were up-regulated ( and ). Hz treatment for 24 h significantly altered expression for 14 genes: 12 were down-regulated (, , , , , , , , , , , and ), while 2 were up-regulated ( and ). Collectively, these results demonstrate that phagocytosis of Hz by PBMCs elicits temporal changes in the transcriptional profiles of genes central to host ubiquitination processes. Results presented here suggest that disruptions in ubiquitination may be a previously undiscovered feature of malaria pathogenesis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Jarratt2022,

title = {A Comprehensive COVID-19 Daily News and Medical Literature Briefing to Inform Health Care and Policy in New Mexico: Implementation Study},

author = {LynnMarie Jarratt and Jenny Situ and Rachel D King and Estefania Montanez Ramos and Hannah Groves and Ryen Ormesher and Melissa Coss\'{e} and Alyse Raboff and Avanika Mahajan and Jennifer Thompson and Randy F Ko and Samantha Paltrow-Krulwich and Allison Price and Ariel May-Ling Hurwitz and Timothy CampBell and Lauren T Epler and Fiona Nguyen and Emma Wolinsky and Morgan Edwards-Fligner and Jolene Lobo and Danielle Rivera and Jens Langsjoen and Lori Sloane and Ingrid Hendrix and Elly O Munde and Clinton O Onyango and Perez K Olewe and Samuel B Anyona and Alexandra V Yingling and Nicolas R Lauve and Praveen Kumar and Shawn Stoicu and Anastasiya Nestsiarovich and Cristian G Bologa and Tudor I Oprea and Kristine Tollestrup and Orrin B Myers and Mari Anixter and Douglas J Perkins and Christophe Gerard Lambert},

doi = {10.2196/23845},

issn = {2369-3762},

year  = {2022},

date = {2022-00-00},

journal = {JMIR Med Educ},

volume = {8},

number = {1},

publisher = {JMIR Publications Inc.},

abstract = {

            Background

            On March 11, 2020, the New Mexico Governor declared a public health emergency in response to the COVID-19 pandemic. The New Mexico medical advisory team contacted University of New Mexico (UNM) faculty to form a team to consolidate growing information on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its disease to facilitate New Mexico’s pandemic management. Thus, faculty, physicians, staff, graduate students, and medical students created the “UNM Global Health COVID-19 Intelligence Briefing.”

          

          

            Objective

            In this paper, we sought to (1) share how to create an informative briefing to guide public policy and medical practice and manage information overload with rapidly evolving scientific evidence; (2) determine the qualitative usefulness of the briefing to its readers; and (3) determine the qualitative effect this project has had on virtual medical education.

          

          

            Methods

            Microsoft Teams was used for manual and automated capture of COVID-19 articles and composition of briefings. Multilevel triaging saved impactful articles to be reviewed, and priority was placed on randomized controlled studies, meta-analyses, systematic reviews, practice guidelines, and information on health care and policy response to COVID-19. The finalized briefing was disseminated by email, a listserv, and posted on the UNM digital repository. A survey was sent to readers to determine briefing usefulness and whether it led to policy or medical practice changes. Medical students, unable to partake in direct patient care, proposed to the School of Medicine that involvement in the briefing should count as course credit, which was approved. The maintenance of medical student involvement in the briefings as well as this publication was led by medical students.

          

          

            Results

            An average of 456 articles were assessed daily. The briefings reached approximately 1000 people by email and listserv directly, with an unknown amount of forwarding. Digital repository tracking showed 5047 downloads across 116 countries as of July 5, 2020. The survey found 108 (95%) of 114 participants gained relevant knowledge, 90 (79%) believed it decreased misinformation, 27 (24%) used the briefing as their primary source of information, and 90 (79%) forwarded it to colleagues. Specific and impactful public policy decisions were informed based on the briefing. Medical students reported that the project allowed them to improve on their scientific literature assessment, stay current on the pandemic, and serve their community.

          

          

            Conclusions

            The COVID-19 briefings succeeded in informing and guiding New Mexico policy and clinical practice. The project received positive feedback from the community and was shown to decrease information burden and misinformation. The virtual platforms allowed for the continuation of medical education. Variability in subject matter expertise was addressed with training, standardized article selection criteria, and collaborative editing led by faculty.

          },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Anyona2021,

title = {Differential Gene Expression in Host Ubiquitination Processes in Childhood Malarial Anemia},

author = {Samuel B. Anyona and Evans Raballah and Qiuying Cheng and Ivy Hurwitz and Caroline Ndege and Elly Munde and Walter Otieno and Philip D. Seidenberg and Kristan A. Schneider and Christophe G. Lambert and Benjamin H. McMahon and Collins Ouma and Douglas J. Perkins},

doi = {10.3389/fgene.2021.764759},

issn = {1664-8021},

year  = {2021},

date = {2021-11-22},

journal = {Front. Genet.},

volume = {12},

publisher = {Frontiers Media SA},

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.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bartlett2021,

title = {COVID-19 global pandemic planning: Presence of SARS-CoV-2 fomites in a university hospital setting},

author = {Christopher Bartlett and Jens Langsjoen and Qiuying Cheng and Alexandra V Yingling and Myissa Weiss and Steven Bradfute and Douglas J Perkins and Ivy Hurwitz},

doi = {10.1177/15353702211024597},

issn = {1535-3699},

year  = {2021},

date = {2021-09-00},

journal = {Exp Biol Med (Maywood)},

volume = {246},

number = {18},

pages = {2039--2045},

publisher = {Frontiers Media SA},

abstract = { As severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has surged across the globe, great effort has been expended to understand mechanisms of transmission and spread. From a hospital perspective, this topic is critical to limit and prevent SARS-CoV-2 iatrogenic transmission within the healthcare environment. Currently, the virus is believed to be transmitted primarily through respiratory droplets, but a growing body of evidence suggests that spread is also possible through aerosolized particles and fomites. Amidst a growing volume of patients with coronavirus disease 2019 (COVID-19), the purpose of this study was to evaluate the potential for SARS-CoV-2 transmission through fomites. Samples collected from the exposed skin of clinicians (n = 42) and high-touch surfaces (n = 40) were collected before and after encounters with COVID-19 patients. Samples were analyzed using two assays: the CDC 2019-nCoV Real-Time Reverse Transcription polymerase chain reaction (RT-qPCR) assay, and a SYBR Green assay that targeted a 121 bp region within the S-gene of SARS-CoV-2. None of the samples tested positive with the CDC assay, while two high-touch surface areas tested positive for SARS-CoV-2 using the Spike assay. However, viral culture did not reveal viable SARS-CoV-2 from the positive samples. Overall, the results from this study suggest that SARS-CoV-2 RNA were not widely present either on exposed skin flora or high-touch surface areas in the hospital locations tested. The inability to recover viable virus from samples that tested positive by the molecular assays, however, does not rule out the possibility of SARS-CoV-2 transmission through fomites. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}