Mechanistic Studies of Gut Dysfunction Exacerbation due to SARS-CoV-2 in HIV/SIV infected Individuals
HIV/SIV 感染者中 SARS-CoV-2 导致肠道功能恶化的机制研究
基本信息
- 批准号:10622542
- 负责人:
- 金额:$ 39.75万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2021
- 资助国家:美国
- 起止时间:2021-07-17 至 2024-05-31
- 项目状态:已结题
- 来源:
- 关键词:2019-nCoVAccelerationAcquired Immunodeficiency SyndromeAddressAgingAgreementAnimalsCD4 Positive T LymphocytesCOVID-19COVID-19 impactCOVID-19 mortalityCOVID-19 pandemicCOVID-19 pathogenesisCOVID-19 patientCellsCessation of lifeChronicCirculationClinicalCoculture TechniquesCoronavirus InfectionsDataDisease ProgressionElderlyEmergency SituationEpithelial CellsEpitheliumFailureFunctional disorderGoalsHIVHIV/AIDSImmuneImmunologicsIndividualInfectionInflammationInflammatoryInflammatory Bowel DiseasesInjuryIntestinesLeadLesionMacacaMacaca nemestrinaModelingMononuclearMorbidity - disease rateMucositisMucous MembraneNational Institute of Diabetes and Digestive and Kidney DiseasesNatural HistoryNeutrophil ActivationNeutrophil InfiltrationOrganOutcomePathogenicityPathologicPathway interactionsPatientsPersonsPhagocytesProductionReportingRespiratory Tract InfectionsRiskRisk FactorsSARS-CoV-2 exposureSARS-CoV-2 infectionSIVSeasonsSiteSystemTestingTherapeuticViral PathogenesisVirusVirus Diseasesagedantiretroviral therapycell injuryco-infectioncomorbiditycytokinedesignexperienceextracellulargastrointestinal epitheliumgastrointestinal symptomglobal healthgut healthgut microbiotahigh risk populationimmune activationinhibitorinnovationinsightmicrobial productsmucosal siteneutrophilnonhuman primateolder patientpathogenpreventrestorationsevere COVID-19superinfectionsystemic inflammatory response
项目摘要
Abstract
With more than 60 million SARS-CoV-2 -infected patients worldwide and nearly 1.5 million COVID-19-related
deaths recoreded thus far (November 25), the COVID pandemic is one of the most critical global health problem
ever known to humankind, and a major emergency in the US. COVID-19 disproportionately impacts elders or
subjects with pre-existing conditions. Considering that the majority of persons living with HIV and AIDS (PLWHA)
in the US are aged over 50 years and that even the younger PLWHA present with accelerated aging and multiple
comorbidities related to HIV-induced excessive chronic inflammation, it is expected that COVID-19 will be
particularly severe in this risk group. Similar to HIV, SARS-CoV-2 replicates in the gut, and patients with
gastrointestinal symptoms were reported to have a more severe outcome. The exact mechanism through which
SARS-CoV-2 impacts the gut health remains elusive, however it is very likely that the two viruses can potentiate
each other through exacerbation of the gut lesions. Here, we will test the hypothesis that exacerbation of
the gut dysfunction of the SIV-infected PTMs after SARS-CoV-2 superinfection occurs through triggering
excessive mobilization, activation and NETosis of neutrophils at mucosal site and consequent gut
collateral damages. Such a scenario will result not only in an increased risk of the PLWHA to develop more
severe forms of COVID-19, but also to a significant boost of HIV pathogenicity through (i) losing control of HIV
at mucosal sites; (ii) depletion of mucosal and systemic immune effectors; (iii) increases of mucosal and systemic
levels of inflammation; and (iv) enhancement of pre-existent SIV-related comorbidities. This innovative project is
designed to assess pathogenic pathways impacted by SARS-CoV-2 in the gut, to understand the natural history
of COVID-19 related to either triggering or exacerbating HIV-associated gut dysfunction and comorbidities. We
will identify risk factors that could prompt therapy changes in high-risk individuals, such as the PLWH. Our highly
translational project addresses key scientific questions identified as critical by the NIDDK, thus being highly
responsive to RFA 20-021.
摘要
项目成果
期刊论文数量(0)
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会议论文数量(0)
专利数量(0)
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Ivona Vasile Pandrea其他文献
Ivona Vasile Pandrea的其他文献
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{{ truncateString('Ivona Vasile Pandrea', 18)}}的其他基金
Probing the role of adenosine pathway in SIV pathogenesis
探讨腺苷途径在 SIV 发病机制中的作用
- 批准号:
10760676 - 财政年份:2023
- 资助金额:
$ 39.75万 - 项目类别:
Mechanistic Studies of Gut Dysfunction Exacerbation due to SARS-CoV-2 in HIV/SIV infected Individuals
HIV/SIV 感染者中 SARS-CoV-2 导致肠道功能恶化的机制研究
- 批准号:
10452676 - 财政年份:2021
- 资助金额:
$ 39.75万 - 项目类别:
Mechanistic Studies of Gut Dysfunction Exacerbation due to SARS-CoV-2 in HIV/SIV infected Individuals
HIV/SIV 感染者中 SARS-CoV-2 导致肠道功能恶化的机制研究
- 批准号:
10319695 - 财政年份:2021
- 资助金额:
$ 39.75万 - 项目类别:
Interventions to Reduce Hypercoagulability in Old SIV-Infected NHPs
降低感染 SIV 的旧 NHP 的高凝状态的干预措施
- 批准号:
8983585 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
Impact of NETosis on SIV Pathogenesis and Response to Treatment
NETosis 对 SIV 发病机制和治疗反应的影响
- 批准号:
10666361 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
Interventions to Reduce Hypercoagulability in Old SIV-Infected NHPs
降低感染 SIV 的旧 NHP 的高凝状态的干预措施
- 批准号:
9108998 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
Impact of NETosis on SIV Pathogenesis and Response to Treatment
NETosis 对 SIV 发病机制和治疗反应的影响
- 批准号:
10402152 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
Interventions to Reduce Hypercoagulability in Old SIV-Infected NHPs
降低感染 SIV 的旧 NHP 的高凝状态的干预措施
- 批准号:
9307988 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
Interventions to Reduce Hypercoagulability in Old SIV-Infected NHPs
降低感染 SIV 的旧 NHP 的高凝状态的干预措施
- 批准号:
9555307 - 财政年份:2015
- 资助金额:
$ 39.75万 - 项目类别:
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