2023
Syntaxin 11 Contributes to the Interferon-Inducible Restriction of Coxiella burnetii Intracellular Infection
Ganesan S, Alvarez N, Steiner S, Fowler K, Corona A, Roy C. Syntaxin 11 Contributes to the Interferon-Inducible Restriction of Coxiella burnetii Intracellular Infection. MBio 2023, 14: e03545-22. PMID: 36728431, PMCID: PMC9972978, DOI: 10.1128/mbio.03545-22.Peer-Reviewed Original ResearchConceptsC. burnetii replicationSNARE proteinsHost cellsSyntaxin-11Cell-autonomous responsesIntracellular pathogensMembrane fusion eventsLysosome-derived organellesDefense mechanismsModel bacterial pathogenMultiple cell typesEukaryotic cellsDefense pathwaysDelivery of cargoReplication of pathogensHuman proteinsFusion eventsDissemination of pathogensFusion pathwayHost proteinsIntrinsic defense mechanismsHost vesiclesHost restriction factorsStable expressionSubcellular organelles
2019
Immunoepidemiology of Human Immunodeficiency
Paintsil E. Immunoepidemiology of Human Immunodeficiency. 2019, 165-178. DOI: 10.1007/978-3-030-25553-4_10.Peer-Reviewed Original ResearchAcquired Immunodeficiency SyndromeSimian immunodeficiency virusHIV-1Retrovirus human immunodeficiency virus type 1Immunodeficiency virus type 1Class I human leukocyte antigenHIV-1 diseaseHIV-2 infectionHIV-1 infectionHuman leukocyte antigenHost immune factorsHIV-1 researchImmune selection pressureHost restriction factorsVirus type 1New human hostHuman β-defensinLikelihood of transmissionEnzyme catalytic polypeptideImmunodeficiency syndromeAIDS patientsImmunodeficiency virusLeukocyte antigenHIV-2Preventative vaccine
2018
Short Communication: Expression of Host Restriction Factors by Memory CD4+ T Cells Differs Between Healthy Donors and HIV-1-Infected Individuals with Effective Antiretroviral Therapy
Bachtel ND, Beckerle GA, Mota TM, de Mulder Rougvie M, Raposo RAS, Jones RB, Nixon DF, Apps R. Short Communication: Expression of Host Restriction Factors by Memory CD4+ T Cells Differs Between Healthy Donors and HIV-1-Infected Individuals with Effective Antiretroviral Therapy. AIDS Research And Human Retroviruses 2018, 35: 108-111. PMID: 30198299, PMCID: PMC6343196, DOI: 10.1089/aid.2018.0162.Peer-Reviewed Original ResearchConceptsHIV-1-infected individualsHost restriction factorsRestriction factor expressionEffective antiretroviral therapyAntiretroviral therapyUninfected individualsMemory CD4Viral reservoirRestriction factorsT cellsChronic HIV-1 infectionHIV-1 gag DNAHIV-1 reservoir sizeFactor expressionMemory T cell compartmentQuantitative viral outgrowth assaysART-suppressed individualsSuppressive antiretroviral therapyViral outgrowth assaysHIV-1 infectionT cell compartmentDroplet digital polymerase chain reactionGag DNAViral loadImmune activation
2011
TRIM22 Inhibits HIV-1 Transcription Independently of Its E3 Ubiquitin Ligase Activity, Tat, and NF-κB-Responsive Long Terminal Repeat Elements
Kajaste-Rudnitski A, Marelli SS, Pultrone C, Pertel T, Uchil PD, Mechti N, Mothes W, Poli G, Luban J, Vicenzi E. TRIM22 Inhibits HIV-1 Transcription Independently of Its E3 Ubiquitin Ligase Activity, Tat, and NF-κB-Responsive Long Terminal Repeat Elements. Journal Of Virology 2011, 85: 5183-5196. PMID: 21345949, PMCID: PMC3126207, DOI: 10.1128/jvi.02302-10.Peer-Reviewed Original ResearchConceptsHIV-1 replicationHIV-1 transcriptionHuman immunodeficiency virus type 1 (HIV-1) replicationU937 promonocytic cell lineHIV-1 restriction factorsTumor necrosis factor alphaInhibits HIV-1 transcriptionType 1 replicationRestriction factorsHIV-1 productionNecrosis factor alphaLower peak levelsPermissive cellsHIV-1 LTRHost restriction factorsPromonocytic cell lineU937 cellsReplication-competent virusNF-κB binding siteFactor alphaT cellsHIV-1Overexpression of TRIM22NF-κBLTR transactivation
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