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dc.contributor.authorCampbell, Jennifer H.en_US
dc.contributor.authorRatai, Eva-Mariaen_US
dc.contributor.authorAutissier, Patricken_US
dc.contributor.authorNolan, David J.en_US
dc.contributor.authorTse, Samanthaen_US
dc.contributor.authorMiller, Andrew D.en_US
dc.contributor.authorGonzález, R. Gilbertoen_US
dc.contributor.authorSalemi, Marcoen_US
dc.contributor.authorBurdo, Tricia H.en_US
dc.contributor.authorWilliams, Kenneth C.en_US
dc.date.accessioned2015-01-05T18:28:01Z
dc.date.issued2014en_US
dc.identifier.citationCampbell, Jennifer H., Eva-Maria Ratai, Patrick Autissier, David J. Nolan, Samantha Tse, Andrew D. Miller, R. Gilberto González, Marco Salemi, Tricia H. Burdo, and Kenneth C. Williams. 2014. “Anti-α4 Antibody Treatment Blocks Virus Traffic to the Brain and Gut Early, and Stabilizes CNS Injury Late in Infection.” PLoS Pathogens 10 (12): e1004533. doi:10.1371/journal.ppat.1004533. http://dx.doi.org/10.1371/journal.ppat.1004533.en
dc.identifier.issn1553-7366en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:13581192
dc.description.abstractFour SIV-infected monkeys with high plasma virus and CNS injury were treated with an anti-α4 blocking antibody (natalizumab) once a week for three weeks beginning on 28 days post-infection (late). Infection in the brain and gut were quantified, and neuronal injury in the CNS was assessed by MR spectroscopy, and compared to controls with AIDS and SIV encephalitis. Treatment resulted in stabilization of ongoing neuronal injury (NAA/Cr by 1H MRS), and decreased numbers of monocytes/macrophages and productive infection (SIV p28+, RNA+) in brain and gut. Antibody treatment of six SIV infected monkeys at the time of infection (early) for 3 weeks blocked monocyte/macrophage traffic and infection in the CNS, and significantly decreased leukocyte traffic and infection in the gut. SIV – RNA and p28 was absent in the CNS and the gut. SIV DNA was undetectable in brains of five of six early treated macaques, but proviral DNA in guts of treated and control animals was equivalent. Early treated animals had low-to-no plasma LPS and sCD163. These results support the notion that monocyte/macrophage traffic late in infection drives neuronal injury and maintains CNS viral reservoirs and lesions. Leukocyte traffic early in infection seeds the CNS with virus and contributes to productive infection in the gut. Leukocyte traffic early contributes to gut pathology, bacterial translocation, and activation of innate immunity.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.ppat.1004533en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4263764/pdf/en
dash.licenseLAAen_US
dc.subjectBiology and Life Sciencesen
dc.subjectAnatomyen
dc.subjectHistologyen
dc.subjectCell Biologyen
dc.subjectCellular Typesen
dc.subjectAnimal Cellsen
dc.subjectBlood Cellsen
dc.subjectWhite Blood Cellsen
dc.subjectMonocytesen
dc.subjectT Cellsen
dc.subjectImmune Cellsen
dc.subjectDevelopmental Biologyen
dc.subjectMolecular Developmenten
dc.subjectCytokinesen
dc.subjectImmunologyen
dc.subjectClinical Immunologyen
dc.subjectImmunopathologyen
dc.subjectNeuroimmunologyen
dc.subjectImmune Systemen
dc.subjectNeuroscienceen
dc.subjectNeuroimagingen
dc.subjectHistochemistry and Cytochemistry Techniquesen
dc.subjectImmunohistochemistry Techniquesen
dc.subjectImmunohistochemical Analysisen
dc.subjectImmunologic Techniquesen
dc.subjectImmunoassaysen
dc.titleAnti-α4 Antibody Treatment Blocks Virus Traffic to the Brain and Gut Early, and Stabilizes CNS Injury Late in Infectionen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS Pathogensen
dash.depositing.authorRatai, Eva-Mariaen_US
dc.date.available2015-01-05T18:28:01Z
dc.identifier.doi10.1371/journal.ppat.1004533*
dash.contributor.affiliatedRatai, Eva-Maria


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