HIV Inhibition by Lactobacilli: Easier in a Test Tube Than in Real Life

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorWITKIN, Steven S.
dc.contributor.authorLINHARES, Lara M.
dc.date.accessioned2016-02-11T14:19:17Z
dc.date.available2016-02-11T14:19:17Z
dc.date.issued2015
dc.description.abstractA lactobacillus-dominant vaginal microbiota has been shown to decrease heterosexual HIV transmission. Nunn et al. now report that a vaginal microbiota dominated by Lactobacillus crispatus is associated with a relative inability of HIV pseudoviral particles to transverse cervicovaginal mucus CVM) in vitro [mBio 65): e01084-15, 2015, doi: 10.1128/mBio.01084-15]. The purported inhibitory mechanism is the interaction between carboxyl groups present on HIV and in CVM that occurred only under acidic conditions when carboxyl groups were protonated. L. crispatus produces high levels of lactic acid and results in the lowest vaginal pH when it is the dominant vaginal bacterium. In addition, high levels of lactic acid inhibit the proliferation of other bacteria that might negatively affect CVM structure. The utility of enhancing L. crispatus dominance to inhibit HIV transmission awaits assessment of the influence of ejaculated semen on this property and investigations on the role of Lactobacillus products such as D-lactic acid in this property.
dc.description.indexMEDLINE
dc.identifier.citationMBIO, v.6, n.5, article ID e01485-15, 2p, 2015
dc.identifier.doi10.1128/mBio.01485-15
dc.identifier.issn2150-7511
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/12856
dc.language.isoeng
dc.publisherAMER SOC MICROBIOLOGY
dc.relation.ispartofMbio
dc.rightsopenAccess
dc.rights.holderCopyright AMER SOC MICROBIOLOGY
dc.subject.othergenital-tract
dc.subject.othertransmission
dc.subject.wosMicrobiology
dc.titleHIV Inhibition by Lactobacilli: Easier in a Test Tube Than in Real Life
dc.typearticle
dc.type.categoryeditorial material
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalWITKIN, Steven S.:Weill Cornell Med Coll, Dept Obstet & Gynecol, Div Infect Dis & Immunol, New York, NY 10065 USA
hcfmusp.citation.scopus6
hcfmusp.contributor.author-fmusphcIARA MORENO LINHARES
hcfmusp.description.articlenumbere01485-15
hcfmusp.description.issue5
hcfmusp.description.volume6
hcfmusp.origemWOS
hcfmusp.origem.pubmed26443461
hcfmusp.origem.scopus2-s2.0-84946607115
hcfmusp.origem.wosWOS:000364523100062
hcfmusp.publisher.cityWASHINGTON
hcfmusp.publisher.countryUSA
hcfmusp.relation.referenceRahkonen L, 2009, HUM REPROD, V24, P2693, DOI 10.1093/humrep/dep284
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hcfmusp.relation.referenceMirmonsef P, 2014, AM J REPROD IMMUNOL, V71, P531, DOI 10.1111/aji.12232
hcfmusp.relation.referenceNunn KL, 2015, MBIO, V6, DOI 10.1128/mBio.01084-15
hcfmusp.relation.referenceO'Hanlon DE, 2010, BMC INFECT DIS, V10, DOI 10.1186/1471-2334-10-120
hcfmusp.relation.referenceRavel J, 2012, MBIO, V3, DOI 10.1128/mBio.00370-12
hcfmusp.relation.referenceWitkin SS, 2013, MBIO, V4, DOI 10.1128/mBio.00460-13
hcfmusp.scopus.lastupdate2024-05-17
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relation.isAuthorOfPublication.latestForDiscovery725393ab-c113-412f-af2c-e7e7e9af2df8
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