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Conference Paper: The effects of HIV-1 Tat protein on mycobacterial infection

TitleThe effects of HIV-1 Tat protein on mycobacterial infection
Authors
Issue Date2013
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
The Annual Meeting of the American Association of Immunologists (AAI) on Immunology (Immunology 2013), Honolulu, Hawaii, 3-7 May 2013. In Journal of Immunology, 2013, v. 190 n. Meeting Abstract Supplement, p. abstract no. 130.9 How to Cite?
AbstractHuman immunodeficiency virus infection remains a worldwide threat. With the emergence of HIV-1 induced immunodeficiency in the host, mycobacterial infection becomes a common opportunistic infection as its prevalence is dramatic increased. HIV-1 Tat is an important viral regulatory protein in promoting HIV replication and modulating the cytokine production, as demonstrated by our previous publications. In light of that, we would like to investigate whether HIV-1 Tat could affect mycobacteria induced immune responses. We first examined whether HIV-1 Tat could mediate mycobacteria induced cytokine production. The results demonstrated that HIV-1 Tat suppressed mycobacteria-induced TNF-α in human primary macrophage. Next, we examined whether HIV-1 Tat also suppress the intracellular survival of mycobacteria. Under the pretreatment of HIV-1 Tat in human primary macrophages, intracellular growth of mycobacteria was enhanced significantly. Since TNF-α is proposed to regulate mycobacterial survival, we would like to verify this hypothesis in order to provide the evidence to support our findings that HIV-1 Tat downregulated mycobacteria induced TNF-α is participated in suppressing the mycobacterial survival. The results showed that when we neutralized the mycobacteria produced TNF-α by antibodies, the survival of mycobacteria is increased. In summary, HIV-1 Tat may play a role in favouring mycobacterial opportunistic infection during AIDS progression.
Persistent Identifierhttp://hdl.handle.net/10722/206057
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549

 

DC FieldValueLanguage
dc.contributor.authorLi, CBen_US
dc.contributor.authorPong, CHen_US
dc.contributor.authorLau, ASYen_US
dc.date.accessioned2014-10-20T11:47:26Z-
dc.date.available2014-10-20T11:47:26Z-
dc.date.issued2013en_US
dc.identifier.citationThe Annual Meeting of the American Association of Immunologists (AAI) on Immunology (Immunology 2013), Honolulu, Hawaii, 3-7 May 2013. In Journal of Immunology, 2013, v. 190 n. Meeting Abstract Supplement, p. abstract no. 130.9en_US
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/206057-
dc.description.abstractHuman immunodeficiency virus infection remains a worldwide threat. With the emergence of HIV-1 induced immunodeficiency in the host, mycobacterial infection becomes a common opportunistic infection as its prevalence is dramatic increased. HIV-1 Tat is an important viral regulatory protein in promoting HIV replication and modulating the cytokine production, as demonstrated by our previous publications. In light of that, we would like to investigate whether HIV-1 Tat could affect mycobacteria induced immune responses. We first examined whether HIV-1 Tat could mediate mycobacteria induced cytokine production. The results demonstrated that HIV-1 Tat suppressed mycobacteria-induced TNF-α in human primary macrophage. Next, we examined whether HIV-1 Tat also suppress the intracellular survival of mycobacteria. Under the pretreatment of HIV-1 Tat in human primary macrophages, intracellular growth of mycobacteria was enhanced significantly. Since TNF-α is proposed to regulate mycobacterial survival, we would like to verify this hypothesis in order to provide the evidence to support our findings that HIV-1 Tat downregulated mycobacteria induced TNF-α is participated in suppressing the mycobacterial survival. The results showed that when we neutralized the mycobacteria produced TNF-α by antibodies, the survival of mycobacteria is increased. In summary, HIV-1 Tat may play a role in favouring mycobacterial opportunistic infection during AIDS progression.-
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org-
dc.relation.ispartofJournal of Immunologyen_US
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org-
dc.titleThe effects of HIV-1 Tat protein on mycobacterial infectionen_US
dc.typeConference_Paperen_US
dc.identifier.emailLi, CB: jamesli@graduate.hku.hken_US
dc.identifier.emailPong, CH: jchpong@hku.hken_US
dc.identifier.emailLau, ASY: asylau@hku.hken_US
dc.identifier.authorityLi, CB=rp00496en_US
dc.identifier.authorityLau, ASY=rp00474en_US
dc.identifier.hkuros241337en_US
dc.identifier.volume190-
dc.identifier.issueMeeting Abstract Supplement-
dc.publisher.placeUnited States-

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