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Host and viral factors contribute to...

Denekamp, Lynn Marie.

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Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages./
Author:	Denekamp, Lynn Marie.
Description:	188 p.
Notes:	Adviser: Gregory Viglianti.
Contained By:	Dissertation Abstracts International68-03B.
Subject:	Biology, Microbiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3254457

Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages.
Denekamp, Lynn Marie.

Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages. - 188 p.

Adviser: Gregory Viglianti.

Thesis (Ph.D.)--Boston University, 2007.

Taken together, these data underscore the importance of investigating the pathways that relay exogenous signals to the HIV-1 LTR and modulate virus replication.Subjects--Topical Terms:

1017734
Biology, Microbiology.

Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages.
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035 $a (UMI)AAI3254457
035 $a AAI3254457
040 $a UMI $c UMI
100 1 $a Denekamp, Lynn Marie. $3 1263312
245 1 0 $a Host and viral factors contribute to modulation of human immunodeficiency virus replication in monocytes/macrophages.
300 $a 188 p.
500 $a Adviser: Gregory Viglianti.
500 $a Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1422.
502 $a Thesis (Ph.D.)--Boston University, 2007.
520 $a Taken together, these data underscore the importance of investigating the pathways that relay exogenous signals to the HIV-1 LTR and modulate virus replication.
520 $a Serum vitamin A levels are inversely correlated with HIV-1 viremia and, in Africa, supplementation with vitamin A reduces morbidity in malnourished, infected children. Retinoic acid (RA), a bioactive metabolite of vitamin A, is known to indirectly repress replication of HIV-1 through a mechanism that requires new protein synthesis and subsequent inhibition of chromatin remodeling of the HIV-1 long terminal repeat (LTR). Transcription factor binding sites within the LTR, including those for NF-kappaB and Sp1, are required for RA mediated repression. The contribution of viral and host factors in RA mediated repression of HIV-1 in monocytes/macrophages was investigated. I found that LTR reporter constructs representing the HIV-1 subtypes (A through G) and containing natural mutations in essential transcription factor binding sites, including Sp1, were all repressible by RA in transfection experiments. Repression of LTR reporter constructs required RA pretreatment for at least 24 hours and occurred in the presence of Tat trans activator. Furthermore, RA repressed the replication of primary HIV-1 isolates representing subtypes B and C in primary human monocyte-derived macrophages (MDMs). Treatment of monocytes/macrophages with RA increased the accumulation of both unmodified and sumoylated isoforms of the HIV-1 transcriptional repressor Sp3 suggesting that it might play a role in RA-mediated repression.
520 $a The role of Toll-like receptors (TLRs) in activation of the HIV-1 LTR was investigated as a model for sexually transmitted co-infections (STI). Clinically, an increase in plasma viral load has been demonstrated in HIV-1 infected patients with acute STIs. Lipopolysaccharide (LPS) and other bacterial products bind to TLRs and induce activation of transcription factors known to regulate the LTR. The bacterial product peptidoglycan (PGN) and the STI pathogen Neisseria gonorrhoeae both activated replication of HIV-1 in monocytes and lymphocyte cultures. MAP kinase inhibitors known to block signaling through TLRs inhibited PGN- and N. gonorrhoeae -mediated activation of virus, suggesting that TLRs provide a link between bacterial products and increased virus replication.
590 $a School code: 0017.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Virology. $3 1019068
690 $a 0410
690 $a 0720
710 2 $a Boston University. $3 1017454
773 0 $t Dissertation Abstracts International $g 68-03B.
790 $a 0017
790 1 0 $a Viglianti, Gregory, $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3254457