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Co-receptors for HIV-1 entry.
Moore JP, Trkola A, Dragic T. Moore JP, et al. Among authors: trkola a. Curr Opin Immunol. 1997 Aug;9(4):551-62. doi: 10.1016/s0952-7915(97)80110-0. Curr Opin Immunol. 1997. PMID: 9287172 Review.
Potent, broad-spectrum inhibition of human immunodeficiency virus type 1 by the CCR5 monoclonal antibody PRO 140.
Trkola A, Ketas TJ, Nagashima KA, Zhao L, Cilliers T, Morris L, Moore JP, Maddon PJ, Olson WC. Trkola A, et al. J Virol. 2001 Jan;75(2):579-88. doi: 10.1128/JVI.75.2.579-588.2001. J Virol. 2001. PMID: 11134270 Free PMC article.
CCR5 serves as a requisite fusion coreceptor for clinically relevant strains of human immunodeficiency virus type 1 (HIV-1) and provides a promising target for antiviral therapy. ...In this study, PRO 140 was tested against a panel of primary HIV-1 isolates s …
CCR5 serves as a requisite fusion coreceptor for clinically relevant strains of human immunodeficiency virus type 1 (HIV-1) and provi …
The HIV-1 Entry Process: A Stoichiometric View.
Brandenberg OF, Magnus C, Regoes RR, Trkola A. Brandenberg OF, et al. Among authors: trkola a. Trends Microbiol. 2015 Dec;23(12):763-774. doi: 10.1016/j.tim.2015.09.003. Epub 2015 Nov 2. Trends Microbiol. 2015. PMID: 26541228 Review.
HIV-1 infection starts with fusion of the viral and the host cell membranes, a process mediated by the HIV-1 envelope glycoprotein trimer. ...Initial estimates suggested a unanimous entry stoichiometry across HIV-1 strains while recent findings showed that HIV-1 str …
HIV-1 infection starts with fusion of the viral and the host cell membranes, a process mediated by the HIV-1 envelope glycoprotein tr …
HIV-host interactions: vital to the virus and key to its inhibition.
Trkola A. Trkola A. Curr Opin Microbiol. 2004 Oct;7(5):555-9. doi: 10.1016/j.mib.2004.08.001. Curr Opin Microbiol. 2004. PMID: 15499686 Review.
HIV-host interactions: vital to the virus and key to its inhibition.
Trkola A. Trkola A. Curr Opin Microbiol. 2004 Aug;7(4):407-11. doi: 10.1016/j.mib.2004.06.002. Curr Opin Microbiol. 2004. PMID: 15358260 Corrected and republished. Review.
HIV-1 escape from a small molecule, CCR5-specific entry inhibitor does not involve CXCR4 use.
Trkola A, Kuhmann SE, Strizki JM, Maxwell E, Ketas T, Morgan T, Pugach P, Xu S, Wojcik L, Tagat J, Palani A, Shapiro S, Clader JW, McCombie S, Reyes GR, Baroudy BM, Moore JP. Trkola A, et al. Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):395-400. doi: 10.1073/pnas.012519099. Proc Natl Acad Sci U S A. 2002. PMID: 11782552 Free PMC article.
To study HIV-1 escape from a coreceptor antagonist, the R5 primary isolate CC1/85 was passaged in peripheral blood mononuclear cells with increasing concentrations of the CCR5-specific small molecule inhibitor, AD101. By 19 passages, an escape mutant emerged with a
To study HIV-1 escape from a coreceptor antagonist, the R5 primary isolate CC1/85 was passaged in peripheral blood mononuclear cells …
Estimating the stoichiometry of human immunodeficiency virus entry.
Magnus C, Rusert P, Bonhoeffer S, Trkola A, Regoes RR. Magnus C, et al. Among authors: trkola a. J Virol. 2009 Feb;83(3):1523-31. doi: 10.1128/JVI.01764-08. Epub 2008 Nov 19. J Virol. 2009. PMID: 19019953 Free PMC article.
Virol. 79: 12132-12147, 2005), we estimated that the number of trimer-receptor interactions required for HIV to infect a target cell is approximately eight, which is higher than previous estimates. ...
Virol. 79: 12132-12147, 2005), we estimated that the number of trimer-receptor interactions required for HIV to infect a target cell …
Use of alternate coreceptors on primary cells by two HIV-1 isolates.
Cilliers T, Willey S, Sullivan WM, Patience T, Pugach P, Coetzer M, Papathanasopoulos M, Moore JP, Trkola A, Clapham P, Morris L. Cilliers T, et al. Among authors: trkola a. Virology. 2005 Aug 15;339(1):136-44. doi: 10.1016/j.virol.2005.05.027. Virology. 2005. PMID: 15992849
The R5 isolate grew in Delta32/Delta32 CCR5 PBMC in the absence or presence of AMD3100, a CXCR4-specific inhibitor, indicating that it uses a receptor other than CCR5 or CXCR4 on primary cells. It was insensitive to the CCR5 entry inhibitors RANTES and PRO140, but w …
The R5 isolate grew in Delta32/Delta32 CCR5 PBMC in the absence or presence of AMD3100, a CXCR4-specific inhibitor, indicating that i …
The differential sensitivity of human and rhesus macaque CCR5 to small-molecule inhibitors of human immunodeficiency virus type 1 entry is explained by a single amino acid difference and suggests a mechanism of action for these inhibitors.
Billick E, Seibert C, Pugach P, Ketas T, Trkola A, Endres MJ, Murgolo NJ, Coates E, Reyes GR, Baroudy BM, Sakmar TP, Moore JP, Kuhmann SE. Billick E, et al. Among authors: trkola a. J Virol. 2004 Apr;78(8):4134-44. doi: 10.1128/jvi.78.8.4134-4144.2004. J Virol. 2004. PMID: 15047829 Free PMC article.
However, the binding of a conformation-dependent monoclonal antibody to human CCR5 is inhibited by SCH-C only when residue 198 is isoleucine. These observations, taken together, suggest that the antiviral effects of SCH-C and AD101 involve stabilization, or induction, of …
However, the binding of a conformation-dependent monoclonal antibody to human CCR5 is inhibited by SCH-C only when residue 198 is iso …
Analysis of the mechanism by which the small-molecule CCR5 antagonists SCH-351125 and SCH-350581 inhibit human immunodeficiency virus type 1 entry.
Tsamis F, Gavrilov S, Kajumo F, Seibert C, Kuhmann S, Ketas T, Trkola A, Palani A, Clader JW, Tagat JR, McCombie S, Baroudy B, Moore JP, Sakmar TP, Dragic T. Tsamis F, et al. Among authors: trkola a. J Virol. 2003 May;77(9):5201-8. doi: 10.1128/jvi.77.9.5201-5208.2003. J Virol. 2003. PMID: 12692222 Free PMC article.
Human immunodeficiency virus type 1 (HIV-1) entry is mediated by the consecutive interaction of the envelope glycoprotein gp120 with CD4 and a coreceptor such as CCR5 or CXCR4. ...Alanine mutagenesis of the transmembrane domain of CCR5 suggests that AD101 and SCH-C bind to …
Human immunodeficiency virus type 1 (HIV-1) entry is mediated by the consecutive interaction of the envelope glycoprotein gp120 with CD4 and …
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