scholarly journals Single-Dose Nevirapine Exposure Affects T Cell Response and Cytokine Levels in HIV Type 1-Infected Women

2009 ◽  
Vol 25 (10) ◽  
pp. 1049-1053 ◽  
Author(s):  
Sharon Shalekoff ◽  
Stephen Meddows-Taylor ◽  
Diana B. Schramm ◽  
Glenda Gray ◽  
Gayle Sherman ◽  
...  
2006 ◽  
Vol 22 (4) ◽  
pp. 330-332 ◽  
Author(s):  
Fabrizio Poccia ◽  
Cristiana Gioia ◽  
Angela Corpolongo ◽  
Gianpiero D'Offizi ◽  
Pasquale Narcisco ◽  
...  

2005 ◽  
Vol 21 (4) ◽  
pp. 319-324 ◽  
Author(s):  
Dana Jones ◽  
Neil Parkin ◽  
Sarah E. Hudelson ◽  
Laura A. Guay ◽  
Philippa Musoke ◽  
...  

2007 ◽  
Vol 23 (8) ◽  
pp. 1055-1061 ◽  
Author(s):  
Seble Kassaye ◽  
Esther Lee ◽  
Rami Kantor ◽  
Elizabeth Johnston ◽  
Mark Winters ◽  
...  

2008 ◽  
Vol 83 (2) ◽  
pp. 540-551 ◽  
Author(s):  
Andreas Mörner ◽  
Iyadh Douagi ◽  
Mattias N. E. Forsell ◽  
Christopher Sundling ◽  
Pia Dosenovic ◽  
...  

ABSTRACT Currently there is limited information about the quality of immune responses elicited by candidate human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (Env)-based immunogens in primates. Here we describe a comprehensive analysis of neutralizing antibody and T-cell responses obtained in cynomolgus macaques by three selected immunization regimens. We used the previously described YU2-based gp140 protein trimers administered in an adjuvant, preceded by two distinct priming strategies: either alphavirus replicon particles expressing matched gp140 trimers or gp120 core proteins stabilized in the CD4-bound conformation. The rationale for priming with replicon particles was to evaluate the impact of the expression platform on trimer immunogenicity. The stable core proteins were chosen in an attempt to expand selectively lymphocytes recognizing common determinants between the core and trimers to broaden the immune response. The results presented here demonstrate that the platform by which Env trimers were delivered in the priming (either protein or replicon vector) had little impact on the overall immune response. In contrast, priming with stable core proteins followed by a trimer boost strikingly focused the T-cell response on the core sequences of HIV-1 Env. The specificity of the T-cell response was distinctly different from that of the responses obtained in animals immunized with trimers alone and was shown to be mediated by CD4+ T cells. However, this regimen showed limited or no improvement in the neutralizing antibody responses, suggesting that further immunogen design efforts are required to successfully focus the B-cell response on conserved neutralizing determinants of HIV-1 Env.


Immunology ◽  
2006 ◽  
Vol 117 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Takeshi Kikuchi ◽  
Shuichiro Uehara ◽  
Haruyuki Ariga ◽  
Takeshi Tokunaga ◽  
Ai Kariyone ◽  
...  

2014 ◽  
Vol 210 (4) ◽  
pp. 641-645 ◽  
Author(s):  
Mark A. Micek ◽  
Sandra Dross ◽  
Ana Judith Blanco ◽  
Ingrid A. Beck ◽  
Laurinda Matunha ◽  
...  

2004 ◽  
Vol 78 (13) ◽  
pp. 7069-7078 ◽  
Author(s):  
Todd M. Allen ◽  
Marcus Altfeld ◽  
Xu G. Yu ◽  
Kristin M. O'Sullivan ◽  
Mathias Lichterfeld ◽  
...  

ABSTRACT Numerous studies now support that human immunodeficiency virus type 1 (HIV-1) evolution is influenced by immune selection pressure, with population studies showing an association between specific HLA alleles and mutations within defined cytotoxic T-lymphocyte epitopes. Here we combine sequence data and functional studies of CD8 T-cell responses to demonstrate that allele-specific immune pressures also select for mutations flanking CD8 epitopes that impair antigen processing. In persons expressing HLA-A3, we demonstrate consistent selection for a mutation in a C-terminal flanking residue of the normally immunodominant Gag KK9 epitope that prevents its processing and presentation, resulting in a rapid decline in the CD8 T-cell response. This single amino acid substitution also lies within a second HLA-A3-restricted epitope, with the mutation directly impairing recognition by CD8 T cells. Transmission of the mutation to subjects expressing HLA-A3 was shown to prevent the induction of normally immunodominant acute-phase responses to both epitopes. However, subsequent in vivo reversion of the mutation was coincident with delayed induction of new CD8 T-cell responses to both epitopes. These data demonstrate that mutations within the flanking region of an HIV-1 epitope can impair recognition by an established CD8 T-cell response and that transmission of these mutations alters the acute-phase CD8+ T-cell response. Moreover, reversion of these mutations in the absence of the original immune pressure reveals the potential plasticity of immunologically selected evolutionary changes.


1999 ◽  
Vol 73 (9) ◽  
pp. 7619-7626 ◽  
Author(s):  
Morgan E. Wallace ◽  
Rachael Keating ◽  
William R. Heath ◽  
Francis R. Carbone

ABSTRACT Many virus infections give rise to surprisingly limited T-cell responses directed to very few immunodominant determinants. We have been examining the cytotoxic T-lymphocyte (CTL) response to herpes simplex virus type 1 (HSV-1) infection. Previous studies have identified the glycoprotein B-derived peptide from residues 498 to 505 (gB498–505) as one of at least three determinants recognized by HSV-1-specific CTLs isolated from C57BL/6 mice. We had previously found that in vitro-derived CTLs directed to gB498–505 show a characteristic pattern of T-cell receptor (TCR) usage, with 60% of gB498–505-specific CD8+ T cells expressing BV10+ TCR β chains and a further 20% expressing BV8S1. In this report, we confirm that this TCR V-region bias is also reflected in the ex vivo response to HSV-1 infection. A high proportion of activated CD8+draining lymph node cells were found to express these dominant V regions, suggesting that a substantial number of in vivo responding T cells were directed to this one viral determinant. The use of an HSV-1 deletion mutant lacking the gB498–505 determinant in combination with accurate intracellular gamma interferon staining allowed us to quantify the extent of gB-specific T-cell dominance. Together, these results suggested that between 70 and 90% of all CD8+ HSV-1-specific T cells target gB498–505. While deletion of this determinant resulted in an attenuated CD8+ T-cell response, it also permitted the emergence of one or more previously unidentified cryptic specificities. Overall, HSV-1 infection of C57BL/6 mice results in an extremely focused pattern of CD8+ T-cell selection in terms of target specificity and TCR expression.


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