scholarly journals HLA class II diversity in HIV-1 uninfected individuals from the placebo arm of the RV144 Thai vaccine efficacy trial

2015 ◽  
Vol 85 (2) ◽  
pp. 117-126 ◽  
Author(s):  
K. M. Baldwin ◽  
P. K. Ehrenberg ◽  
A. Geretz ◽  
H. A. Prentice ◽  
S. Nitayaphan ◽  
...  
2014 ◽  
Vol 30 (S1) ◽  
pp. A40-A40
Author(s):  
Heather Prentice ◽  
Daniel Geraghty ◽  
Georgia D. Tomaras ◽  
Youyi Fong ◽  
Wyatt Nelson ◽  
...  

2018 ◽  
Vol 79 ◽  
pp. 29
Author(s):  
Aviva Geretz ◽  
Shida Shangguan ◽  
Chris Bryant ◽  
Philip Ehrenberg ◽  
Merlin Robb ◽  
...  

2015 ◽  
Vol 11 (2) ◽  
pp. e1003973 ◽  
Author(s):  
Paul T. Edlefsen ◽  
Morgane Rolland ◽  
Tomer Hertz ◽  
Sodsai Tovanabutra ◽  
Andrew J. Gartland ◽  
...  

2005 ◽  
Vol 12 (9) ◽  
pp. 1020-1028 ◽  
Author(s):  
Thumbi Ndung'u ◽  
Simani Gaseitsiwe ◽  
Enoch Sepako ◽  
Florence Doualla-Bell ◽  
Trevor Peter ◽  
...  

ABSTRACT Southern Africa is facing an unprecedented public health crisis due to the high prevalence of human immunodeficiency virus type 1 (HIV-1). Vaccine development and testing efforts, mainly based on elicitation of HIV-specific T cells, are under way. To understand the role of human leukocyte antigen (HLA) class II alleles in HIV pathogenesis and to facilitate HLA-based HIV-1 vaccine design, we analyzed the frequencies of HLA class II alleles within the southern African country of Botswana. Common HLA class II alleles were identified within the Batswana population through the molecular genotyping of DRB and DQB1 loci. The DRB1 allele groups DRB1*01, DRB1*02/15, DRB1*03, DRB1*11, and DRB1*13 were encountered at frequencies above 20%. Within the DQB1 locus, DQB1*06 (47.7%) was the most common allele group, followed by DQB1*03 (39.2%) and DQB1*04 (25.8%). We found that DRB1*01 was more common in HIV-negative than in HIV-positive individuals and that those who expressed DRB1*08 had lower median viral loads. We demonstrate that the frequencies of certain HLA class II alleles in this Batswana population differ substantially from those in North American populations, including African-Americans. Common allele groups within Botswana cover large percentages of other African populations and could be targeted in regional vaccine designs.


2014 ◽  
Vol 30 (S1) ◽  
pp. A25-A26
Author(s):  
Paul T. Edlefsen ◽  
Morgane Rolland ◽  
Tomer Hertz ◽  
Sodsai Tovanabutra ◽  
Andrew J. Gartland ◽  
...  

1998 ◽  
Vol 188 (10) ◽  
pp. 1785-1793 ◽  
Author(s):  
Gillian C. Harcourt ◽  
Sarah Garrard ◽  
Miles P. Davenport ◽  
Anne Edwards ◽  
Rodney E. Phillips

Effective long-term antiviral immunity requires specific cytotoxic T lymphocytes and CD4+ T lymphocyte help. Failure of these helper responses can be a principle cause of viral persistence. We sought evidence that variation in HIV-1 CD4+ T helper epitopes might contribute to this phenomenon. To determine this, we assayed fresh peripheral blood mononuclear cells from 43 asymptomatic HIV-1+ patients for proliferative responses to HIV-1 antigens. 12 (28%) showed a positive response, and we went on to map dominant epitopes in two individuals, to p24 Gag restricted by human histocompatibility leukocyte antigen (HLA)-DR1 and to p17 Gag restricted by HLA-DRB52c. Nine naturally occurring variants of the p24 Gag epitope were found in the proviral DNA of the individual in whom this response was detected. All variants bound to HLA-DR1, but three of these peptides failed to stimulate a CD4+ T lymphocyte line which recognized the index sequence. Antigenic variation was also detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized by a specific CD4+ T lymphocyte line, whereas several natural mutants were not. Importantly, variants detected at both epitopes also failed to stimulate fresh uncultured cells while index peptide stimulated successfully. These results demonstrate that variant antigens arise in HIV-1+ patients which fail to stimulate the T cell antigen receptor of HLA class II–restricted lymphocytes, although the peptide epitopes are capable of being presented on the cell surface. In HIV-1 infection, naturally occurring HLA class II–restricted altered peptide ligands that fail to stimulate the circulating T lymphocyte repertoire may curtail helper responses at sites where variant viruses predominate.


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