scholarly journals Phenotypic characterization of regulatory T cells from antiretroviral-naive HIV-1-infected people

Immunology ◽  
2017 ◽  
Vol 151 (4) ◽  
pp. 405-416 ◽  
Author(s):  
Georgia N. Ambada ◽  
Claudine E. Ntsama ◽  
Nadesh N. Nji ◽  
Loveline N. Ngu ◽  
Carole N. Sake ◽  
...  
2013 ◽  
Vol 9 (1) ◽  
pp. e1003140 ◽  
Author(s):  
Chun Li ◽  
Ilona Toth ◽  
Julian Schulze zur Wiesch ◽  
Florencia Pereyra ◽  
Jennifer Rychert ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e20375 ◽  
Author(s):  
Jennifer A. Slyker ◽  
Grace C. John-Stewart ◽  
Tao Dong ◽  
Barbara Lohman-Payne ◽  
Marie Reilly ◽  
...  

2017 ◽  
Vol 32 (7) ◽  
pp. 1098-1104 ◽  
Author(s):  
Adriele A. Queiroz ◽  
Eduardo L. França ◽  
Cristiane C. P. Hara ◽  
Mariana S. Honorio ◽  
Danny L. G. Fagundes ◽  
...  

2005 ◽  
Vol 175 (12) ◽  
pp. 8415-8423 ◽  
Author(s):  
Brent E. Palmer ◽  
Naomi Blyveis ◽  
Andrew P. Fontenot ◽  
Cara C. Wilson

2004 ◽  
Vol 136 (2) ◽  
pp. 373-378 ◽  
Author(s):  
J. HEIKKINEN ◽  
M. MOTTONEN ◽  
A. ALANEN ◽  
O. LASSILA

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Gabriella Tedeschi ◽  
Elisa Maffioli ◽  
Armando Negri ◽  
Andrea Romagnani ◽  
Fabio Grassi

2017 ◽  
Author(s):  
Sean Matthew McCauley ◽  
Kyusik Kim ◽  
Anetta Nowosielska ◽  
Ann Dauphin ◽  
Leonid Yurkovetskiy ◽  
...  

ABSTRACTHIV-1-infected people who take drugs that suppress viremia to undetectable levels are protected from developing AIDS. Nonetheless, these individuals have chronic inflammation associated with heightened risk of cardiovascular pathology. HIV-1 establishes proviruses in long-lived CD4+memory T cells, and perhaps other cell types, that preclude elimination of the virus even after years of continuous antiviral therapy. Though the majority of proviruses that persist during antiviral therapy are defective for production of infectious virions, many are expressed, raising the possibility that the HIV-1provirus or its transcripts contribute to ongoing inflammation. Here we found that the HIV-1 provirus activated innate immune signaling in isolated dendritic cells, macrophages, and CD4+T cells. Immune activation required transcription from the HIV-1 provirus and expression of CRM1-dependent, Rev-dependent, RRE-containing, unspliced HIV-1 RNA. Ifrevwas providedin trans, all HIV-1 coding sequences were dispensable for activation except thosecis-acting sequences required for replication or splicing. These results indicate that the complex, post-transcriptional regulation intrinsic to HIV-1 RNA is detected by the innate immune system as a danger signal, and that drugs which disrupt HIV-1 transcription or HIV-1 RNA metabolism would add qualitative benefit to current antiviral drug regimens.


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