scholarly journals Association of TRIM22 with the Type 1 Interferon Response and Viral Control during Primary HIV-1 Infection

2010 ◽  
Vol 85 (1) ◽  
pp. 208-216 ◽  
Author(s):  
R. Singh ◽  
G. Gaiha ◽  
L. Werner ◽  
K. McKim ◽  
K. Mlisana ◽  
...  
2020 ◽  
Vol 228 ◽  
pp. 83-85
Author(s):  
James J. DiNicolantonio ◽  
Jorge Barroso-Aranda ◽  
Mark F. McCarty

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e45839 ◽  
Author(s):  
Tom H. M. Ottenhoff ◽  
Ranjeeta Hari Dass ◽  
Ninghan Yang ◽  
Mingzi M. Zhang ◽  
Hazel E. E. Wong ◽  
...  

2004 ◽  
Vol 78 (7) ◽  
pp. 3233-3243 ◽  
Author(s):  
Agatha Masemola ◽  
Tumelo Mashishi ◽  
Greg Khoury ◽  
Phineas Mohube ◽  
Pauline Mokgotho ◽  
...  

ABSTRACT An understanding of the relationship between the breadth and magnitude of T-cell epitope responses and viral loads is important for the design of effective vaccines. For this study, we screened a cohort of 46 subtype C human immunodeficiency virus type 1 (HIV-1)-infected individuals for T-cell responses against a panel of peptides corresponding to the complete subtype C genome. We used a gamma interferon ELISPOT assay to explore the hypothesis that patterns of T-cell responses across the expressed HIV-1 genome correlate with viral control. The estimated median time from seroconversion to response for the cohort was 13 months, and the order of cumulative T-cell responses against HIV proteins was as follows: Nef > Gag > Pol > Env > Vif > Rev > Vpr > Tat > Vpu. Nef was the most intensely targeted protein, with 97.5% of the epitopes being clustered within 119 amino acids, constituting almost one-third of the responses across the expressed genome. The second most targeted region was p24, comprising 17% of the responses. There was no correlation between viral load and the breadth of responses, but there was a weak positive correlation (r = 0.297; P = 0.034) between viral load and the total magnitude of responses, implying that the magnitude of T-cell recognition did not contribute to viral control. When hierarchical patterns of recognition were correlated with the viral load, preferential targeting of Gag was significantly (r = 0.445; P = 0.0025) associated with viral control. These data suggest that preferential targeting of Gag epitopes, rather than the breadth or magnitude of the response across the genome, may be an important marker of immune efficacy. These data have significance for the design of vaccines and for interpretation of vaccine-induced responses.


2016 ◽  
Vol 06 (01) ◽  
pp. 15-23 ◽  
Author(s):  
Samuel V. Nuvor ◽  
Hilton Whittle ◽  
Sarah Rowland-Jones ◽  
Assan Jaye

2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 191-191
Author(s):  
Megan Shoemaker ◽  
Natalia Smirnova ◽  
Hana Van Campen ◽  
Helle Bielefeldt-Ohmann ◽  
Kathy Austin ◽  
...  

Retrovirology ◽  
2011 ◽  
Vol 8 (1) ◽  
pp. 49 ◽  
Author(s):  
Thomas Pertel ◽  
Christian Reinhard ◽  
Jeremy Luban

2018 ◽  
Vol 319 ◽  
pp. 117-129 ◽  
Author(s):  
Virginia D. McLane ◽  
Saurabh Kumar ◽  
Reno Leeming ◽  
Sanjay Rau ◽  
Colin L. Willis ◽  
...  

Viruses ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1227
Author(s):  
Yu-Min Choi ◽  
Hyein Jeong ◽  
Uni Park ◽  
Nam-Hyuk Cho ◽  
Bum-Joon Kim

The current COVID-19 pandemic has highlighted the urgent need to develop effective therapeutic strategies. We evaluated the in vitro antiviral effect against SARS-CoV-2 of a hepatitis B virus (HBV) hexamer peptide, Poly6, which is capable of eliciting an antiviral effect against human immunodeficiency virus -1 (HIV-1), as a novel HIV-1 integrase inhibitor, and a strong anticancer immune response in an IFN-I-dependent manner, as a novel potential adjuvant in anticancer immunotherapy. Here, we report that Poly6 exerts an anti-SARS-CoV-2 effect, with an estimated 50% inhibitory concentration of 2.617 µM, in the human bronchial epithelial cell line, Calu-3 but not in Vero-E6 cells, which are deficient in type 1 interferon (IFN-I) signaling. We proved via assays based on mRNA profiles, inhibitors, or blocking antibodies that Poly6 can exert an anti-SARS-CoV-2 effect in an IFN-I-dependent manner. We also found that Poly6 inhibits IL-6 production enhanced by SARS-CoV-2 in infected Calu-3 cells at both the transcription and the translation levels, mediated via IL-10 induction in an IFN-I-dependent manner. These results indicate the feasibility of Poly6 as an IFN-I-inducing COVID-19 drug with potent antiviral and anti-inflammatory activities.


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