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Bolduan, S. ; Koppensteiner, H. ; Businger, R.* ; Rebensburg, S. ; Kunze, C. ; Brack-Werner, R. ; Draenert, R.* ; Schindler, M.

T cells with low CD2 levels express reduced restriction factors and are preferentially infected in therapy naïve chronic HIV-1 patients.

J. Int. AIDS Soc. 20:21865 (2017)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Bolduan S et al; licensee International AIDS Society. Introduction: Restriction factors (RFs) suppress HIV-1 in cell lines and primary cell models. Hence, RFs might be attractive targets for novel antiviral strategies, but their importance for virus control in vivo is controversial. Methods: We profiled the expression of RFs in primary blood-derived mononuclear cells (PBMC) from therapy-naïve HIV-1 patients and quantified infection. Results: Overall, there was no correlation between individual RF expression and HIV-1 status in total PBMC. However, we identified a T cell population with low levels of intracellular CD2 and reduced expression of SAMHD1, p21 and SerinC5. CD2 low T cells with reduced RF expression were markedly positive for HIV-1 p24. In contrast, CD2+ T cells were less infected and expressed higher levels of RFs. CD2 low T cell infection correlated with viral loads and was associated with HIV-1 disease progression. Conclusions: In untreated therapy naïve chronic HIV-1 patients, RF expression in T cells is associated with CD2 expression and seems to influence viral loads. Our study suggests that RFs help to control HIV-1 infection in certain T cells in vivo and supports the potential for RFs as promising targets for therapeutic intervention.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Hiv-1 ; In Vivo Relevance ; P21 ; Restriction Factors ; Risp ; Samhd1 ; Serinc5 ; Tetherin; Hepatitis-c Virus; In-vivo; Antiretroviral Activity; Immunodeficiency-virus; Elite Controllers; Host; Nef; Vpu; Surface; Samhd1
ISSN (print) / ISBN 1758-2652
e-ISSN 1758-2652
Quellenangaben Band: 20, Heft: 1, Seiten: , Artikelnummer: 21865 Supplement: ,
Verlag Springer
Verlagsort Berlin ; Heidelberg
Begutachtungsstatus Peer reviewed