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Sulforaphane Inhibits HIV Infection of Macrophages through Nrf2
#MMPMID27093399
Furuya AK
; Sharifi HJ
; Jellinger RM
; Cristofano P
; Shi B
; de Noronha CM
PLoS Pathog
2016[Apr]; 12
(4
): e1005581
PMID27093399
show ga
Marburg virus, the Kaposi's sarcoma-associated herpesvirus (KSHV) and Dengue
virus all activate, and benefit from, expression of the transcription regulator
nuclear erythroid 2-related factor 2 (Nrf2). The impact of Nrf2 activation on
human immunodeficiency virus (HIV) infection has not been tested. Sulforaphane
(SFN), produced in cruciferous vegetables after mechanical damage, mobilizes Nrf2
to potently reprogram cellular gene expression. Here we show for the first time
that SFN blocks HIV infection in primary macrophages but not in primary T cells.
Similarly SFN blocks infection in PMA-differentiated promonocytic cell lines, but
not in other cell lines tested. siRNA-mediated depletion of Nrf2 boosted HIV
infectivity in primary macrophages and reduced the anti-viral effects of SFN
treatment. This supports a model in which anti-viral activity is mediated through
Nrf2 after it is mobilized by SFN. We further found that, like the type I
interferon-induced cellular anti-viral proteins SAMHD1 and MX2, SFN treatment
blocks infection after entry, but before formation of 2-LTR circles.
Interestingly however, neither SAMHD1 nor MX2 were upregulated. This shows for
the first time that Nrf2 action can potently block HIV infection and highlights a
novel way to trigger this inhibition.
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