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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Retrovirology
2016 ; 13
(1
): 63
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Impact of APOL1 polymorphism and IL-1? priming in the entry and persistence of
HIV-1 in human podocytes
#MMPMID27599995
Mikulak J
; Oriolo F
; Portale F
; Tentorio P
; Lan X
; Saleem MA
; Skorecki K
; Singhal PC
; Mavilio D
Retrovirology
2016[Sep]; 13
(1
): 63
PMID27599995
show ga
BACKGROUND: Patients of African ancestry with untreated HIV-1 infection and
carrying the G1 or G2 kidney disease risk variants (Vs) at the APOL1 gene have a
tenfold higher risk of developing HIV-associated nephropathy (HIVAN) compared to
those with the non-risk wild type (WT) G0 variant. However, the mechanistic
contribution of the APOL1 allelic state to kidney injury in HIV-1 infection
remains to be elucidated. RESULTS: Non-risk WT APOL1 is associated with lower
intracellular levels of HIV-1 in conditionally immortalized human podocytes,
while the over expression of G1 or G2 risk Vs significantly increases viral
accumulation. The priming of podocytes with exogenous IL-1? facilitates HIV-1
entry, via the up-regulation of DC-SIGN. The over expression of APOL1 G1 and G2
risk Vs in combination with an increase in IL-1? levels causes a greater increase
in viral concentration than either condition alone. In turn, HIV-1 and exogenous
IL-1? together induce a de novo secretion of endogenous IL-1? and an increase of
APOL1 gene expression. CONCLUSIONS: Our findings indicate that the presence of
risk Vs of APOL1 is permissive of HIV-1 persistence in human podocytes in synergy
with IL-1?, a cytokine that characterizes the inflammatory milieu of acute and
chronic phases of HIV-1 infection. The elucidation of these molecular mechanisms
explains, at least in part, the higher frequency of HIVAN in populations carrying
the risk polymorphic genetic variant of APOL1 gene.
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