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2017 ; 91
(11
): ä Nephropedia Template TP
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Hili Inhibits HIV Replication in Activated T Cells
#MMPMID28331090
Peterlin BM
; Liu P
; Wang X
; Cary D
; Shao W
; Leoz M
; Hong T
; Pan T
; Fujinaga K
J Virol
2017[Jun]; 91
(11
): ä PMID28331090
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P-element-induced wimpy-like (Piwil) proteins restrict the replication of mobile
genetic elements in the germ line. They are also expressed in many transformed
cell lines. In this study, we discovered that the human Piwil 2 (Hili) protein
can also inhibit HIV replication, especially in activated CD4(+) T cells that are
the preferred target cells for this virus in the infected host. Although resting
cells did not express Hili, its expression was rapidly induced following T cell
activation. In these cells and transformed cell lines, depletion of Hili
increased levels of viral proteins and new viral particles. Further studies
revealed that Hili binds to tRNA. Some of the tRNAs represent rare tRNA species,
whose codons are overrepresented in the viral genome. Targeting tRNA(Arg)(UCU)
with an antisense oligonucleotide replicated effects of Hili and also inhibited
HIV replication. Finally, Hili also inhibited the retrotransposition of the
endogenous intracysternal A particle (IAP) by a similar mechanism. Thus, Hili
joins a list of host proteins that inhibit the replication of HIV and other
mobile genetic elements.IMPORTANCE Piwil proteins inhibit the movement of mobile
genetic elements in the germ line. In their absence, sperm does not form and male
mice are sterile. This inhibition is thought to occur via small Piwi-interacting
RNAs (piRNAs). However, in some species and in human somatic cells, Piwil
proteins bind primarily to tRNA. In this report, we demonstrate that human Piwil
proteins, especially Hili, not only bind to select tRNA species, including rare
tRNAs, but also inhibit HIV replication. Importantly, T cell activation induces
the expression of Hili in CD4(+) T cells. Since Hili also inhibited the movement
of an endogenous retrovirus (IAP), our finding shed new light on this
intracellular resistance to exogenous and endogenous retroviruses as well as
other mobile genetic elements.
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