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Correspondence to Thomas J. Hope: thope{at}northwestern.edu
TRIM5 proteins constitute a class of restriction factors that prevent host cell infection by retroviruses from different species. TRIM5
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restricts retroviral infection early after viral entry, before the generation of viral reverse transcription products. However, the underlying restriction mechanism remains unclear. In this study, we show that during rhesus macaque TRIM5
(rhTRIM5
)–mediated restriction of HIV-1 infection, cytoplasmic HIV-1 viral complexes can associate with concentrations of TRIM5
protein termed cytoplasmic bodies. We observe a dynamic interaction between rhTRIM5
and cytoplasmic HIV-1 viral complexes, including the de novo formation of rhTRIM5
cytoplasmic body–like structures around viral complexes. We observe that proteasome inhibition allows HIV-1 to remain stably sequestered into large rhTRIM5
cytoplasmic bodies, preventing the clearance of HIV-1 viral complexes from the cytoplasm and revealing an intermediate in the restriction process. Furthermore, we can measure no loss of capsid protein from viral complexes arrested at this intermediate step in restriction, suggesting that any rhTRIM5
-mediated loss of capsid protein requires proteasome activity.
, rhesus macaque TRIM5
; RT, reverse transcription; VSV-G, vesicular stomatitis virus G. ![]()
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J. Cell Biol. 2008 180: 444.
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