8 research outputs found

    Splitting ‘intervocalic’: Expanding the typology of lenition environments

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    The basic types of lenition environments (‘initial’, ‘intervocalic’, ‘final’) need to be separately evaluated as they differ along parameters like word position (e.g., pre-consonantal vs. final codas) or stress relations. This paper argues that we need to recognise an additional such parameter: the length of the vowel preceding an intervocalic consonant. We show that a number of phenomena from varieties of English and German show lenition patterns which draw a distinction between reflexes found in post-short (vc) and post-long (vvc) environments. The theoretical consequence of our observations is that phonological theory needs to be able to account for the post-short vs. post-long distinction in the form of a parametrically-determined representational difference

    SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx

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    International audienceThe primate lentivirus auxiliary protein Vpx counteracts an unknown restriction factor that renders human dendritic and myeloid cells largely refractory to HIV-1 infection. Here we identify SAMHD1 as this restriction factor. SAMHD1 is a protein involved in Aicardi-GoutiĂšres syndrome, a genetic encephalopathy with symptoms mimicking congenital viral infection, that has been proposed to act as a negative regulator of the interferon response. We show that Vpx induces proteasomal degradation of SAMHD1. Silencing of SAMHD1 in non-permissive cell lines alleviates HIV-1 restriction and is associated with a significant accumulation of viral DNA in infected cells. Concurrently, overexpression of SAMHD1 in sensitive cells inhibits HIV-1 infection. The putative phosphohydrolase activity of SAMHD1 is probably required for HIV-1 restriction. Vpx-mediated relief of restriction is abolished in SAMHD1-negative cells. Finally, silencing of SAMHD1 markedly increases the susceptibility of monocytic-derived dendritic cells to infection. Our results demonstrate that SAMHD1 is an antiretroviral protein expressed in cells of the myeloid lineage that inhibits an early step of the viral life cycle
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