Measles virus matrix protein inhibits host cell transcription

Xuelian Yu, Shadi Shahriari, Hongmei Li, Reena GHILDYAL

Research output: Contribution to journalArticle

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Abstract

Measles virus (MeV) is a highly contagious virus that still causes annual epidemics in developing countries despite the availability of a safe and effective vaccine. Additionally, importation from endemic countries causes frequent outbreaks in countries where it has been eliminated. The M protein of MeV plays a key role in virus assembly and cytopathogenesis; interestingly, M is localised in nucleus, cytoplasm and membranes of infected cells. We have used transient expression of M in transfected cells and in-cell transcription assays to show that only some MeV M localizes to the nucleus, in addition to cell membranes and the cytoplasm as previously described, and can inhibit cellular transcription via binding to nuclear factors. Additionally, MeV M was able to inhibit in vitro transcription in a dose-dependent manner. Importantly, a proportion of M is also localized to nucleus of MeV infected cells at early times in infection, correlating with inhibition of cellular transcription. Our data show, for the first time, that MeV M may play a role early in infection by inhibiting host cell transcription.
Original languageEnglish
Article numbere0161360
Pages (from-to)1-15
Number of pages15
JournalPLoS One
Volume11
Issue number8
DOIs
Publication statusPublished - 23 Aug 2016

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Measles virus
Transcription
Viruses
Proteins
proteins
cells
cell membranes
Cytoplasm
cytoplasm
Cell Membrane
Virus Assembly
Infection
infection
Developing Countries
Disease Outbreaks
developing countries
Cell membranes
Vaccines
Developing countries
vaccines

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Yu, Xuelian ; Shahriari, Shadi ; Li, Hongmei ; GHILDYAL, Reena. / Measles virus matrix protein inhibits host cell transcription. In: PLoS One. 2016 ; Vol. 11, No. 8. pp. 1-15.
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Measles virus matrix protein inhibits host cell transcription. / Yu, Xuelian; Shahriari, Shadi; Li, Hongmei; GHILDYAL, Reena.

In: PLoS One, Vol. 11, No. 8, e0161360, 23.08.2016, p. 1-15.

Research output: Contribution to journalArticle

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