TY - JOUR
T1 - Measles virus matrix protein inhibits host cell transcription
AU - Yu, Xuelian
AU - Shahriari, Shadi
AU - Li, Hongmei
AU - GHILDYAL, Reena
N1 - Funding Information:
XYL was supported by The Shanghai Municipal Health Bureau Talents Development Foundation Grant No.:GWDTR201201.
Publisher Copyright:
© 2016 Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2016/8/23
Y1 - 2016/8/23
N2 - 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.
AB - 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.
KW - Cell Membrane/genetics
KW - Cell Nucleus/genetics
KW - Chromatin/genetics
KW - Glycoproteins/genetics
KW - Host-Pathogen Interactions/genetics
KW - Humans
KW - Measles/genetics
KW - Measles virus/genetics
KW - Protein Binding
KW - Transcription Factors/genetics
KW - Transcription, Genetic
KW - Viral Matrix Proteins/genetics
KW - Virus Assembly/genetics
UR - http://www.scopus.com/inward/record.url?scp=84984623417&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0161360
DO - 10.1371/journal.pone.0161360
M3 - Article
C2 - 27551716
SN - 1932-6203
VL - 11
SP - 1
EP - 15
JO - PLoS One
JF - PLoS One
IS - 8
M1 - e0161360
ER -