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@ARTICLE{Dupr:634624,
author = {Dupré, Juliette and Dolata, Katarzyna Magdalena and Pei,
Gang and Molouki, Aidin and Goatley, Lynnette C. and
Küchler, Richard and Soh, Timothy K. and Bosse, Jens
Bernhard and Fablet, Aurore and Le Dimna, Mireille and
Karadjian, Grégory and Hirchaud, Edouard and Netherton,
Christopher L. and Dixon, Linda K. and Reis, Ana Luisa and
Vitour, Damien and Le Potier, Marie-Frédérique and Karger,
Axel and Caignard, Grégory},
title = {{E}xploring virus-host interactions through combined
proteomic approaches identifies {BANF}1 as a new essential
factor for {A}frican {S}wine {F}ever {V}irus},
journal = {Molecular $\&$ cellular proteomics},
volume = {24},
number = {9},
issn = {1535-9476},
address = {Bethesda, Md.},
publisher = {The American Society for Biochemistry and Molecular
Biology},
reportid = {PUBDB-2025-02538},
pages = {101038},
year = {2025},
abstract = {African swine fever virus (ASFV) causes a lethal disease in
pigs and represents a significant threat to the global pork
industry due to the lack of effective vaccines or
treatments. Despite intensive research, many ASFV proteins
remain uncharacterized. This study aimed to elucidate the
functions of two ASFV proteins, pMGF360-21R and pA151R,
through comprehensive analysis of their interactions with
host proteins. Using affinity purification-mass spectrometry
and yeast two-hybrid screening approaches, we identified the
host protein barrier-to-autointegration factor 1 (BANF1) as
a key interactor of both viral proteins. Biochemical and
colocalization assays confirmed these interactions and
demonstrated that MGF360-21R and A151R expression leads to
cytoplasmic relocation of BANF1. Functionally, BANF1
silencing significantly reduced ASFV replication, indicating
its proviral role. Given BANF1's established function in
regulating the cGAS/STING-dependent type I interferon
(IFN-I) response, we postulated that A151R and MGF360-21R
could inhibit this pathway. Using different strategies, we
showed that both A151R and MGF360-21R did indeed inhibit
IFN-I induction. Generation of ASFV deficient of A151R or
MGF360-21R showed that both mutant viruses enhanced the host
IFN response in primary porcine macrophages compared to
wild-type virus. However, their capacity to inhibit this
pathway could occur through mechanisms independent of BANF1.
Proteomic analysis of BANF1 interactors during ASFV
infection highlighted potentially roles in chromatin
remodeling, nuclear transport, and innate immune response
pathways. Altogether, our data provide new insights into
ASFV-host interactions, identifying BANF1 as an important
new host factor required for replication and uncovering
novel functions for A151R and MGF360-21R.},
cin = {CSSB-MHH-JB},
ddc = {610},
cid = {I:(DE-H253)CSSB-MHH-JB-20210520},
pnm = {899 - ohne Topic (POF4-899) / DFG project
G:(GEPRIS)390874280 - EXC 2155: RESIST - Resolving Infection
Susceptibility (390874280) / GRK 2771 - GRK 2771: Mensch und
Mikrobe: Reorganisation von Zellkompartimenten und
Molekülkomplexen während der Infektion (453548970) / ICRAD
- INTERNATIONAL COORDINATION OF RESEARCH ON INFECTIOUS
ANIMAL DISEASES (862605)},
pid = {G:(DE-HGF)POF4-899 / G:(GEPRIS)390874280 /
G:(GEPRIS)453548970 / G:(EU-Grant)862605},
experiment = {EXP:(DE-MLZ)NOSPEC-20140101},
typ = {PUB:(DE-HGF)16},
doi = {10.1016/j.mcpro.2025.101038},
url = {https://bib-pubdb1.desy.de/record/634624},
}