Gerald McInerney Group
Regulation of Gene Expression during Viral Infection
All viruses, regardless of their host tropism, genome structure or any other properties, must use components of the host cell gene expression machinery in order to propagate. This reliance has led to the development of an evolutionary arms-race between viruses and hosts. Viral strategies have evolved to ensure access to this machinery while host cells have developed means to recognize viruses as foreign entities and to restrict their expression. In turn, viruses have developed methods to counteract these restrictions and to reduce the cells ability to communicate with its neighbouring cells. Our work concerns the mechanisms of regulation of gene expression during the early stages of viral infections. Using Semliki Forest virus as a model, we are studying viral interactions with diverse cellular pathways and systems including the translation machinery, the type I interferon system and protein degradation systems.
Read more about our group activities at alphavirus.org
Group Members
| Paula Eiben | Associated | ||
 | Benjamin Götte | PhD student, Graduate Student | |
 | Leo Hanke | Associated | |
 | Lifeng Liu | PhD student, Graduate Student | |
 | Gerald McInerney | Senior researcher | |
 | Ainhoa Moliner Morro | PhD student, Graduate Student | |
 | Marc Panas | Associated | |
| Hendrik Reuper | Associated |
Former Group Members
Post Doc Bastian Thaa
Post Doc Roberta Biasiotto
PhD Student Kai Eng
Post Doc Thomas Kuri
Selected Publications
Alphavirus-induced hyperactivation of PI3K/AKT directs pro-viral metabolic changes.
PLoS Pathog. 2018 01;14(1):e1006835
A Link Between a Common Mutation in CFTR and Impaired Innate and Adaptive Viral Defense.
J. Infect. Dis. 2017 Dec;216(10):1308-1317
The Antiviral Alkaloid Berberine Reduces Chikungunya Virus-Induced Mitogen-Activated Protein Kinase Signaling.
J. Virol. 2016 Nov;90(21):9743-9757
Combined structural, biochemical and cellular evidence demonstrates that both FGDF motifs in alphavirus nsP3 are required for efficient replication.
Open Biol 2016 Jul;6(7):
G3BP-Caprin1-USP10 complexes mediate stress granule condensation and associate with 40S subunits.
J. Cell Biol. 2016 Mar;212(7):845-60
Differential Phosphatidylinositol-3-Kinase-Akt-mTOR Activation by Semliki Forest and Chikungunya Viruses Is Dependent on nsP3 and Connected to Replication Complex Internalization.
J. Virol. 2015 Nov;89(22):11420-37
FGDF motif regulation of stress granule formation.
DNA Cell Biol. 2015 Sep;34(9):557-60
Methods for the characterization of stress granules in virus infected cells.
Methods 2015 Nov;90():57-64
Viral and cellular proteins containing FGDF motifs bind G3BP to block stress granule formation.
PLoS Pathog. 2015 Feb;11(2):e1004659
Real-time resolution of point mutations that cause phenovariance in mice.
Proc. Natl. Acad. Sci. U.S.A. 2015 Feb;112(5):E440-9
The host nonsense-mediated mRNA decay pathway restricts Mammalian RNA virus replication.
Cell Host Microbe 2014 Sep;16(3):403-11
The C-terminal repeat domains of nsP3 from the Old World alphaviruses bind directly to G3BP.
J. Virol. 2014 May;88(10):5888-93
Sequestration of G3BP coupled with efficient translation inhibits stress granules in Semliki Forest virus infection.
Mol. Biol. Cell 2012 Dec;23(24):4701-12
Accumulation of autophagosomes in Semliki Forest virus-infected cells is dependent on expression of the viral glycoproteins.
J. Virol. 2012 May;86(10):5674-85
A novel quantitative flow cytometry-based assay for autophagy.
Autophagy 2010 Jul;6(5):634-41
Semliki Forest virus nonstructural protein 2 is involved in suppression of the type I interferon response.
J. Virol. 2007 Aug;81(16):8677-84
Semliki Forest virus nonstructural protein 2 is involved in suppression of the type I interferon response.
J. Virol. 2007 Aug;81(16):8677-84
Importance of eIF2alpha phosphorylation and stress granule assembly in alphavirus translation regulation.
Mol. Biol. Cell 2005 Aug;16(8):3753-63
Further Publications
Further Publications on PubMed