TY  - JOUR
A1  - Goettsch, Winfried
A1  - Beerenwinkel, Niko
A1  - Deng, Li
A1  - Dölken, Lars
A1  - Dutilh, Bas E.
A1  - Erhard, Florian
A1  - Kaderali, Lars
A1  - Kleist, Max von
A1  - Marquet, Roland
A1  - Matthijnssens, Jelle
A1  - McCallin, Shawna
A1  - McMahon, Dino
A1  - Rattei, Thomas
A1  - Van Rij, Ronald P.
A1  - Robertson, David L.
A1  - Schwemmle, Martin
A1  - Stern-Ginossar, Noam
A1  - Marz, Manja
T1  - ITN—VIROINF: Understanding (harmful) virus-host interactions by linking virology and bioinformatics
JF  - Viruses
N2  - Many recent studies highlight the fundamental importance of viruses. Besides their important role as human and animal pathogens, their beneficial, commensal or harmful functions are poorly understood. By developing and applying tailored bioinformatical tools in important virological models, the Marie Skłodowska-Curie Initiative International Training Network VIROINF will provide a better understanding of viruses and the interaction with their hosts. This will open the door to validate methods of improving viral growth, morphogenesis and development, as well as to control strategies against unwanted microorganisms. The key feature of VIROINF is its interdisciplinary nature, which brings together virologists and bioinformaticians to achieve common goals.
KW  - bioinformatic
KW  - virus
KW  - virology
KW  - virus host interaction
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-236687
SN  - 1999-4915
VL  - 13
IS  - 5
ER  - 
TY  - JOUR
A1  - Libre, Camille
A1  - Seissler, Tanja
A1  - Guerrero, Santiago
A1  - Batisse, Julien
A1  - Verriez, Cédric
A1  - Stupfler, Benjamin
A1  - Gilmer, Orian
A1  - Cabrera-Rodriguez, Romina
A1  - Weber, Melanie M.
A1  - Valenzuela-Fernandez, Agustin
A1  - Cimarelli, Andrea
A1  - Etienne, Lucie
A1  - Marquet, Roland
A1  - Paillart, Jean-Christophe
T1  - A conserved uORF regulates APOBEC3G translation and is targeted by HIV-1 Vif protein to repress the antiviral factor
JF  - Biomedicines
N2  - The HIV-1 Vif protein is essential for viral fitness and pathogenicity. Vif decreases expression of cellular restriction factors APOBEC3G (A3G), A3F, A3D and A3H, which inhibit HIV-1 replication by inducing hypermutation during reverse transcription. Vif counteracts A3G at several levels (transcription, translation, and protein degradation) that altogether reduce the levels of A3G in cells and prevent its incorporation into viral particles. How Vif affects A3G translation remains unclear. Here, we uncovered the importance of a short conserved uORF (upstream ORF) located within two critical stem-loop structures of the 5′ untranslated region (5′-UTR) of A3G mRNA for this process. A3G translation occurs through a combination of leaky scanning and translation re-initiation and the presence of an intact uORF decreases the extent of global A3G translation under normal conditions. Interestingly, the uORF is also absolutely required for Vif-mediated translation inhibition and redirection of A3G mRNA into stress granules. Overall, we discovered that A3G translation is regulated by a small uORF conserved in the human population and that Vif uses this specific feature to repress its translation.
KW  - HIV-1
KW  - APOBEC3G
KW  - Vif
KW  - mRNA
KW  - translation
KW  - uORF
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-252147
SN  - 2227-9059
VL  - 10
IS  - 1
ER  -