<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gong, Meijiao</style></author><author><style face="normal" font="default" size="100%">Myster, Françoise</style></author><author><style face="normal" font="default" size="100%">Azouz, Abdulkader</style></author><author><style face="normal" font="default" size="100%">Guillem Sanchez Sanchez</style></author><author><style face="normal" font="default" size="100%">Shifang Li</style></author><author><style face="normal" font="default" size="100%">Benoit Charloteaux</style></author><author><style face="normal" font="default" size="100%">Yang, Bin</style></author><author><style face="normal" font="default" size="100%">Jenna Nichols</style></author><author><style face="normal" font="default" size="100%">Lucas Lefevre</style></author><author><style face="normal" font="default" size="100%">Javaux, Justine</style></author><author><style face="normal" font="default" size="100%">Sylvain Leemans</style></author><author><style face="normal" font="default" size="100%">Olivier Nivelles</style></author><author><style face="normal" font="default" size="100%">Willem Van Campe</style></author><author><style face="normal" font="default" size="100%">S. Roels</style></author><author><style face="normal" font="default" size="100%">Laurent Mostin</style></author><author><style face="normal" font="default" size="100%">Thierry van den Berg</style></author><author><style face="normal" font="default" size="100%">Davison, Andrew J</style></author><author><style face="normal" font="default" size="100%">Gillet, Laurent</style></author><author><style face="normal" font="default" size="100%">Timothy Connelley</style></author><author><style face="normal" font="default" size="100%">David Vermijlen</style></author><author><style face="normal" font="default" size="100%">Stanislas Goriely</style></author><author><style face="normal" font="default" size="100%">Vanderplasschen, Alain</style></author><author><style face="normal" font="default" size="100%">Dewals, Benjamin G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Unraveling clonal CD8 T cell expansion and identification of essential factors in γ-herpesvirus-induced lymphomagenesis.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cattle</style></keyword><keyword><style  face="normal" font="default" size="100%">CD8-Positive T-Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Gammaherpesvirinae</style></keyword><keyword><style  face="normal" font="default" size="100%">Herpesviridae Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Malignant Catarrh</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2024 Aug 06</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">121</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Alcelaphine gammaherpesvirus 1 (AlHV-1) asymptomatically persists in its natural host, the wildebeest. However, cross-species transmission to cattle results in the induction of an acute and lethal peripheral T cell lymphoma-like disease (PTCL), named malignant catarrhal fever (MCF). Our previous findings demonstrated an essential role for viral genome maintenance in infected CD8 T lymphocytes but the exact mechanism(s) leading to lymphoproliferation and MCF remained unknown. To decipher how AlHV-1 dysregulates T lymphocytes, we first examined the global phenotypic changes in circulating CD8 T cells after experimental infection of calves. T cell receptor repertoire together with transcriptomics and epigenomics analyses demonstrated an oligoclonal expansion of infected CD8 T cells displaying effector and exhaustion gene signatures, including GZMA, GNLY, PD-1, and TOX2 expression. Then, among viral genes expressed in infected CD8 T cells, we uncovered A10 that encodes a transmembrane signaling protein displaying multiple tyrosine residues, with predicted ITAM and SH3 motifs. Impaired A10 expression did not affect AlHV-1 replication in vitro but rendered AlHV-1 unable to induce MCF. Furthermore, A10 was phosphorylated in T lymphocytes in vitro and affected T cell signaling. Finally, while AlHV-1 mutants expressing mutated forms of A10 devoid of ITAM or SH3 motifs (or both) were able to induce MCF, a recombinant virus expressing a mutated form of A10 unable to phosphorylate its tyrosine residues resulted in the lack of MCF and protected against a wild-type virus challenge. Thus, we could characterize the nature of this γ-herpesvirus-induced PTCL-like disease and identify an essential mechanism explaining its development.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">32</style></issue></record></records></xml>