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Prevention of tumor formation by latent gammaherpesvirus infection.

PLoS ONE 10:e0145678 (2015)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Recent reports suggested that chronic herpesvirus infection, as a constituent of the so-called virome, may not only exert harmful effects but may also be beneficial to the host, for example mediating increased resistance to secondary infections or to tumors. To further challenge this concept, specifically regarding increased resistance to tumors, we infected chimeric HLA-DR4-H2-E (DR4) mice, a mouse strain which spontaneously develops hematological tumors, with the rodent herpesvirus murine gammaherpesvirus 68 (MHV-68). Using this model, we observed that infection with wildtype MHV-68 completely prevented tumor formation. This happened, however, at the cost of hyposplenism. In contrast to wildtype infection, infection with a latency-deficient mutant of MHV-68 neither prevented tumor formation nor induced hyposplenism. The underlying mechanisms are not known but might be related to an infection-mediated priming of the immune response, resulting in the suppression of a tumor promoting endogenous retrovirus. Thus, under certain circumstances, chronic herpesvirus infection may prevent the development of tumors.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2015
HGF-Berichtsjahr 2015
ISSN (print) / ISBN 1932-6203
Zeitschrift PLoS ONE
Quellenangaben Band: 10, Heft: 12, Seiten: , Artikelnummer: e0145678 Supplement: ,
Verlag Public Library of Science (PLoS)
Verlagsort Lawrence, Kan.
Begutachtungsstatus Peer reviewed
POF Topic(s) 30203 - Molecular Targets and Therapies
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-501500-006
G-501790-001
PubMed ID 26714031
Scopus ID 84958225164
Erfassungsdatum 2015-12-31