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作 者:Manrico SEBASTIANO Olivier CHASTEL Benoit DE THOBY Marcel EENS David COSTANTINI
机构地区:[1]Behavioural Ecology and Ecophysiology Group, Department of Biology, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Belgium [2]Centre d'Etudes Biologiques de Chize (CEBC), UMR7372 - Centre National de la Recherche Scientifique/Universit La Rochelle [3]Laboratory of Virus-Host Interactions. Institut Pasteur de la Guyane, French Guiana, France [4]Institute of Biodiversity, Animal Health & Comparative Medicine (IBAHCM), University of Glasgow, Glasgow, UK
出 处:《Current Zoology》2016年第4期325-332,共8页动物学报(英文版)
摘 要:Herpes viruses are responsible for a variety of pathological effects in humans and in both wild and domestic animals. One mechanism that has been proposed to facilitate replication and activity of herpes viruses is oxidative stress (OS). We used meta-analytical techniques to test the hypotheses that (1) herpes virus infection causes OS and (2) supplementation of antioxidants reduces virus load, indicating that replication is favoured by a state of OS. Results based on studies on mammals, including humans, and birds show that (1) OS is indeed increased by herpes virus infection across multiple tissues and species, (2) biomarkers of OS may change differently between tissues, and (3) the effect size does not differ among different virus strains. In addition, the increase of oxidative damage in blood (tissue commonly available in ecological studies) was similar to that in the tissues most sensitive to the herpes virus. Our results also show that administration of antioxidants re- duces virus yield, indicating that a condition of OS is favorable for the viral replication. In addition, some antioxidants may be more efficient than others in reducing herpes virus yield. Our results point to a potential mechanism linking herpes virus infection to individual health status.
关 键 词:ANTIOXIDANTS herpes virus infection immune response interaction host-pathogen oxidative stress.
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