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Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis.

ABSTRACT: 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 reduces 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.

SUBMITTER: Sebastiano M

PROVIDER: S-EPMC5829443 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature

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Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis.

Sebastiano Manrico M Chastel Olivier O de Thoisy Benoît B Eens Marcel M Costantini David D

Current zoology 20160317 4

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, includi ...[more]

PMID: 29491920

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Project description:Inferring from patterns observed in biomedical research, ecoimmunological theory predicts that oxidative stress is a ubiquitous physiological cost that contributes to generating variation in immune function between individuals or species. This prediction is, however, often challenged by empirical studies testing the relationship between immune response or infection and oxidative status markers. This points out the importance of combining ecological immunology and oxidative stress ecology to further our understanding of the proximate causes and fitness consequences of individual variation in health, and adaptability to natural and anthropogenic environmental changes. I reviewed evidence and performed phylogenetic meta-analyses of changes in oxidative status markers owing to either injection of an antigen or infection in captive and free-living vertebrates (141 studies, 1262 effect sizes, 97 species). The dataset was dominated by studies on fish, birds and mammals, which provided 95.8% of effect sizes. Both antigen injection and parasite exposure were associated with changes of oxidative status. There were significant effects of taxonomic class and experimental environment (captivity vs. wild). In contrast with my predictions, age category (young vs. adult), study design (correlational vs. experimental) and proxies of pace of life (clutch size, litter size, and body mass; for birds and mammals only) were negligible in this dataset. Several methodological aspects (type of immunostimulant, laboratory assay, tissue analysed) showed significant effects on both strength and direction of effect. My results suggest that alterations of oxidative status are a widespread consequence of immune function across vertebrates. However, this work also identified heterogeneity in strength and direction of effect sizes, which suggests that immune function does not necessarily result in oxidative stress. Finally, this work identifies methodological caveats that might be relevant for the interpretation and comparability of results and for the application in conservation programs.

Project description:BackgroundThe burden of herpes zoster (HZ) is significant worldwide, with millions affected and the incidence rising. Current literature has identified some risk factors for this disease; however, there is yet to be a comprehensive study that pools all evidence to provide estimates of risk. Therefore, the purpose of this study is to identify various risk factors, excluding immunosuppressive medication, that may predispose an individual to developing HZ.MethodsThe literature search was conducted in MEDLINE, EMBASE, and Cochrane Central, yielding case control, cohort, and cross-sectional studies that were pooled from January 1966 to September 2017. Search terms included the following: zoster OR herpe* OR postherpe* OR shingle* AND risk OR immunosupp* OR stress OR trauma OR gender OR ethnicity OR race OR age OR diabetes OR asthma OR chronic obstructive pulmonary disease OR diabetes. Risk ratios (RRs) for key risk factors were calculated via natural logarithms and pooled using random-effects modeling.ResultsFrom a total of 4417 identified studies, 88 were included in analysis (N = 3, 768 691 HZ cases). Immunosuppression through human immunodeficiency virus/acquired immune deficiency syndrome (RR = 3.22; 95% confidence interval [CI], 2.40-4.33) or malignancy (RR = 2.17; 95% CI, 1.86-2.53) significantly increased the risk of HZ compared with controls. Family history was also associated with a greater risk (RR = 2.48; 95% CI, 1.70-3.60), followed by physical trauma (RR = 2.01; 95% CI, 1.39-2.91) and older age (RR = 1.65; 95% CI, 1.37-1.97). A slightly smaller risk was seen those with psychological stress, females, and comorbidities such as diabetes, rheumatoid arthritis, cardiovascular diseases, renal disease, systemic lupus erythematosus, and inflammatory bowel disease compared with controls (RR range, 2.08-1.23). We found that black race had lower rates of HZ development (RR = 0.69; 95% CI, 0.56-0.85).ConclusionsThis study demonstrated a number of risk factors for development of HZ infection. However, many of these characteristics are known well in advance by the patient and clinician and may be used to guide discussions with patients for prevention by vaccination.

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Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis.

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Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis.

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