Physiological costs of infection: herpesvirus replication is linked to blood oxidative stress in equids

Sci Rep. 2018 Jul 9;8(1):10347. doi: 10.1038/s41598-018-28688-0.

Abstract

Viruses may have a dramatic impact on the health of their animal hosts. The patho-physiological mechanisms underlying viral infections in animals are, however, not well understood. It is increasingly recognized that oxidative stress may be a major physiological cost of viral infections. Here we compare three blood-based markers of oxidative status in herpes positive and negative individuals of the domestic horse (Equus ferus caballus) and of both captive and free-ranging Mongolian khulan (Equus hemionus hemionus) and plains zebra (Equus quagga). Herpes positive free-ranging animals had significantly more protein oxidative damage and lower glutathione peroxidase (antioxidant enzyme) than negative ones, providing correlative support for a link between oxidative stress and herpesvirus infection in free-living equids. Conversely, we found weak evidence for oxidative stress in herpes positive captive animals. Hence our work indicates that environment (captive versus free living) might affect the physiological response of equids to herpesvirus infection. The Mongolian khulan and the plains zebra are currently classified as near threatened by the International Union for Conservation of Nature. Thus, understanding health impacts of pathogens on these species is critical to maintaining viable captive and wild populations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DNA, Viral / genetics
  • DNA, Viral / metabolism
  • Equidae
  • Female
  • Glutathione Peroxidase / metabolism
  • Herpesviridae / genetics
  • Herpesviridae / isolation & purification
  • Herpesviridae / physiology*
  • Herpesviridae Infections / pathology*
  • Herpesviridae Infections / veterinary
  • Herpesviridae Infections / virology
  • Horses
  • Least-Squares Analysis
  • Male
  • Oxidative Stress*
  • Protein Carbonylation
  • Species Specificity
  • Virus Replication*

Substances

  • DNA, Viral
  • Glutathione Peroxidase