IMR Press / FBL / Volume 9 / Issue 3 / DOI: 10.2741/1320

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

The involvement of oxidative stress in bovine herpesvirus type 4-mediated apoptosis
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1 Department of Pathology and Animal Health and Department of Structures, Functions and Biological Technologies - School of Veterinary Medicine – University of Naples “Federico II” , Naples, Italy
2 Sbarro Institute for Cancer Reseaerch and Molecular Medicine, College of Science and Technology, Temple University, Philedelphia, Pennsylvania
3 Department of Experimental Pharmacology – School of Pharmacy - University of Naples “Federico II” , Naples, Italy
Academic Editor:Antonio Giordano
Front. Biosci. (Landmark Ed) 2004, 9(3), 2106–2114;
Published: 1 September 2004
(This article belongs to the Special Issue Gene targets for modulating cell growth)

Bovine herpesvirus type 4 (BHV-4) belongs to the gamma-2-herpesviruses of the Gammaherpesvirinae subfamily. BHV-4 has a worldwide distribution and has been isolated in a variety of clinical diseases as well as from healthy cattle. In this report we demonstrate that BHV-4 induces apoptosis in MDBK cells. In the early phases of apoptosis, cells show an increase in the intracellular level of reactive oxygen species, which is indicative of oxidative stress. This precedes DNA fragmentation, a hallmark typical of apoptosis. Cells were protected from apoptosis only by certain antioxidants (butylated hydroxyanisole and ebselen), whereas N-acetylcysteine turned out to be ineffective. Antioxidants that protected cells from apoptosis prevented oxidative stress but failed to block virus growth. These observations suggest that oxidative stress may be a crucial event in the sequence leading to apoptotic cell death but apoptosis is not required for the multiplication of BHV-4.

Herpes virus
Cell death
Reactive oxygen species
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