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Abstract
Equine herpesvirus-1 (EHV-1) infection remains a significant problem despite the widespread use of vaccines. The inability to generate a protective immune response to EHV-1 vaccination or infection is thought to be due to immunomodulatory properties of the virus, and the ORF1 and ORF2 gene products have been hypothesized as potential candidates with immunoregulatory properties. A pony infection study was performed to define immune responses to EHV-1, and to determine if an EHV-1 ORF1/2 deletion mutant (ΔORF1/2) would have different disease and immunoregulatory effects compared to wild type EHV-1 (WT). Infection with either virus led to cytokine responses that coincided with the course of clinical disease, particularly the biphasic pyrexia, which correlates with respiratory disease and viremia, respectively. Similarly, both viruses caused suppression of proliferative T-cell responses on day 7 post infection (pi). The ΔORF1/ORF2 virus caused significantly shorter primary pyrexia and significantly reduced nasal shedding, and an attenuated decrease in PBMC IL-8 as well as increased Tbet responses compared to WT-infected ponies. In conclusion, our findings are (i) that infection of ponies with EHV-1 leads to modulation of immune responses, which are correlated with disease pathogenesis, and (ii) that the ORF1/2 genes are of importance for disease outcome and modulation of cytokine responses.
Highlights
Equine herpesvirus-1 remains one of the most common viral infections of horses causing respiratory disease, epidemic abortion, and outbreaks of equine herpes myeloencephalopathy (EHM) [1]
The sequential characterization of cytokine responses during the first seven days following infection with Ab4 wild type EHV-1 (WT) virus shows that increases in pro-inflammatory (IL-1, IFN-a, TNF-a), T-helper 1 associated (IFN-g,) and regulatory cytokines (TGF-b and IL-10) coincide with the biphasic increases in body temperature and the onset of respiratory disease and viremia respectively
Cytokine responses decreased in Ab4 WTinfected ponies, while decreases in IL-8 were attenuated in Ab4 ΔORF1/2 virus infected ponies and Tbet responses were increased compared to Ab4 WT-infected ponies and controls
Summary
Equine herpesvirus-1 remains one of the most common viral infections of horses causing respiratory disease, epidemic abortion, and outbreaks of equine herpes myeloencephalopathy (EHM) [1]. Primary infections with EHV-1 lead to establishment of latent infection within the first weeks or months of life. The two main strategies for controlling EHV-1 infection and disease are management practices and vaccination, immunity established after either infection or vaccination is short lived and incomplete [1]. While virusneutralizing (VN) antibodies play a role in reduction of nasal viral shedding [2], cytotoxic T-lymphocytes (CTLs) are most critical for protection from clinical disease, Viruses have developed an array of strategies to circumvent host immunity, and for EHV-1 it is thought that the lack of long-lasting immunity is due to immunomodulatory properties of the virus [6,7,8,9,10,11]. Strategies employed by EHV-1 include interference and modulation of NK-cell lysis, alteration of cytokine network responses that affect B- and T-cell responses, loss of efficient antigen presentation and chemoattraction of professional antigen presenting cells, antibody dependent cytotoxicity, and CTL responses [12]
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