Abstract

Gammaherpesviruses (GHVs) are host specific DNA viruses that infect a large range of mammalian species. These viruses preferentially target host lymphocyte cell populations and infection may lead to morbidity or mortality in immunocompromised, co-infected, or non-adapted hosts. In this study, we tested for the presence of Lynx rufus gammaherpesvirus 1 (LruGHV1) in a northeastern United States population of wild bobcats (L. rufus). We estimated prevalence of infection and viral load in infected individuals using quantitative real-time PCR analysis of spleen DNA from 64 Vermont bobcats. We observed an overall prevalence of 64% using this methodology. Bobcat age was significantly positively associated with GHV infection status, and we noted a trend for higher viral loads in young animals, but prevalence and viral load were similar in male and female bobcats. A single LruGHV1 variant was identified from the sequencing of the viral glycoprotein B gene of Vermont bobcats. This gene sequence was 100% similar to that reported in Florida bobcats and slightly variant from other isolates identified in the Western USA. Our work suggests broad geographic distribution and high prevalence of LruGHV1 in bobcat populations across the United States with infection attributes that suggest horizontal transmission of the agent. Geographic differences in viral genotype may reflect historical migration and expansion events among bobcat populations.

Highlights

  • Herpesviruses are large, enveloped, double-stranded DNA viruses capable of both lytic and latent infection of their hosts (Speck & Ganem, 2010)

  • 64.1% of the 64 bobcats were positive for GHV via polymerase chain reaction (PCR), and infected animals were identified throughout the state of Vermont (Fig. 1)

  • We document for the first time the presence of gammaherpesvirus in a population of wild felids living in the northeast United States

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Summary

Introduction

Herpesviruses are large, enveloped, double-stranded DNA viruses capable of both lytic (i.e., productive) and latent infection of their hosts (Speck & Ganem, 2010). This ability to express true latency results in lifelong infection punctuated by episodes of reactivation and productive infection in response to environmental stimuli. GHV-associated disease is primarily observed in immunocompromised hosts as a consequence of latent infection, and to a lesser extent, reactivation of lytic infection (Ackermann, 2006; O’Toole & Li, 2014). Latent infection with GHVs, such as Epstein–Barr virus (EBV) and Karposi sarcoma-associated herpesvirus, may lead to a variety of lymphoproliferative disorders (LPDs) in individuals with impaired immunity due to HIV infection and AIDS, therapeutic immunosuppression, or congenital immunodeficiency (Cesarman, 2011, 2014)

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