Abstract
Reactivation of latent Gammaherpesvirus in the genital tract can lead to reproductive failure in domestic animals. Nevertheless, this pathophysiology has not received formal study in wild mammals. High prevalence of Mustelid gammaherpesvirus 1 (MusGHV-1) DNA detected in the genital tracts of European badgers (Meles meles) implies that this common pathogen may be a sexual transmitted infection. Here we used PCR to test MusGHV-1 DNA prevalence in genital swabs collected from 144 wild badgers in Ireland (71 males, 73 females) to investigate impacts on male fertility indicators (sperm abundance and testes weight) and female fecundity (current reproductive output). MusGHV-1 reactivation had a negative effect on female reproduction, but not on male fertility; however males had a higher risk of MusGHV-1 reactivation than females, especially during the late-winter mating season, and genital MusGHV-1 reactivation differed between age classes, where 3–5 year old adults had significantly lower reactivation rates than younger or older ones. Negative results in foetal tissues from MusGHV-1 positive mothers indicated that cross-placental transmission was unlikely. This study has broader implications for how wide-spread gammaherpesvirus infections could affect reproductive performance in wild Carnivora species.
Highlights
The herpesviridae comprise four subfamilies, the alphaherpesvirinae, betaherpesvirinae, gammaherpesvirinae [1], and the newly assigned deltaherpesvirinae [2], which can all maintain lifelong infection, and exhibit prolonged latency and repeated reactivation
Genital discharge was present in 74.2% (23/31) of females during spring, and 7.5% (3/40) of females and none of the males (0/40) in winter, but was not associated with MusGHV-1 reactivation
(0/40) inrates winter, but Irish was not associated with MusGHV-1 reactivation
Summary
The herpesviridae comprise four subfamilies, the alphaherpesvirinae, betaherpesvirinae, gammaherpesvirinae [1], and the newly assigned deltaherpesvirinae [2], which can all maintain lifelong infection, and exhibit prolonged latency and repeated reactivation. Stimuli associated with reactivation include physical or mental stress [7,8], trauma [9], hypoxia [10], coinfection with other pathogens [11], pregnancy [12], hormonal changes [13], and aging [14]. Reactivation from latency, during pregnancy can be serious, causing reproductive failure, including infertility, embryonic reabsorption, foetal abortion, preterm birth, stillbirth, poor neonatal condition, or neonatal death [15,16]. Direct herpesvirus-induced abortions are usually associated with viremia by primary infection or reactivation during pregnancy, leading to heavy viral loads in uterine vessels and cross-placental transmission to the foetus(es), resulting in reabsorption, abortion, or neonatal death
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