Insights on Immune Function in Free-Ranging Green Sea Turtles (Chelonia mydas) with and without Fibropapillomatosis

Abstract

Chelonid alphaherpesviruses 5 and 6 (ChHV5 and ChHV6) are viruses that affect wild sea turtle populations. ChHV5 is associated with the neoplastic disease fibropapillomatosis (FP), which affects green turtles (Chelonia mydas) in panzootic proportions. ChHV6 infection is associated with lung-eye-trachea disease (LETD), which has only been observed in maricultured sea turtles, although antibodies to ChHV6 have been detected in free-ranging turtles. To better understand herpesvirus prevalence and host immunity in various green turtle foraging aggregations in Florida, USA, our objectives were to compare measures of innate and adaptive immune function in relation to (1) FP tumor presence and severity, and (2) ChHV5 and ChHV6 infection status. Free-ranging, juvenile green turtles (N = 45) were captured and examined for external FP tumors in Florida’s Big Bend, Indian River Lagoon, and Lake Worth Lagoon. Blood samples were collected upon capture and analyzed for ChHV5 and ChHV6 DNA, antibodies to ChHV5 and ChHV6, in vitro lymphocyte proliferation using a T-cell mitogen (concanavalin A), and natural killer cell activity. Despite an overall high FP prevalence (56%), ChHV5 DNA was only observed in one individual, whereas 20% of turtles tested positive for antibodies to ChHV5. ChHV6 DNA was not observed in any animals and only one turtle tested positive for ChHV6 antibodies. T-cell proliferation was not significantly related to FP presence, tumor burden, or ChHV5 seroprevalence; however, lymphocyte proliferation in response to concanavalin A was decreased in turtles with severe FP (N = 3). Lastly, green turtles with FP (N = 9) had significantly lower natural killer cell activity compared to FP-free turtles (N = 5). These results increase our understanding of immune system effects related to FP and provide evidence that immunosuppression occurs after the onset of FP disease.

First Evidence of Chelonid Herpesvirus 5 (ChHV5) Infection in Green Turtles (Chelonia mydas) from Sabah, Borneo

“…It was also documented that the viral particle could survive in the ocean for a short period of time before the virus capsid protein degrades [1]. Environment co-factors such as water temperature and habitat degradation have been suggested to play a role in FP pathogenesis [34,35]. Similarly, viral latency, viral load thresholds, and other ecological factors contribute in the tumour expression [30,35].…”

“…Environment co-factors such as water temperature and habitat degradation have been suggested to play a role in FP pathogenesis [34,35]. Similarly, viral latency, viral load thresholds, and other ecological factors contribute in the tumour expression [30,35].…”

Adaptive evolution of major histocompatibility complex class I immune genes and disease associations in coastal juvenile sea turtles

“…FP consequences range from complete tumour regression and recovery to turtle mortality [35,36]. Immunosuppression is associated with FP [37] and may develop after FP onset [26,38,39]. While the prevalence of FP in coastal habitats has led to speculation that environmental cofactors such as chemical pollutants and degraded environmental quality contribute to disease development [40,41], their precise role in FP aetiology remains uncertain.…”

“…While the prevalence of FP in coastal habitats has led to speculation that environmental cofactors such as chemical pollutants and degraded environmental quality contribute to disease development [40,41], their precise role in FP aetiology remains uncertain. The interplay of FP, environmental change, pathogens and host immune defences has remained largely uncharacterized until recently, with studies indicating reduced or altered immune function in turtles with FP [39] and in turtles in degraded habitat [42], as well as differential immune expression in FP-afflicted Ch. mydas [43–46].…”

Sea Turtles in the Cancer Risk Landscape: A Global Meta-Analysis of Fibropapillomatosis Prevalence and Associated Risk Factors

“…Fibropapillomatosis tumors range in size from 0.1 cm to greater than 30 cm in diameter [24]. These tumors debilitate the host by impeding movement and foraging ability, and reducing host immune function, while consuming energetic resources [33,34]. These tumors can be concomitant to other parasitic infections (i.e., trematodes [28]), but also become secondary infection sites for other parasitic species (i.e., bacterial infections, [35]).…”