In Vitro Exposure of Harbor Seal Immune Cells to Aroclor 1260 Alters Phocine Distemper Virus Replication

Abstract

In the last 30 years, several large-scale marine mammal mortality events have occurred, often in close association with highly polluted regions, leading to suspicions that contaminant-induced immunosuppression contributed to these epizootics. Some of these recent events also identified morbillivirus as a cause of or contributor to death. The role of contaminant exposures regarding morbillivirus mortality is still unclear. The results of this study aimed to address the potential for a mixture of polychlorinated biphenyls (PCBs), specifically Aroclor 1260, to alter harbor seal T-lymphocyte proliferation and to assess if exposure resulted in increased likelihood of phocine distemper virus (PDV USA 2006) to infect susceptible seals in an in vitro system. Exposure of peripheral blood mononuclear cells to Aroclor 1260 did not significantly alter lymphocyte proliferation (1, 5, 10, and 20 ppm). However, using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), lymphocytes exposed to 20 ppm Aroclor 1260 exhibited a significant decrease in PDV replication at day 7 and a significant increase at day 11 compared with unexposed control cells. Similar and significant differences were apparent on exposure to Aroclor 1260 in monocytes and supernatant. The results here indicate that in harbor seals, Aroclor 1260 exposure results in a decrease in virus early during infection and an increase during late infection. The consequences of this contaminant-induced infection pattern in a highly susceptible host could result in a greater potential for systemic infection with greater viral load, which could explain the correlative findings seen in wild populations exposed to a range of persistent contaminants that suffer from morbillivirus epizootics.

The initial steps toward the formation of somatic tissue banks and cell cultures derived from captive Antillean manatee (Trichechus manatus manatus) skin biopsies

“…The establishment of somatic tissue banks for different species (Borges et al, 2017; Costa et al, 2020; Lira et al, 2021), especially those threatened with extinction (Boroda et al, 2015; Praxedes et al, 2019), is important for the development of these conservation strategies for the species of interest. Moreover, specifically for marine mammals, these banks can be used for acquiring knowledge regarding the species (Yajing et al, 2018), as well as for studying the influence of fuel and its derivatives (Wise et al, 2014), the impact of chlorine derivatives (Marsili et al, 2014), the toxicity of heavy metals (Wise et al, 2015), and performing immunological and physiological studies (Bogomolni et al, 2016). Moreover, development of primary cell cultures represents an interesting tool for elucidating the molecular etiology of physiological modifications, a step in accelerating genome‐to‐phenome studies (Lam et al, 2020).…”

California sea lion (Zalophus californianus) lymph-node explant reveals involvement and possible transcriptional regulation of SLAM and nectin-4 during phocine distemper virus infection

“…In vitro methods to study the PDV pathogenesis have mainly used stable and transformed Vero and CHO cell lines; 27,45 however, those cells have limitations since they were originally obtained from species other than pinnipeds. Experiments investigating replication of PDV in culture have used gray seal and harbor seal peripheral-blood mononuclear cells 6,7 and primary seal kidney cells. 31 Although, both types of cell lines are from pinnipeds, they also have some limitations.…”

Environmental toxicity influences disease spread in consumer population

“…This may be a result of toxin-induced immunity suppression which is ubiquitous in many epidemic scenarios (Coors and De Meester, 2008) and well demonstrated in plenty of experimental studies (de Swart et al, 1994;De Swart et al, 1996;Ross et al, 1996;Bogomolni et al, 2016). Especially, aquatic species and more specifically many marine mammals are known to be vulnerable to immuno-toxic contaminants (Ross, 2000(Ross, , 2002de Swart et al, 1994;De Swart et al, 1996;Ross et al, 1996;Bogomolni et al, 2016). For instance, harbor seals would be less immune if they fed on fish from the more polluted Baltic Sea and less susceptible in case their predation is associated with the less polluted Atlantic sea (Ross et al, 1996;de Swart et al, 1994).…”

“…However, high environmental toxin may also lead to increased susceptibility of the host to disease (Coors and De Meester, 2008;Beck and Levander, 2000). This may be a result of toxin-induced immunity suppression which is ubiquitous in many epidemic scenarios (Coors and De Meester, 2008) and well demonstrated in plenty of experimental studies (de Swart et al, 1994;De Swart et al, 1996;Ross et al, 1996;Bogomolni et al, 2016). Especially, aquatic species and more specifically many marine mammals are known to be vulnerable to immuno-toxic contaminants (Ross, 2000(Ross, , 2002de Swart et al, 1994;De Swart et al, 1996;Ross et al, 1996;Bogomolni et al, 2016).…”