U.S. flag

An official website of the United States government

Dot gov

Official websites use .gov
A .gov website belongs to an official government organization in the United States.


Secure .gov websites use HTTPS
A lock ( ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites.


Main content area

Saxitoxin increases phocine distemper virus replication upon in-vitro infection in harbor seal immune cells

Andrea L. Bogomolni, Anna L. Bass, Spencer Fire, Lindsay Jasperse, Milton Levin, Ole Nielsen, Gordon Waring, Sylvain De Guise
Harmful algae 2016 v.51 pp. 89-96
algal blooms, infectious diseases, dolphins, neurotoxicity, T-lymphocytes, algae, seals, Phoca vitulina, Phocine morbillivirus, viruses, immunotoxicity, virus replication, lymphocyte proliferation, mortality, Northeastern United States
Several marine mammal epizootics have been closely linked to infectious diseases, as well as to the biotoxins produced by harmful algal blooms (HABs). In two of three saxitoxin (STX) associated mortality events, dolphin morbillivirus (DMV) or phocine distemper virus (PDV) was isolated in affected individuals. While STX is notorious for its neurotoxicity, immunotoxic effects have also been described. This study investigated the role of STX in altering immune function, specifically T lymphocyte proliferation, in harbor seals (Phoca vitulina concolor) upon in-vitro exposure. In addition, the study also examined whether exposure to STX could alter the susceptibility of harbor seal immune cells to PDV infection upon in-vitro exposure. STX caused an increase in harbor seal lymphocyte proliferation at 10ppb and exposure to STX significantly increased the amount of virus present in lymphocytes. These results suggest that low levels of STX within the range of those reported in northeast U.S. seals may affect the likelihood of systemic PDV infection upon in-vivo exposure in susceptible seals. Given the concurrent increase in morbillivirus epizootics and HAB events in the last 25 years, the relationship between low level toxin exposure and host susceptibility to morbillivirus needs to be further explored.