Densovirus associated with sea-star wasting disease and mass mortality
- aDepartment of Microbiology, Cornell University, Ithaca, NY 14853;
- bDepartment of Biology, Western Washington University, Bellingham, WA 98225;
- cZoological Health Program, Wildlife Conservation Society, Bronx, NY 10460;
- dSchool of Veterinary Medicine, University of California, Davis, CA 95616;
- eCalifornia Science Center, Los Angeles, CA 90089;
- fNatural History Museum of Los Angeles County, Los Angeles, CA 90007;
- gMonterey Bay Aquarium, Monterey, CA 93940;
- hOlympic National Park, National Parks Service, Port Angeles, WA 98362;
- iCollege of Marine Science, University of South Florida, St. Petersburg, FL 33701;
- jWestern Ecological Research Center, US Geological Survey c/o Marine Science Institute, University of California, Santa Barbara, CA 93106;
- kDepartment of Ecology & Evolutionary Biology, University of California, Santa Cruz, CA 95064;
- lSeattle Aquarium, Seattle, WA 98101;
- mSchool of Aquatic & Fishery Sciences, University of Washington, Seattle, WA 98195;
- nDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269;
- oVancouver Aquarium, Vancouver, BC, Canada V6G 3E2; and
- pDepartment of Ecology & Evolutionary Biology, Cornell University, Ithaca, NY 14853
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Edited by James L. Van Etten, University of Nebraska-Lincoln, Lincoln, NE, and approved October 21, 2014 (received for review August 28, 2014)

Significance
Sea stars inhabiting the Northeast Pacific Coast have recently experienced an extensive outbreak of wasting disease, leading to their degradation and disappearance from many coastal areas. In this paper, we present evidence that the cause of the disease is transmissible from disease-affected animals to apparently healthy individuals, that the disease-causing agent is a virus-sized microorganism, and that the best candidate viral taxon, the sea star-associated densovirus (SSaDV), is in greater abundance in diseased than in healthy sea stars.
Abstract
Populations of at least 20 asteroid species on the Northeast Pacific Coast have recently experienced an extensive outbreak of sea-star (asteroid) wasting disease (SSWD). The disease leads to behavioral changes, lesions, loss of turgor, limb autotomy, and death characterized by rapid degradation (“melting”). Here, we present evidence from experimental challenge studies and field observations that link the mass mortalities to a densovirus (Parvoviridae). Virus-sized material (i.e., <0.2 μm) from symptomatic tissues that was inoculated into asymptomatic asteroids consistently resulted in SSWD signs whereas animals receiving heat-killed (i.e., control) virus-sized inoculum remained asymptomatic. Viral metagenomic investigations revealed the sea star-associated densovirus (SSaDV) as the most likely candidate virus associated with tissues from symptomatic asteroids. Quantification of SSaDV during transmission trials indicated that progression of SSWD paralleled increased SSaDV load. In field surveys, SSaDV loads were more abundant in symptomatic than in asymptomatic asteroids. SSaDV could be detected in plankton, sediments and in nonasteroid echinoderms, providing a possible mechanism for viral spread. SSaDV was detected in museum specimens of asteroids from 1942, suggesting that it has been present on the North American Pacific Coast for at least 72 y. SSaDV is therefore the most promising candidate disease agent responsible for asteroid mass mortality.
Footnotes
- ↵1To whom correspondence should be addressed. Email: hewson{at}cornell.edu.
↵2Present address: Institute for Marine and Environmental Technology, University of Maryland, Baltimore County, Baltimore, MD 21202.
Author contributions: I.H. and B.M. designed research; I.H., J.B.B., B.M.G., B.M., A.L.N., J.K.G., J.W., C.L.G., G.H., M.M., S.F., E.F., C.M.M., P.R., L.L., S.D., M.H., J.M., C.A.B., M.E.E., and C.D.H. performed research; I.H., J.B.B., B.M.G., M.B., K.D.L., A.M.K., and C.S.F. analyzed data; I.H., J.B.B., B.M.G., B.M., A.L.N., G.H., M.M., M.B., K.D.L., A.M.K., C.M.M., P.R., C.S.F., M.H., C.A.B., M.E.E., and C.D.H. wrote the paper; I.H. is senior author; I.H., J.B.B., B.M.G., and E.F. analyzed genomic data; I.H., C.A.B., and M.E.E. performed viral challenge experiments; I.H. and J.B.B. performed molecular biological analyses; B.M., J.W., M.M., S.F., C.M.M., P.R., L.L., M.H., J.M., C.A.B., and C.D.H. collected samples; B.M., J.K.G., J.W., M.M., S.F., C.M.M., P.R., L.L., M.H., J.M., C.A.B., and C.D.H. made field observations; A.L.N. and S.D. performed histological and microscopic examination; I.H., J.K.G., M.B., and C.S.F. interpreted results; I.H., C.L.G., and G.H. analyzed museum specimens; and I.H., K.D.L., and A.M.K. performed statistical analyses.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. PRJNA253121).
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1416625111/-/DCSupplemental.
Freely available online through the PNAS open access option.