In the journal of Clinical Infectious Diseases 1998;26:434-9 it is shown that a calicivirus previously isolated from the flippers of northern fur seals [San Miguel sea lion virus serotype 5 (SMSV-5)] is now a human pathogen.

In the journal article "In Vitro Isolation and Characterization of a Calicivirus Causing a Vesicular Disease of the Hands and Feet" by A. W. Smith, E. S. Berry,, D. E. Skilling, J. E. Barlough, S. E. Poet, T. Berke, J. Mead. and D. O. Matson

from the College of Veterinary Medicine, Laboratory for Calicivirus Studies, Oregon State University, Corvallis, Oregon; Department of Veterinary Science/Microbiology, North Dakota State University, Fargo , North Dakota; Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, California; Department of Medical Microbiology, College of Veterinary Medicine, University of Georgia, Athens, Georgia; Center for Pediatric Research, Children's Hospital of The King's Daughters and Eastern Virginia Medical School, Norfolk, Virginia; and American Red Cross, National Testing Laboratory, Portland, Oregon

The following introductory passage is of great interest in describing the capabilities of San Miguel sea lion virus serotype 5 (SMSV-5).

The authors reported:

"We report that a calicivirus of oceanic origin, San Miguel sea lion virus serotype 5 (SMSV-5), is a human pathogen. This biotype was isolated originally from blisters on the flippers of northern fur seals (Callorhinus ursinus) and replicates readily in primate and human cell lines. It infects a phylogenetically diverse array of hosts (poikilotherms to primates) and induces type-specific neu- tralizing antibodies in exposed humans. Group antibody against a pooled antigen of SMSV-5 and two other serotypes was also observed in 18% of 300 blood donors from a population in the northwestern United States. The human calicivirus isolate designated SMSV-5 Homosapien-1 (SMSV-5 Hom-1) was recovered from a laboratory worker with systemic illness, including vesicular lesions on all four extremities. We believe this newly described human disease represents a para- digmatic shift in calicivirus disease recognition."

They went on to report

"Serological evidence can suggest that animal viruses are also human pathogens [1, 2], and occasionally this is confirmed by a single case, as we report herein and as was reported with regard to Cache Valley virus [3]. At other times, with no prior warning, a single case signals the arrival of a new zoonotic disease, as occurred with the death of a horse trainer in Austra- lia infected with a previously unknown morbillivirus [4]. Such events can occur when shifts in ecologic relationships cause intermixing of species and result in increased "viral traffic" [5]. In turn, "viral traffic" encourages adaptive shifts in viral genomes and host-parasite relationships, which can result in emerging new diseases, especially zoonoses [5]. "Viral traffic" for one calicivirus was deliberately increased in Australia where a recently recognised ( I 984) hemorrhagic virus of rab- bits [6-8) has been spread as a biological control agent, re- sulting in a continent-wide calicivirus challenge of naive and diverse populations.

The early detection of and appropriate responses to emerging viral diseases that may result from this or similar events that heighten "viral traffic" will require preventative programs involving research, early diagnosis, public health awareness, and reporting. In this context, the caliciviral traffic between oceanic hosts and humans that we report herein, with regard to a laboratory workers illness caused by San Miguel sea lion calicivirus (SMSV), provides an example of a new disease manifestation and observation. To provide further evidence of probable human exposure and infection with this group of pathogenic caliciviruses, we also report the serum reactivity to group SMSV antigens in blood donors living along the Pacific Coast of North America."