Rabbit coronavirus (RbCV) was apparently first encountered in 1961 when Scandinavian investigators observed occasional mortality in rabbits used to propagate the Nichols strain of Treponema pallidum. Mortality rates reached 50 percent by 1968 and 75 percent by 1970. Contaminated samples of I. pallidum were brought to the Johns Hopkins University School of Medicine, a World Health Organization center for the study of treponematoses. There it was established that the causative agent was filterable, the heart was the target organ, and the agent was determined by electron microscopy to be a coronavirus. Also, complement fixing antibodies to the human coronaviruses 229E (two way cross) and OC43 (one way cross) were demonstrated in surv1v1ng rabbits. Immunofluorescent staining with anti-229E serum localized fluorescence in the interstitial tissue of the myocardium. Antiserum to RbCV cross reacted with coronaviruses of three other diseases, feline infectious peritonitis (FIPV), canine coronavirus diarrhea (CCV), and transmissible gastroenteritis (TGEV) by radioimmunoassay. In plaque neutralization tests, a slight reduction was observed against TGE and CCV but not against FIP. Antiserum to 229EV, CCV, FIPV and to a lesser degree TGEV partially blocked the clinical course of the disease and reduced mortality. Slight protection was afforded rabbits by vaccination with, in descending order of survivors, CCV, FIPV, and TGEV. Vaccination with calf diarrhea coronavirus (CDCV) provided no protection. M. M. C. Lai et al. (eds.