Sabia Virus

Epidemiology and History:

Only one known case of naturally contracted Sabia virus infection has been documented, yet the virus remains important due to at least two laboratory infections that have occurred. The original natural case of Sabia virus infection occurred in a woman staying in the village of Sabia, outside of Sao Paulo Brazil, in 1990. In this instance, severe liver damage led physicians to an initial diagnosis of yellow fever. However, this was soon ruled out through a thorough blood test. Following the patient’s death, the agent was identified as a then unknown arenavirus. The viriologist who was responsible for this identification, however, contracted the disease as during the course of his research; he, fortunately, survived. Four years later, while working under level 3 biohazard conditions, a researcher at the Tropical Medicine Clinic at Yale-New Haven Hospital was exposed to the virus. Exposure apparently resulted when a centrifuge bottle containing infected tissue cracked and leaked into the spinning centrifuge, releasing aerosolized virus particles into the air. New World arenaviruses, or those members of the family that are endemic to the Americas, are being discovered at a rate of close to one every three years, a fact that brands Sabia and its cousins as some of the most important emerging viruses of their regions.


Like other New World arenaviruses, transmission is assumed to be via aerosolized virus particles. Close contact with infected individuals or suspected animal reservoirs or vectors are key factors in Sabia diagnosis. Though the animal reservoir is as yet unknown, a rodent found throughout the region surrounding the small village of Sabia has been implicated. In the history of the virus, laboratory-related infection has been a primary method of transmission, and therefore necessitates the utmost caution when handling the virus in a laboratory setting.


In discussing Sabia virus and the other New World arenaviruses, diagnosis is one of the most important areas of concern. Especially in initial stages, infection with Sabia and its relatives is often indistinguishable from other common viral diseases, including the prevalent pathogen yellow fever. Should the disease develop hemorrhagic manifestations, dengue hemorrhagic fever is also a possibility. Consequently, virologic testing is incontrovertibly necessary in any cases of suspected arenavirus infection. Swift diagnosis is necessary in cases of infection with any of the New World arenaviruses, as death may sometimes occur even before antibodies are detected. Antigen-capture ELISA remains the preferred method of diagnosis.


Due to the small number of individuals infected with Sabia virus, future cases may elaborate upon current known symptoms. Fever, headache, myalgia, nausea, vomiting, weakness, and pronounced sore throat were symptoms exhibited in all cases of Sabia infection. Additional symptoms include conjunctivitis, diarrhea, epigastric pain, and bleeding gums. In both cases that occurred in 1990, symptoms lasted approximately 15 days. However, symptoms ceased in the index case due to death, while the laboratory technician convalesced following this time period. Leucopenia, thrombocytopenia, and proteinuria were all present in each case, though these are hardly unique to the virus. Gastro-intestinal hemorrhage was marked in the index case, though generalized hemorrhagic fever appears to have been exhibited in all documented cases.


Like other arenaviruses, Sabia virus proved to be responsive to treatment with ribavirin. In confirmed cases of Sabia infection, ribavirin is unquestionably the most appropriate treatment. Additionally, treatment of symptoms related to dehydration and bleeding is also recommended. Hemorrhage is most often the primary concern, meaning that fluid intake should be monitored carefully to compensate for vascular leaking and edema.


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Profile: Sabia Virus
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Jamie Dyal and Ben Fohner Stanford University Humans and Viruses Class of 2005