Background
In May 1993, an unusual cluster of deaths occurred in the southwestern United States. The deaths were characterized by a febrile prodrome that preceded acute respiratory failure and shock. Physicians from the Indian Health Service and the Centers for Disease Control and Prevention (CDC) determined that a rodent vector was responsible for the infection and identified the responsible virus as a member of the Hantavirus family.
Sin Nombre virus (SNV), as it is now known, is the primary agent responsible for Hantavirus pulmonary syndrome (HPS) and the deadliest member of the Hantavirus family. However, there are numerous other pathogenic hantaviruses. The New York virus has been identified as the cause of HPS in New York and Rhode Island, and the Bayou and Black Creek Canal viruses, found in the southeastern United States, produce a variant of the syndrome that includes a greater degree of renal failure. The more distantly related Hantaan, Seoul, Dobrava/Belgrade, and Puumala hantaviruses produce a distinct syndrome of hemorrhagic fever and renal failure (HFRS).
The hantaviruses are RNA zoonotic viruses that are generally spherical in shape, measuring 70-100 nm in diameter, and can be identified by inclusion bodies and distinctive gridlike patterns on electron microscopy. They are transmitted to humans from rodent hosts, including possibly from pet rats,
but, except for the Andes hantavirus, have not been shown to be capable of human-to-human transmission.
Retrospective analyses indicate that HPS has been present in North America since as early as 1959, and Hantavirus infections have now been reported in at least 32 states in the United States, as well as in Canada and South America.