Reston ebolavirus is a species of the genus Ebolavirus first recognized during an outbreak among cynomolgus macaques at a primate quarantine facility in Reston, Virginia, in 1989. The virus belongs to the family Filoviridae and possesses a negative‑sense, single‑stranded RNA genome of about 19 kilobases encoding seven structural proteins. Unlike other ebolaviruses, Reston ebolavirus is known to cause disease in non‑human primates and pigs but has not been associated with clinical illness in humans despite evidence of infection.
Taxonomy and Biological Features
Reston ebolavirus shares the general architecture of ebolaviruses: filamentous, enveloped virions containing a helical nucleocapsid and seven gene segments encoding nucleoprotein, VP35, VP40, glycoprotein, VP30, VP24 and the RNA‑dependent RNA polymerase. Phylogenetic analyses show it is more closely related to Sudan ebolavirus and Bundibugyo ebolavirus than to Zaire ebolavirus. The virus was first isolated in 1989 when imported macaques from the Philippines developed hemorrhagic fever at a facility in Reston, Virginia; similar outbreaks occurred at facilities in Texas and Pennsylvania. Several human handlers seroconverted, indicating infection, but none developed Ebola virus disease symptoms. Additional outbreaks in 1990 and 1996 in facilities in the United States and Italy confirmed its presence in macaque breeding centers in the Philippines. In 2008, Reston ebolavirus was detected in domestic pigs in Bulacan and Pangasinan provinces of the Philippines; workers at affected farms had antibodies but remained healthy. Experimental studies in non‑human primates demonstrate that Reston ebolavirus causes severe disease resembling other ebolavirus infections, with systemic viral replication and immune dysregulation. The lack of human pathogenicity may result from viral genetic differences or host factors. Reston ebolavirus remains a biosafety level‑4 pathogen due to uncertainty about its potential to adapt to humans.
Outbreak History and Public Health Considerations
The 1989 Reston outbreak was traced to a shipment of macaques from Ferlite Farms in the Philippines. The affected animals displayed fever, anorexia and high mortality, prompting euthanasia of entire cohorts. The virus was isolated and initially misidentified as simian hemorrhagic fever virus; sequencing revealed an ebolavirus distinct from known species. Subsequent outbreaks in 1990 in the same quarantine facility and in 1996 at an Italian facility were linked to contaminated shipments. These events led to enhanced surveillance of imported primates and revisions to quarantine protocols. The detection of Reston ebolavirus in pigs in 2008 raised concerns about food safety and the potential for reassortment or mutation that could alter host range. Philippine authorities culled affected herds and implemented farm biosecurity measures. Although human infections have remained asymptomatic, serologic evidence of exposure underscores the need for continued monitoring. Reston ebolavirus underscores that ebolaviruses can circulate in a variety of hosts, including livestock, and highlights the importance of early detection and strict biosafety practices in animal trade.
Reston ebolavirus is an anomaly among ebolaviruses, causing fatal disease in monkeys and pigs while sparing humans. Ongoing surveillance, research into viral determinants of host specificity, and adherence to biosecurity in animal facilities are crucial to mitigate potential risks.
Related Terms: Zaire Ebolavirus, Sudan Ebolavirus, Bundibugyo Ebolavirus, Taï Forest Ebolavirus, Bombali Ebolavirus