Abstract

African swine fever virus (ASFV) is the sole member of the family Asfarviridae, and the only known DNA arbovirus. Since its identification in Kenya in 1921, ASFV has remained endemic in Africa, maintained in a sylvatic cycle between Ornithodoros soft ticks and warthogs (Phacochoerus africanus) which do not develop clinical disease with ASFV infection. However, ASFV causes a devastating and economically significant disease of domestic (Sus scrofa domesticus) and feral (Sus scrofa ferus) swine. There is no ASFV vaccine available, and current control measures consist of strict animal quarantine and culling procedures. The virus is highly stable and easily spreads by infected swine, contaminated pork products and fomites, or via transmission by the Ornithodoros vector. Competent Ornithodoros argasid soft tick vectors are known to exist not only in Africa, but also in parts of Europe and the Americas. Once ASFV is established in the argasid soft tick vector, eradication can be difficult due to the long lifespan of Ornithodoros ticks and their proclivity to inhabit the burrows of warthogs or pens and shelters of domestic pigs. Establishment of endemic ASFV infections in wild boar populations further complicates the control of ASF. Between the late 1950s and early 1980s, ASFV emerged in Europe, Russia and South America, but was mostly eradicated by the mid-1990s. In 2007, a highly virulent genotype II ASFV strain emerged in the Caucasus region and subsequently spread into the Russian Federation and Europe, where it has continued to circulate and spread. Most recently, ASFV emerged in China and has now spread to several neighboring countries in Southeast Asia. The high morbidity and mortality associated with ASFV, the lack of an efficacious vaccine, and the complex makeup of the ASFV virion and genome as well as its lifecycle, make this pathogen a serious threat to the global swine industry and national economies. Topics covered by this review include factors important for ASFV infection, replication, maintenance, and transmission, with attention to the role of the argasid tick vector and the sylvatic transmission cycle, current and future control strategies for ASF, and knowledge gaps regarding the virus itself, its vector and host species.

Highlights

  • Reviewed by: Marie Rene Culhane, University of Minnesota, United States Faten Abdelaal Okda, St

  • Once African swine fever virus (ASFV) is established in the argasid soft tick vector, eradication can be difficult due to the long lifespan of Ornithodoros ticks and their proclivity to inhabit the burrows of warthogs or pens and shelters of domestic pigs

  • While the situation remains ever-changing due to continued outbreaks and spread of ASFV globally, information from peer-reviewed manuscripts, situation reports, and press releases provide some indication of the impact of ASFV emergence on animal health and economics of effected countries

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Summary

ASFV Emergence and Arbovirology

Since its identification in Kenya in 1921 [1, 2], African swine fever virus (ASFV) has remained endemic in Africa, affecting up to 35 African countries [3]. Between the late 1950s and early 1980s, ASFV genotype I emerged in Europe, Russia, the Caribbean and South America. While the situation remains ever-changing due to continued outbreaks and spread of ASFV globally, information from peer-reviewed manuscripts, situation reports, and press releases provide some indication of the impact of ASFV emergence on animal health and economics of effected countries. Since the first reported outbreak in China in August 2018, ASF has been detected in at least 8 other countries in Asia and has resulted in the death or culling of more than 5 million pigs, with losses accounting for more than 10 percent of the total pig population in China, Mongolia and Vietnam [(11, 12); FAO situation update, www.fao.org; FAO press release, 09/08/2019, “One year on, close to 5 million pigs lost to Asia’s swine fever

Estimated animal losses
Ornithodoros Soft Ticks
ASFV Sylvatic Cycle
MOLECULAR PROPERTIES OF ASFV
Target Cells
ASFV Entry and Early Events in the Infectious Cycle
ASFV Gene Expression and Replication
Virion Assembly and Transport of Mature Virus Particles
ASFV Gene Functions and Virulence Factors
CONTROL OF ASFV
Detection and Diagnosis
CONCLUDING REMARKS
Findings
ONLINE CITATIONS
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