| African swine fever virus | |
|---|---|
| Electron micrograph of a virus particle | |
| Virus classification | |
| Group: | Group I (dsDNA) |
| Family: | Asfarviridae |
| Genus: | Asfivirus |
| Species: | African swine fever virus |
African swine fever virus (ASFV) is the causative agent of African swine fever (ASF). ASFV is a large, double-stranded DNA virus which replicates in the cytoplasm of infected cells, and is the only member of the Asfarviridae family.[1] ASFV infects domestic pigs, warthogs and bushpigs, as well as soft ticks (Ornithodoros), which are likely vectors. ASFV is the only virus with a DNA genome transmitted by arthropods. The virus causes a lethal haemorraghic disease in domestic pigs. Some isolates can cause death of animals within as little as a week after infection. In all other species, the virus causes no obvious disease. ASFV is endemic to sub-Saharan Africa and exists in the wild through a cycle of infection between ticks and wild pigs, bushpigs and warthogs. ASFV was first described after European settlers brought pigs into areas endemic with ASFV and, as such, is an example of an 'emerging infection'.
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African swine fever was restricted to the continent that bears its name until 1957, when the disease was reported in Lisbon, Portugal. A further outbreak occurred there in 1960. Subsequent to these initial introductions, the disease became established in the Iberian peninsula and sporadic outbreaks occurred in France, Belgium and other European countries during the 1980s. Both Spain and Portugal had managed to eradicate the disease by the mid 1990s through a slaughter policy. During the late 1970s, ASFV crossed the Atlantic Ocean and outbreaks were reported in some Caribbean islands, including Cuba and the Dominican Republic. Major outbreaks of ASF in Africa are regularly reported to the World Organisation for Animal Health (previously called l'office international des épizooties (OIE)). The most recent outbreak of ASF outside Africa started at the beginning of 2007 in Georgia, and has since spread to the countries of Armenia, Azerbaijan, Iran and Russia.
The appearance of ASF in the Western hemisphere at the same time as the emergence of AIDS led to some interest in whether the two were related, and a report appeared in the Lancet supporting this in 1986. However, AIDS is now known to be caused by human immunodeficiency virus (HIV); no link between ASFV and AIDS has been proven or is suspected.
The clinical symptoms of ASF are very similar to classical swine fever virus, and the two diseases normally have to be distinguished by laboratory diagnosis.
ASFV is a large, double-stranded DNA virus with a genome containing at least 150 genes. The number of genes differs slightly between different isolates of the virus. ASFV has similarities to the other large DNA viruses, e.g., poxvirus, iridovirus and mimivirus. In common with other viral haemorrhagic fevers, the main target cells for replication are those of monocyte, macrophage lineage. The virus causes a haemorrhagic fever with high mortality rates in pigs, but persistently infects its natural hosts, warthogs, bushpigs and soft ticks of the Ornithodoros genus, with no disease signs. The virus encodes enzymes required for replication and transcription of the genome, including elements of a base excision repair system, structural proteins and many proteins that are not essential for replication in cells, but have roles in virus survival and transmission in its hosts. Virus replication takes place in perinuclear factory areas. Assembly of the icosahedral capsid occurs on modified membranes from the endoplasmic reticulum. Products from proteolytically-processed polyproteins form the core shell between the internal membrane and the nucleoprotein core. An additional outer membrane is gained as particles bud from the plasma membrane. The virus encodes proteins that inhibit signalling pathways in infected macrophages and thus modulate transcriptional activation of immune response genes. In addition, the virus encodes proteins which inhibit apoptosis of infected cells to facilitate production of progeny virions. Viral membrane proteins with similarity to cellular adhesion proteins modulate interaction of virus-infected cells and extracellular virions with host components.[1]