African swine fever virus

African swine fever virus (ASFV) is a large, double-stranded DNA virus in the Asfarviridae family. It is the causative agent of African swine fever (ASF). The virus causes a haemorrhagic fever with high mortality rates in domestic pigs; some isolates can cause death of animals as quickly as a week after infection. It persistently infects its natural hosts, warthogs, bushpigs, and soft ticks of the genus Ornithodoros, which likely act as a vector, with no disease signs. It does not cause disease in humans. 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. The disease was first described after European settlers brought pigs into areas endemic with ASFV and, as such, is an example of an 'emerging infectious disease'. African swine fever virus (ASFV) is a large, double-stranded DNA virus in the Asfarviridae family. It is the causative agent of African swine fever (ASF). The virus causes a haemorrhagic fever with high mortality rates in domestic pigs; some isolates can cause death of animals as quickly as a week after infection. It persistently infects its natural hosts, warthogs, bushpigs, and soft ticks of the genus Ornithodoros, which likely act as a vector, with no disease signs. It does not cause disease in humans. 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. The disease was first described after European settlers brought pigs into areas endemic with ASFV and, as such, is an example of an 'emerging infectious disease'. ASFV replicates in the cytoplasm of infected cells. It is the only known virus with a double-stranded DNA genome to be transmitted by arthropods. ASFV is a large, icosahedral, double-stranded DNA virus with a linear genome containing at least 150 genes. The number of genes differs slightly among 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 hemorrhagic fevers, the main target cells for replication are those of monocyte, macrophage lineage. Entry of the virus into the host cell is receptor-mediated, but the precise mechanism of endocytosis is presently unclear. The virus encodes enzymes required for replication and transcription of its genome, including elements of a base excision repair system, structural proteins, and many proteins that are not essential for replication in cells, but instead have roles in virus survival and transmission in its hosts. Virus replication takes place in perinuclear factory areas. It is a highly orchestrated process with at least four stages of transcription—immediate-early, early, intermediate, and late. The majority of replication and assembly occurs in discrete, perinuclear regions of the cell called virus factories, and finally progeny virions are transported to the plasma membrane along microtubules where they bud out or are propelled away along actin projections to infect new cells. As the virus progresses through its lifecycle, most if not all of the host cell's organelles are modified, adapted, or in some cases destroyed. 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. Based on sequence variation in the C-terminal region of the B646L gene encoding the major capsid protein p72, 22 ASFV genotypes (I–XXIII) have been identified. All ASFV p72 genotypes have been circulating in eastern and southern Africa. Genotype I has been circulating in Europe, South America, the Caribbean, and western Africa. Genotype VIII is confined to four East African countries. The virus is thought to be derived from a virus of soft tick (genus Ornithodoros) that infects wild swine, including giant forest hogs (Hylochoerus meinertzhageni), warthogs (Phacochoerus africanus), and bushpigs (Potamochoerus porcus). In these wild hosts, infection is generally asymptomatic. This virus appears to have evolved around 1700 AD. This date is corroborated by the historical record. Pigs were initially domesticated in North Africa and Eurasia. They were introduced into southern Africa from Europe and the Far East by the Portuguese (300 years ago) and Chinese (600 years ago), respectively. At the end of the 19th century, the extensive pig industry in the native region of ASFV (Kenya) started after massive losses of cattle due to a rinderpest outbreak. Pigs were imported on a massive scale for breeding by colonizers from Seychelles in 1904 and from England in 1905. Pig farming was free-range at that time. The first outbreak of ASF was reported in 1907. In the acute form of the disease caused by highly virulent strains, pigs may develop a high fever, but show no other noticeable symptoms for the first few days. They then gradually lose their appetites and become depressed. In white-skinned pigs, the extremities turn blueish-purple and hemorrhages become apparent on the ears and abdomen. Groups of infected pigs lie huddled together shivering, breathing abnormally, and sometimes coughing. If forced to stand, they appear unsteady on their legs; this is called congenital tremor type A-I in newborn piglets. Within a few days of infection, they enter a comatose state and then die. In pregnant sows, spontaneous abortions occur. In milder infections, affected pigs lose weight, becoming thin, and develop signs of pneumonia, skin ulcers, and swollen joints.