Thursday, August 26, 2021

08-26-2021-0848 - African Swine Fever Virus

African Swine Fever Virus

ASFV possesses two distinct lipid membranes: an external one, obtained from the cellular membrane during budding, and an internal one that surrounds the inner core of the particle and is likely derived from the endoplasmic reticulum of the infected cell.

From: Encyclopedia of Microbiology (Third Edition), 2009

Asfarviridae

In Virus Taxonomy, 2012

List of species in the genus Asfivirus

African swine fever virus
African swine fever virus Benin97/1	[AM712239]	(ASFV-Benin97)
ASFV-BA71V	[U18466=NC_001659]
ASFV-Ken	[AY261360]
ASFV-Mal	[AY261361]
ASFV-Mku	[AY261362]
ASFV-OurT88/3	[AM712240]
ASFV-Pret	[AY261363]
ASFV-Teng	[AY261364]
ASFV-War	[AY261366]
ASFV-Warm	[AY261365]
ASFV-E75	[FN557520]

Species names are in italic script; names of isolates and strains are in roman script. Full genome sequence accession numbers [ ] and assigned abbreviations ( ) are also listed.

African Swine Fever Virus

L.K. Dixon, D. Chapman, in Encyclopedia of Virology (Third Edition), 2008

Classification and Relationship with Other Virus Families

ASFV was first classified as a member of the family Iridoviridaebecause of its large size, cytoplasmic location, and double-stranded DNA genome. However, studies of replication strategy and the genome revealed similarities with the Poxviridae, although the viruses differ structurally. ASFV was therefore placed as the species African swine fever virus into a separate virus family, the Asfarviridae, of which it is the sole member of the single genus, the Asfivirus genus. ASFV has also been considered to be part of a larger grouping of nucleo-cytoplasmic large DNA viruses (NCLDV) which, apart from the families mentioned above, includes the family Phycodnaviridae (large DNA viruses that infect blue-green algae) and the genus Mimivirus(which infect amebae). Replication of all families in the NCLDVgrouping involves at least some stage in the cytoplasm, although each family has varying requirements for host nuclear functions. For example, both ASFV and poxviruses encode their own RNA polymerase which is packaged into virus particles so that transcription of early genes begins immediately following virus entry. Members of the Iridoviridae have a greater requirement for the nucleus since virus particles do not contain an RNA polymerase and early virus gene transcription and replication take place in the nucleus and are initiated by host enzymes. At later stages, virus DNA replication, transcription, and virus assembly take place in the cytoplasm. Less is known about the replication strategies of the Phycodnaviridae and Mimivirus, although they exhibit a greater involvement of nuclear functions in replication compared to the Poxviridae and Asfarviridae.

Analysis of the gene complements of different families in the grouping has indicated that the ancestral NCLDV may have encoded at least 40 genes involved in replication, transcription, packaging, and assembly. Each family has evolved to encode genes that represent adaptations to its particular ecological niche. Genome analysis suggests there are two major lineages, one consisting of the Poxviridae and Asfarviridae and other of the Iridoviridae, Phycodnaviridae, and Mimivirus.

Comparison of the NCLDV families suggests that genes have been acquired by horizontal transfer from eukaryotic and prokaryotic hosts as well as possibly from other viruses. However, there are few genes which show evidence of recent acquisition. Another feature of the NCLDV is the presence of MGFs which have evolved by processes of gene duplication and sequence divergence. The remarkable adaptation of ASFV to replicate in its tick vector suggests that its ancestor may have replicated only in arthropods and later acquired the ability to replicate also in mammalian hosts. The independence of the virus from host transcriptional machinery facilitates virus replication in both mammalian and arthropod hosts since the gene promoters do not have to be recognised by both the mammalian and arthropod host transcriptional machinery. This could have facilitated the jump from arthropod to mammalian hosts. However, ASFV also encodes proteins (such as CD2v) that are clearly derived from a higher eukaryotic host, suggesting that growth in such hosts has substantially influenced ASFV evolution. Replication in macrophages provides the virus with opportunities to manipulate the host response to infection. This advantage may offset difficulties encountered by replicating in the harsh, microbiocidal environment of the macrophage cytoplasm.

Asfarviridae and Iridoviridae

In Fenner's Veterinary Virology (Fifth Edition), 2017

Classification

African swine fever virus is a large enveloped double-stranded DNA virus that is the sole member of the genus Asfivirus within the family Asfarviridae (Asfar=African swine fever and related viruses). African swine fever virus is the only known DNA arbovirus and is transmitted by soft ticks of the genus Ornithodoros. Virus strains are distinguished by their virulence to swine, which ranges from highly lethal to subclinical infection. Virus strains can also be differentiated by their genetic sequences, and various virus-encoded genes, including p72 (also referred to as p73), can be used for genotyping the virus; however, the genomic diversity of the virus in nature remains to be thoroughly characterized. The genome of African swine fever virus contains a unique complement of multigene families.

African Swine Fever Virus Polyprotein Processing Proteinase

Alí Alejo, ... María L. Salas, in Handbook of Proteolytic Enzymes (Third Edition), 2013

Structural Chemistry

ASFV gene S273R encodes a protein of 273 amino acid residues with a predicted pI of 8.85 and a molecular mass of 31 kDa, as determined by SDS-polyacrylamide gel electrophoresis, which is consistent with the 31.5 kDa mass deduced from the amino acid sequence.

The catalytic domain, located between residues 168 and 252, is preceded by an N-terminal region of 167 amino acids that is unrelated to the N terminus of other Clan CE peptidases. In particular, the ASFV enzyme lacks the Ulp1 motifs that interact with SUMO substrates [17]. These motifs are also absent from the adenovirus protease.

The Double Stranded DNA Viruses

CONTRIBUTED BY, ... D. Raoult, in Virus Taxonomy, 2005

BIOLOGICAL PROPERTIES

ASFV infects domestic and wild swine (Sus scrofa domesticus and S. s. ferus), warthogs (Phacochoerus aethiopicus) and bushpigs (Potamochoerus porcus). Disease signs are only apparent in domestic and wild swine. Soft ticks of the genus Ornithodoros are also infected and O. moubata acts as a vector in parts of Africa south of the Sahara and O. erraticus acted as a vector in S.W. Spain and Portugal. Virus can be transmitted in ticks trans-stadially, trans-ovarially and sexually. Warthogs, bushpigs and swine can be infected by bites from infected ticks. Neither vertical nor horizontal transfer of virus between warthogs is thought to occur. However, transmission between domestic swine can occur by direct contact, or by ingestionof infected meat, or fomites, or mechanically by biting flies. Warthogs, bushpigs, wild swine and ticks act as reservoirs of virus. Disease is endemic in domestic swine in many African countries and in Europe in Sardinia. ASFV was first reported in Madagscar in 1998 and remains endemic there. Disease was first introduced into Europe in Portugal in 1957 and was endemic in parts of the Iberian peninsula from 1960 until 1995. Sporadic outbreaks have occurred in and been eradicated from Belgium, Brazil, Cuba, the Dominican Republic, France, Haiti, Holland and Malta.

https://www.sciencedirect.com/topics/medicine-and-dentistry/african-swine-fever-virus

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