Identification of a variable region of the African swine fever virus genome that has undergone separate DNA rearrangements leading to expansion of minisatellite-like sequences

1990 ◽  
Vol 216 (3) ◽  
pp. 677-688 ◽  
Author(s):  
Linda K. Dixon ◽  
Christine Bristow ◽  
Philip J. Wilkinson ◽  
Keith J. Sumption
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Variable Region ◽  
Virus Genome ◽  
Fever Virus ◽  
Dna Rearrangements

scholarly journals Novel Swine Virulence Determinant in the Left Variable Region of the African Swine Fever Virus Genome

2002 ◽  
Vol 76 (7) ◽  
pp. 3095-3104 ◽  
Author(s):  
J. G. Neilan ◽  
L. Zsak ◽  
Z. Lu ◽  
G. F. Kutish ◽  
C. L. Afonso ◽  
...  
Keyword(s):  
Deletion Mutant ◽  
Gene Deletion ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Variable Region ◽  
Fever Virus ◽  
Marker Rescue ◽  
Virulence Determinant ◽  
Gene Deletion Mutant

ABSTRACT Previously we have shown that the African swine fever virus (ASFV) NL gene deletion mutant E70ΔNL is attenuated in pigs. Our recent observations that NL gene deletion mutants of two additional pathogenic ASFV isolates, Malawi Lil-20/1 and Pr4, remained highly virulent in swine (100% mortality) suggested that these isolates encoded an additional virulence determinant(s) that was absent from E70. To map this putative virulence determinant, in vivo marker rescue experiments were performed by inoculating swine with infection-transfection lysates containing E70 NL deletion mutant virus (E70ΔNL) and cosmid DNA clones from the Malawi NL gene deletion mutant (MalΔNL). A cosmid clone representing the left-hand 38-kb region (map units 0.05 to 0.26) of the MalΔNL genome was capable of restoring full virulence to E70ΔNL. Southern blot analysis of recovered virulent viruses confirmed that they were recombinant E70ΔNL genomes containing a 23- to 28-kb DNA fragment of the Malawi genome. These recombinants exhibited an unaltered MalΔNL disease and virulence phenotype when inoculated into swine. Additional in vivo marker rescue experiments identified a 20-kb fragment, encoding members of multigene families (MGF) 360 and 530, as being capable of fully restoring virulence to E70ΔNL. Comparative nucleotide sequence analysis of the left variable region of the E70ΔNL and Malawi Lil-20/1 genomes identified an 8-kb deletion in the E70ΔNL isolate which resulted in the deletion and/or truncation of three MGF 360 genes and four MGF 530 genes. A recombinant MalΔNL deletion mutant lacking three members of each MGF gene family was constructed and evaluated for virulence in swine. The mutant virus replicated normally in macrophage cell culture but was avirulent in swine. Together, these results indicate that a region within the left variable region of the ASFV genome containing the MGF 360 and 530 genes represents a previously unrecognized virulence determinant for domestic swine.

Two Novel Multigene Families, 530 and 300, in the Terminal Variable Regions of African Swine Fever Virus Genome

Virology ◽  
1994 ◽  
Vol 202 (2) ◽  
pp. 997-1002 ◽  
Author(s):  
T. Yozawa ◽  
G.F. Kutish ◽  
C.L. Afonso ◽  
Z. Lu ◽  
D.L. Rock
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Virus Genome ◽  
Fever Virus ◽  
Multigene Families ◽  
Variable Regions

Characterization of the African swine fever virus protein p49: a new late structural polypeptide

Microbiology ◽  
2000 ◽  
Vol 81 (1) ◽  
pp. 59-65 ◽  
Author(s):  
Inmaculada Galindo ◽  
Eladio Viñuela ◽  
Angel L. Carrascosa
Keyword(s):  
Cell Attachment ◽  
African Swine Fever Virus ◽  
Rabbit Antiserum ◽  
African Swine Fever ◽  
Virus Genome ◽  
Fever Virus ◽  
Virus Protein ◽  
Significant Similarity ◽  
Reading Frame ◽  
Cell Extracts

The open reading frame B438L, located within the EcoRI B fragment of the African swine fever virus genome, is predicted to encode a protein of 438 amino acids with a molecular mass of 49·3 kDa. It presents a cell attachment RGD (Arg–Gly–Asp) motif but no other significant similarity to protein sequences in databases. Northern blot and primer extension analysis showed that B438L is transcribed only at late times during virus infection. The B438L gene product has been expressed in Escherichia coli, purified and used as an antigen for antibody production. The rabbit antiserum specific for pB438L recognized a protein of about 49 kDa in virus-infected cell extracts. This protein was synthesized late in infection by all the virus strains tested, was located in cytoplasmic virus factories and appeared as a structural component of purified virus particles.

scholarly journals Increased resolution of African Swine Fever Virus genome patterns based on profile HMM protein domains

2020 ◽  
Author(s):  
Charles Masembe ◽  
My V.T. Phan ◽  
David L. Robertson ◽  
Matthew Cotten
Keyword(s):  
African Swine Fever Virus ◽  
Antiviral Agents ◽  
Protein Domains ◽  
African Swine Fever ◽  
Virus Genome ◽  
Fever Virus ◽  
Functional Protein ◽  
A Genome ◽  
Genomic Relationships ◽  
Genome Scale

ABSTRACTAfrican Swine Fever Virus (ASFV) was originally described in Africa almost 100 years ago and is now spreading uncontrolled across Europe and Asia and threatening to destroy the domestic pork industry. Neither effective antiviral drugs nor a protective vaccine are currently available. Efforts to understand the basis for viral pathogenicity and the development of attenuated potential vaccine strains are complicated by the large and complex ASFV genome. We report here a novel method of documenting viral diversity based on profile Hidden Markov Model domains on a genome scale. The method can be used to infer genomic relationships independent of genome alignments and also reveal ASFV genome sequence differences that alter the presence of functional protein domains in the virus. We show that the method can quickly identify differences and shared patterns between virulent and attenuated ASFV strains and will be a useful tool for developing much-needed vaccines and antiviral agents to help control this virus. The tool is rapid to run and easy to implement, readily available as a simple Docker image.

scholarly journals Deletion of the African Swine Fever Virus Gene DP148R Does Not Reduce Virus Replication in Culture but Reduces Virus Virulence in Pigs and Induces High Levels of Protection against Challenge

2017 ◽  
Vol 91 (24) ◽  
Author(s):  
Ana L. Reis ◽  
Lynnette C. Goatley ◽  
Tamara Jabbar ◽  
Pedro J. Sanchez-Cordon ◽  
Christopher L. Netherton ◽  
...  
Keyword(s):  
Virus Replication ◽  
Infectious Virus ◽  
African Swine Fever Virus ◽  
Clinical Signs ◽  
African Swine Fever ◽  
Virus Genome ◽  
Fever Virus ◽  
Virulent Virus ◽  
Ifn Γ ◽  
Reduce Virus Replication

ABSTRACT Many of the approximately 165 proteins encoded by the African swine fever virus (ASFV) genome do not have significant similarity to known proteins and have not been studied experimentally. One such protein is DP148R. We showed that the DP148R gene is transcribed at early times postinfection. Deletion of this gene did not reduce virus replication in macrophages, showing that it is not essential for replication in these cells. However, deletion of this gene from a virulent isolate, Benin 97/1, producing the BeninΔDP148R virus, dramatically reduced the virulence of the virus in vivo. All pigs infected with the BeninΔDP148R virus survived infection, showing only transient mild clinical signs soon after immunization. Following challenge with the parental virulent virus, all pigs immunized by the intramuscular route (11/11) and all except one immunized by the intranasal route (5/6) survived. Mild or no clinical signs were observed after challenge. As expected, control nonimmune pigs developed signs of acute African swine fever (ASF). The virus genome and infectious virus were observed soon after immunization, coincident with the onset of clinical signs (∼106 genome copies or 50% tissue culture infective doses/ml). The levels of the virus genome declined over an extended period up to 60 days postimmunization. In contrast, infectious virus was no longer detectable by days 30 to 35. Gamma interferon (IFN-γ) was detected in serum between days 4 and 7 postimmunization, and IFN-γ-producing cells were detected in all pigs analyzed following stimulation of immune lymphocytes with whole virus. ASFV-specific antibodies were first detected from day 10 postimmunization. IMPORTANCE African swine fever (ASF) is endemic in Africa, parts of the Trans Caucasus, the Russian Federation, and several European countries. The lack of a vaccine hinders control. Many of the ASF virus genes lack similarity to known genes and have not been characterized. We have shown that one of these, DP148R, is transcribed early during virus replication in cells and can be deleted from the virus genome without reducing virus replication. The virus with the gene deletion, BeninΔDP148R, caused mild clinical signs in pigs and induced high levels of protection against challenge with the parental virulent virus. Therefore, deletion of this gene can provide a target for the rational development of vaccines.

scholarly journals Amino Acid Tandem Repeats within a Late Viral Gene Define the Central Variable Region of African Swine Fever Virus

Virology ◽  
1996 ◽  
Vol 220 (1) ◽  
pp. 20-27 ◽  
Author(s):  
P.M. IRUSTA ◽  
M.V. BORCA ◽  
G.F. KUTISH ◽  
Z. LU ◽  
E. CALER ◽  
...  
Keyword(s):  
Amino Acid ◽  
Tandem Repeats ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Variable Region ◽  
Fever Virus ◽  
Viral Gene ◽  
Central Variable Region

scholarly journals Evaluation of Lesions and Viral Antigen Distribution in Domestic Pigs Inoculated Intranasally with African Swine Fever Virus Ken05/Tk1 (Genotype X)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 768
Author(s):  
Pedro J. Sánchez-Cordón ◽  
Tobias Floyd ◽  
Daniel Hicks ◽  
Helen R. Crooke ◽  
Stephen McCleary ◽  
...  
Keyword(s):  
Viral Antigen ◽  
African Swine Fever Virus ◽  
Clinical Signs ◽  
African Swine Fever ◽  
Virus Genome ◽  
Virus Antigen ◽  
Fever Virus ◽  
Control Measures ◽  
Vascular Lesions ◽  
Domestic Pigs

The understanding of the pathogenic mechanisms and the clinicopathological forms caused by currently circulating African swine fever virus (ASFV) isolates is incomplete. So far, most of the studies have been focused on isolates classified within genotypes I and II, the only genotypes that have circulated outside of Africa. However, less is known about the clinical presentations and lesions induced by isolates belonging to the other twenty-two genotypes. Therefore, the early clinicopathological identification of disease outbreaks caused by isolates belonging to, as yet, not well-characterised ASFV genotypes may be compromised, which might cause a delay in the implementation of control measures to halt the virus spread. To improve the pathological characterisation of disease caused by diverse isolates, we have refined the macroscopic and histopathological evaluation protocols to standardise the scoring of lesions. Domestic pigs were inoculated intranasally with different doses (high, medium and low) of ASFV isolate Ken05/Tk1 (genotype X). To complement previous studies, the distribution and severity of macroscopic and histopathological lesions, along with the amount and distribution of viral antigen in tissues, were characterised by applying the new scoring protocols. The intranasal inoculation of domestic pigs with high doses of the Ken05/Tk1 isolate induced acute forms of ASF in most of the animals. Inoculation with medium doses mainly induced acute forms of disease. A less severe but longer clinical course, typical of subacute forms, characterised by the presence of more widespread and severe haemorrhages and oedema, was observed in one pig inoculated with the medium dose. The severity of vascular lesions (haemorrhages and oedema) induced by high and medium doses was not associated with the amount of virus antigen detected in tissues, therefore these might be attributed to indirect mechanisms not evaluated in the present study. The absence of clinical signs, lesions and detectable levels of virus genome or antigen in blood from the animals inoculated with the lowest dose ruled out the existence of possible asymptomatic carriers or persistently infected pigs, at least for the 21 days period of the study. The results corroborate the moderate virulence of the Ken05/Tk1 isolate, as well as its capacity to induce both the acute and, occasionally, subacute forms of ASF when high and medium doses were administered intranasally.

scholarly journals In-yeast reconstruction of the African swine fever virus genome isolated from clinical samples

2021 ◽  
Vol 2 (3) ◽  
pp. 100803
Author(s):  
Fabien Labroussaa ◽  
Kemal Mehinagic ◽  
Valentina Cippa ◽  
Matthias Liniger ◽  
Hatice Akarsu ◽  
...  
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Virus Genome ◽  
Fever Virus ◽  
Clinical Samples

scholarly journals A Method for the Analysis of African Swine Fever by Viral Metagenomic Sequencing

2021 ◽  
Vol 8 ◽  
Author(s):  
ChiHai Ji ◽  
JingZhe Jiang ◽  
YingFang Wei ◽  
ZhiYuan Wang ◽  
YongJie Chen ◽  
...  
Keyword(s):  
Genome Sequencing ◽  
African Swine Fever Virus ◽  
Gene Prediction ◽  
African Swine Fever ◽  
Epidemiological Studies ◽  
Virus Genome ◽  
Fever Virus ◽  
Whole Genome ◽  
Sequencing Analysis ◽  
Metagenomic Sequencing

In 2018, there was an outbreak of African swine fever (ASF) in China, which spread to other provinces in the following 3 years and severely damaged China's pig industry. ASF is caused by the African swine fever virus (ASFV). Given that the genome of the African swine fever virus is very complex and whole genome information is currently inadequate, it is important to efficiently obtain virus genome sequences for genomic and epidemiological studies. The prevalent ASFV strains have low genetic variability; therefore, whole genome sequencing analysis provides a basis for the study of ASFV. We provide a method for the efficient sequencing of whole genomes, which requires only a small number of tissues. The database construction method was selected according to the genomic types of ASFV, and the whole ASFV genome was obtained through data filtering, host sequence removal, virus classification, data assembly, virus sequence identification, statistical analysis, gene prediction, and functional analysis. Our proposed method will facilitate ASFV genome sequencing and novel virus discovery.

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