Expression in vivo and in vitro of the major structural protein (VP 73) of African swine fever virus

1992 ◽  
Vol 123 (1-2) ◽  
pp. 111-124 ◽  
Author(s):  
C. Cistu� ◽  
E. Tabar�s
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Structural Protein ◽  
Major Structural Protein

scholarly journals Deletion of a CD2-Like Gene, 8-DR, from African Swine Fever Virus Affects Viral Infection in Domestic Swine

1998 ◽  
Vol 72 (4) ◽  
pp. 2881-2889 ◽  
Author(s):  
M. V. Borca ◽  
C. Carrillo ◽  
L. Zsak ◽  
W. W. Laegreid ◽  
G. F. Kutish ◽  
...  
Keyword(s):  
Viral Infection ◽  
Mononuclear Cells ◽  
African Swine Fever Virus ◽  
Disease Onset ◽  
African Swine Fever ◽  
Fever Virus ◽  
Parental Virus ◽  
Viral Virulence

ABSTRACT An African swine fever virus (ASFV) gene with similarity to the T-lymphocyte surface antigen CD2 has been found in the pathogenic African isolate Malawi Lil-20/1 (open reading frame [ORF] 8-DR) and a cell culture-adapted European virus, BA71V (ORF EP402R) and has been shown to be responsible for the hemadsorption phenomenon observed for ASFV-infected cells. The structural and functional similarities of the ASFV gene product to CD2, a cellular protein involved in cell-cell adhesion and T-cell-mediated immune responses, suggested a possible role for this gene in tissue tropism and/or immune evasion in the swine host. In this study, we constructed an ASFV 8-DR gene deletion mutant (Δ8-DR) and its revertant (8-DR.R) from the Malawi Lil-20/1 isolate to examine gene function in vivo. In vitro, Δ8-DR, 8-DR.R, and the parental virus exhibited indistinguishable growth characteristics on primary porcine macrophage cell cultures. In vivo,8-DR had no obvious effect on viral virulence in domestic pigs; disease onset, disease course, and mortality were similar for the mutant Δ8-DR, its revertant 8-DR.R, and the parental virus. Altered viral infection was, however, observed for pigs infected with Δ8-DR. A delay in spread to and/or replication of Δ8-DR in the draining lymph node, a delay in generalization of infection, and a 100- to 1,000-fold reduction in virus titers in lymphoid tissue and bone marrow were observed. Onset of viremia for Δ8-DR-infected animals was significantly delayed (by 2 to 5 days), and mean viremia titers were reduced approximately 10,000-fold at 5 days postinfection and 30- to 100-fold at later times; moreover, unlike in 8-DR.R-infected animals, the viremia was no longer predominantly erythrocyte associated but rather was equally distributed among erythrocyte, leukocyte, and plasma fractions. Mitogen-dependent lymphocyte proliferation of swine peripheral blood mononuclear cells in vitro was reduced by 90 to 95% following infection with 8-DR.R but remained unaltered following infection with Δ8-DR, suggesting that 8-DR has immunosuppressive activity in vitro. Together, these results suggest an immunosuppressive role for 8-DR in the swine host which facilitates early events in viral infection. This may be of most significance for ASFV infection of its highly adapted natural host, the warthog.

scholarly journals Clinical Indicators of Moribundity in Swine Experimentally Inoculated with African Swine Fever Virus

2020 ◽  
Author(s):  
Benjamin J Hershey ◽  
Jenna L Hagart ◽  
Karyn A Havas
Keyword(s):  
Vaccine Development ◽  
African Swine Fever Virus ◽  
Significant Risk ◽  
African Swine Fever ◽  
Fever Virus ◽  
Complex Nature ◽  
Clinical Indicators ◽  
Record Data

African swine fever virus (ASFV), the causative agent of African Swine Fever (ASF), is an infectious disease of swine that is associated with high rates of morbidity and mortality in naive populations. ASFV is challenging to work with in vitro and the in vivo immune response remains an active area of study. Vaccine development, pathogenesis, and diagnostic assay development studies often require use of live swine housed in high-containment laboratories. Studies of this type are intended to obtain key data yet must minimize the pain and distress experienced by the animals. To implement humane endpoints, pigs are ideally euthanatized by barbiturate overdose prior to death from ASFV infection, as the final stages of ASF can be clinically severe. However, due to the complex nature of ASFV pathogenesis, predicting when an infected animal will become moribund and require euthanasia is difficult. The current study was intended to aid in predicting the onset of moribundity in swine. Toward this end, we performed statistical analyses of historical health record data from 103 swine experimentally infected with ASFV. Regression analysis suggested that rectal temperature has potential utility as a marker for predicting moribundity, whereas viral strain and duration of survival after inoculation were significant risk factors for death due to disease rather than euthanasia.

Mapping and sequence of the gene encoding protein p37, A major structural protein of African swine fever virus

Virus Genes ◽  
1988 ◽  
Vol 1 (3) ◽  
pp. 291-303 ◽  
Author(s):  
C. L�pez-Ot�n ◽  
C. Sim�n ◽  
E. M�ndez ◽  
E. Vi�uela
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Structural Protein ◽  
Gene Encoding ◽  
Major Structural Protein ◽  
Encoding Protein

Phosphorylation of African swine fever virus proteins in vitro and in vivo

Biochimie ◽  
1988 ◽  
Vol 70 (5) ◽  
pp. 627-635 ◽  
Author(s):  
María L. Salas ◽  
José Salas ◽  
Eladio Viñuela
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Virus Proteins

scholarly journals The Major Structural Protein of African Swine Fever Virus, p73, Is Packaged into Large Structures, Indicative of Viral Capsid or Matrix Precursors, on the Endoplasmic Reticulum

1998 ◽  
Vol 72 (6) ◽  
pp. 5215-5223 ◽  
Author(s):  
Christian Cobbold ◽  
Thomas Wileman
Keyword(s):  
Endoplasmic Reticulum ◽  
Complex Formation ◽  
Inner Core ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
In Vitro Translation ◽  
Structural Protein ◽  
Major Structural Protein ◽  
Outer Capsid

ABSTRACT African swine fever virus (ASFV) is a large enveloped DNA virus that shares the striking icosahedral symmetry of iridoviruses. To understand the mechanism of assembly of ASFV, we have been studying the biosynthesis and subcellular distribution of p73, the major structural protein of ASFV. Sucrose density sedimentation of lysates prepared from infected cells showed that newly synthesized p73 was incorporated into a complex with a size of 150 to 250 kDa. p73 synthesized by in vitro translation migrated at 70 kDa, suggesting that cellular and/or viral proteins are required for the formation of the 150- to 250-kDa complex. During a 2-h chase, approximately 50% of the newly synthesized pool of p73 bound to the endoplasmic reticulum (ER). During this period, the membrane-bound pool of p73, but not the cytosolic pool, formed large complexes of approximately 50,000 kDa. The complexes were formed via assembly intermediates, and the entire membrane-associated pool of p73 was incorporated into the 50,000-kDa complex within 2 h. The 50,000-kDa complexes containing p73 were also detected in virions secreted from cells. Immunoprecipitation of sucrose gradients with sera taken from hyperimmune pigs suggested that p73 was the major component of the 50,000-kDa complex. It is possible, therefore, that the complex contains between 600 and 700 copies of p73. The kinetics of complex formation and envelopment of p73 were similar, and complex formation and envelopment were both reversibly inhibited by cycloheximide, suggesting a functional link between complex assembly and ASFV envelopment. A protease protection assay detected 50,000-kDa complexes on the inside and outside of the membranes forming the viral envelope. The identification of a complex containing p73 beneath the envelope of ASFV suggests that p73 may be a component of the inner core shell or matrix of ASFV. The outer pool may represent p73 within the outer capsid layer of the virus. In summary, the data suggest that the assembly of the inner core matrix and outer capsid of ASFV takes place on the ER membrane during envelopment and that these structures are not preassembled in the cytosol.

scholarly journals African swine fever virus: a B cell-mitogenic virus in vivo and in vitro.

1999 ◽  
Vol 80 (6) ◽  
pp. 1453-1461 ◽  
Author(s):  
H Takamatsu ◽  
M S Denyer ◽  
C Oura ◽  
A Childerstone ◽  
J K Andersen ◽  
...  
Keyword(s):  
B Cell ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus

scholarly journals Evaluation in Swine of a Recombinant Georgia 2010 African Swine Fever Virus Lacking the I8L Gene

Viruses ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 39
Author(s):  
Elizabeth Vuono ◽  
Elizabeth Ramirez-Medina ◽  
Sarah Pruitt ◽  
Ayushi Rai ◽  
Ediane Silva ◽  
...  
Keyword(s):  
Virus Replication ◽  
African Swine Fever Virus ◽  
Disease Outbreaks ◽  
African Swine Fever ◽  
Fever Virus ◽  
Transcriptional Analysis ◽  
Economic Losses ◽  
Conserved Gene

African swine fever virus (ASFV) is the causative agent of African swine fever, a disease currently causing significant economic losses in Europe and Asia. Specifically, the highly virulent ASFV strain Georgia 2010 (ASFV-G) is producing disease outbreaks in this large geographical region. The ASFV genome encodes for over 150 genes, most of which are still not experimentally characterized. I8L is a highly conserved gene that has not been studied beyond its initial description as a virus ORF. Transcriptional analysis of swine macrophages infected with ASFV-G demonstrated that the I8L gene is transcribed early during the virus replication cycle. To assess the importance of I8L during ASFV-G replication in vitro and in vivo, as well as its role in virus virulence in domestic swine, we developed a recombinant virus lacking the I8L gene (ASFV-G-ΔI8L). Replication of ASFV-G-ΔI8L was similar to parental ASFV-G replication in primary swine macrophage cultures, suggesting that the I8L gene is not essential for ASFV-G replication in vitro. Similarly, replication of ASFV-G-ΔI8L in swine intramuscularly inoculated with 102 HAD50 displayed replication kinetics similar to ASFV-G. In addition, animals inoculated with ASFV-G-ΔI8L presented with a clinical disease indistinguishable from that induced by the same dose of the virulent parental ASFV-G isolate. We conclude that deletion of the I8L gene from ASFV-G does not affect virus replication in vitro or in vivo, nor changes the disease outcome in swine.

GS-441524 inhibits African swine fever virus infection in vitro

2021 ◽  
pp. 105081
Author(s):  
Zhao Huang ◽  
Lang Gong ◽  
Zezhong Zheng ◽  
Qi Gao ◽  
Xiongnan Chen ◽  
...  
Keyword(s):  
Virus Infection ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus
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