scholarly journals In vitro primary porcine alveolar macrophage cell toxicity and African swine fever virus inactivation using five commercially supply compound disinfectants under various condition

2021 ◽  
Author(s):  
Machimaporn TAESUJI ◽  
Khate RATTANAMAS ◽  
Darsaniya PUNYADARSANIYA ◽  
Thanongsak MAMOM ◽  
Hoa Thi NGUYEN ◽  
...  
Keyword(s):  
Alveolar Macrophage ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Porcine Alveolar Macrophage ◽  
Virus Inactivation ◽  
Cell Toxicity ◽  
Macrophage Cell ◽  
Porcine Alveolar Macrophage Cell

scholarly journals African Swine Fever Virus Multigene Family 360 and 530 Genes Are Novel Macrophage Host Range Determinants

2001 ◽  
Vol 75 (7) ◽  
pp. 3066-3076 ◽  
Author(s):  
L. Zsak ◽  
Z. Lu ◽  
T. G. Burrage ◽  
J. G. Neilan ◽  
G. F. Kutish ◽  
...  
Keyword(s):  
Host Range ◽  
Cell Cultures ◽  
Multigene Family ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Target Cells ◽  
Macrophage Cell ◽  
Range Function

ABSTRACT Pathogenic African swine fever virus (ASFV) isolates primarily target cells of the mononuclear-phagocytic system in infected swine and replicate efficiently in primary macrophage cell cultures in vitro. ASFVs can, however, be adapted to grow in monkey cell lines. Characterization of two cell culture-adapted viruses, MS16 and BA71V, revealed that neither virus replicated in macrophage cell cultures. Cell viability experiments and ultrastructural analysis showed that infection with these viruses resulted in early macrophage cell death, which occurred prior to viral progeny production. Genomic cosmid clones from pathogenic ASFV isolate E70 were used in marker rescue experiments to identify sequences capable of restoring MS16 and BA71V growth in macrophage cell cultures. A cosmid clone representing a 38-kbp region at the left terminus of the genome completely restored the growth of both viruses. In subsequent fine-mapping experiments, an 11-kbp subclone from this region was sufficient for complete rescue of BA71V growth. Sequence analysis indicated that both MS16 and BA71V had significant deletions in the region containing members of multigene family 360 (MGF 360) and MGF530. Deletion of this same region from highly pathogenic ASFV isolate Pr4 significantly reduced viral growth in macrophage cell cultures. These findings indicate that ASFV MGF360 and MGF530 genes perform an essential macrophage host range function(s) that involves promotion of infected-cell survival.

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

scholarly journals Role of African swine fever virus (ASFV) proteins EP153R and EP402R in reducing viral persistence and virulence from attenuated BeninΔDP148R

2021 ◽  
Author(s):  
Vlad Petrovan ◽  
Anusyah Rathakrishnan ◽  
Muneeb Islam ◽  
Lynnette Goatley ◽  
Katy Moffat ◽  
...  
Keyword(s):  
Virus Replication ◽  
Vaccine Development ◽  
African Swine Fever Virus ◽  
Clinical Signs ◽  
African Swine Fever ◽  
Viral Persistence ◽  
Fever Virus ◽  
Post Immunization

The limited knowledge on the role of many of the approximately 170 proteins encoded by African swine fever virus restricts progress towards vaccine development. In this study we investigated the effect of deleting combinations of different genes from a previously attenuated virus, BeninΔDP148R on: virus replication in macrophages, virus persistence and clinical signs post immunization, and induction of protection against challenge. Deletion of either EP402R or EP153R genes individually or in combination from BeninΔDP148R did not reduce virus replication in vitro. However, deletion of EP402R dramatically reduced viral persistence in vivo, whilst maintaining high levels of protection against challenge. The additional deletion of EP153R (BeninΔDP148RΔEP153RΔEP402R) further attenuated the virus and no viremia or clinical signs were observed post immunization. This was associated with decreased protection and detection of moderate levels of challenge virus in blood. Interestingly, the deletion of EP153R alone from BeninΔDP148R did not result in further virus attenuation and a slight increase in virus genome copies in blood was observed at different times post immunization when compared with BeninΔDP148R. These results show that EP402R and EP153R have a synergistic role in promoting viremia, however EP153R alone does not seem to have a major impact on virus levels in blood.

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 African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis

2001 ◽  
Vol 75 (21) ◽  
pp. 10372-10382 ◽  
Author(s):  
Isabelle Vallée ◽  
Stephen W. G. Tait ◽  
Penelope P. Powell
Keyword(s):  
Endothelial Cells ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Surface Expression ◽  
Fever Virus ◽  
Parp Cleavage ◽  
Aortic Endothelial Cells ◽  
Porcine Aortic Endothelial Cells ◽  
Aortic Endothelial

ABSTRACT African swine fever (ASF) is an asymptomatic infection of warthogs and bushpigs, which has become an emergent disease of domestic pigs, characterized by hemorrhage, lymphopenia, and disseminated intravascular coagulation. It is caused by a large icosohedral double-stranded DNA virus, African swine fever virus (ASFV), with infection of macrophages well characterized in vitro and in vivo. This study shows that virulent isolates of ASFV also infect primary cultures of porcine aortic endothelial cells and bushpig endothelial cells (BPECs) in vitro. Kinetics of early and late gene expression, viral factory formation, replication, and secretion were similar in endothelial cells and macrophages. However, ASFV-infected endothelial cells died by apoptosis, detected morphologically by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and nuclear condensation and biochemically by poly(ADP-ribose) polymerase (PARP) cleavage at 4 h postinfection (hpi). Immediate-early proinflammatory responses were inhibited, characterized by a lack of E-selectin surface expression and interleukin 6 (IL-6) and IL-8 mRNA synthesis. Moreover, ASFV actively downregulated interferon-induced major histocompatibility complex class I surface expression, a strategy by which viruses evade the immune system. Significantly, Western blot analysis showed that the 65-kDa subunit of the transcription factor NF-κB, a central regulator of the early response to viral infection, decreased by 8 hpi and disappeared by 18 hpi. Both disappearance of NF-κB p65 and cleavage of PARP were reversed by the caspase inhibitor z-VAD-fmk. Interestingly, surface expression and mRNA transcription of tissue factor, an important initiator of the coagulation cascade, increased 4 h after ASFV infection. These data suggest a central role for vascular endothelial cells in the hemorrhagic pathogenesis of the disease. Since BPECs infected with ASFV also undergo apoptosis, resistance of the natural host must involve complex pathological factors other than viral tropism.

scholarly journals An African swine fever virus ORF with similarity to C-type lectins is non-essential for growth in swine macrophages in vitro and for virus virulence in domestic swine

1999 ◽  
Vol 80 (10) ◽  
pp. 2693-2697 ◽  
Author(s):  
J. G. Neilan ◽  
M. V. Borca ◽  
Z. Lu ◽  
G. F. Kutish ◽  
S. B. Kleiboeker ◽  
...  
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Virus Infectivity ◽  
Mrna Transcription ◽  
Host Cell Interactions ◽  
Lectin Family ◽  
Virus Replication Cycle ◽  
Domestic Swine

An African swine fever virus (ASFV) ORF, 8CR, with similarity to the C-type lectin family of adhesion proteins has been described in the pathogenic isolate Malawi Lil-20/1. The similarity of 8CR to cellular and poxvirus genes associated with cell adhesion, cell recognition and virus infectivity suggested that 8CR may be of significance to ASFV–host cell interactions. Sequence analysis of the 8CR ORF from additional pathogenic ASFV isolates demonstrated conservation among isolates from both pig and tick sources. Northern blot analysis demonstrated 8CR mRNA transcription late in the virus replication cycle. A Malawi Lil-20/1 8CR deletion mutant (Δ8CR) was constructed to analyse 8CR function further. The growth characteristics in vitro of Δ8CR in porcine macrophage cell cultures were identical to those observed for parental virus. In domestic swine, Δ8CR exhibited an unaltered parental Malawi Lil- 20/1 disease and virulence phenotype. Thus, although well conserved among pathogenic ASFV field isolates, 8CR is non-essential for growth in porcine macrophages in vitro and for virus virulence in domestic swine.

scholarly journals Salt inactivation of classical swine fever virus and African swine fever virus in porcine intestines confirms the existing in vitro casings model

2019 ◽  
Vol 238 ◽  
pp. 108424 ◽  
Author(s):  
Tinka Jelsma ◽  
Joris J. Wijnker ◽  
Bregtje Smid ◽  
Eline Verheij ◽  
Wim H.M. van der Poel ◽  
...  
Keyword(s):  
Classical Swine Fever Virus ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Classical Swine Fever ◽  
Fever Virus

Polyadenylation, methylation, and capping of the RNA synthesized in vitro by African swine fever virus

Virology ◽  
1981 ◽  
Vol 113 (2) ◽  
pp. 484-491 ◽  
Author(s):  
María L. Salas ◽  
Juan Kuznar ◽  
Eladio Viñuela
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus

scholarly journals EFFECTS OF MODERATELY VIRULENT AFRICAN SWINE FEVER VIRUS ON INTERLEUKIN-10 PRODUCTION

2019 ◽  
pp. 23-28 ◽  
Author(s):  
A. S. Pershin ◽  
I. V. Shevchenko ◽  
A. S. Igolkin ◽  
Ye. V. Aronova ◽  
N. N. Vlasova
Keyword(s):  
Immune Response ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Noticeable Effect ◽  
Specific Antibodies ◽  
Virulent Virus ◽  
Virus Isolates ◽  
Highly Virulent

A characteristic feature of African swine fever virus (ASFV) is the ability to escape from host immune response, affecting macrophages and replicating in them. Besides, ASFV - specific antibodies do not completely neutralize the virus. Cytokines are important factors for various viral infection pathologies. The virulence of ASFV isolates may depend on the capacity to regulate cytokine expression by macrophages. Thus, when comparing in vitro and in vivo cytokine production by macrophages, it was established that infection with low virulent virus isolates leads to an immune response with a predominance of cytokines involved in cellular immunity, such as INF-α and IL-12p40, as compared with infection with highly virulent isolates. The aim of this paper was to study the effect of African swine fever virus on the production of IL-10, a pleiotropic cytokine that inhibits synthesis of cytokines and shows a strong antiinflammatory effect. For this, 12 piglets were experimentally infected intramuscularly with a continuous cell culture-adapted ASFV isolate Vero25 at a dose of 10 HAdU per animal followed by control infection of surviving animals with the reference virus isolate Arm 07 at a dose of 1,000 HAdU per animal. Temperature measurements were taken and blood sampling to obtain serum was conducted during the experiment. IL-10 amount in blood sera was determined using Invitrogen test systems (Thermo Fisher, USA). A higher IL-10 level (15.8–173 pg/ml) was observed in blood sera of dead animals infected with a moderately virulent virus, as compared with surviving pigs (4–5 pg/ml). No correlation between the speed of appearance of specific antibodies and IL-10 serum levels has been established. No noticeable effect of the IL-10 serum level prior to infection on the survival rate of animals has been observed. Further studies are needed to establish a causal relationship, including study of the expression of various cytokines during infection with both low- and highly virulent virus isolates.

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