Role of B and T lymphocytes in the specific immunosuppression induced by a protein released by a protein monocytes infected with African swine fever virus

1991 ◽  
Vol 3 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Adilia dos Santos Ribelro ◽  
Mário Passalaqua Arala-Chaves ◽  
Manuel Vilanova ◽  
Maria Teresa Porto ◽  
Antonio Coutinho
Keyword(s):  
T Lymphocytes ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
B And T Lymphocytes ◽  
Specific Immunosuppression

scholarly journals The Role of Interleukine-10 and Interferon-γ as Potential Markers of the Evolution of African Swine Fever Virus Infection in Wild Boar

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 757
Author(s):  
Sandra Barroso-Arévalo ◽  
Jose A. Barasona ◽  
Estefanía Cadenas-Fernández ◽  
José M. Sánchez-Vizcaíno
Keyword(s):  
Wild Boar ◽  
Vaccine Candidate ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Interferon Γ ◽  
Fever Virus ◽  
Control Group ◽  
Challenge Virus ◽  
Ifn Γ

African swine fever virus (ASFv) is one of the most challenging pathogens to affect both domestic and wild pigs. The disease has now spread to Europe and Asia, causing great damage to the pig industry. Although no commercial vaccine with which to control the disease is, as yet, available, some potential vaccine candidates have shown good results in terms of protection. However, little is known about the host immune mechanisms underlying that protection, especially in wild boar, which is the main reservoir of the disease in Europe. Here, we study the role played by two cytokines (IL-10 and IFN-γ) in wild boar orally inoculated with the attenuated vaccine candidate Lv17/WB/Rie1 and challenged with a virulent ASFv genotype II isolate. A group of naïve wild boar challenged with the latter isolate was also established as a control group. Our results showed that both cytokines play a key role in protecting the host against the challenge virus. While high levels of IL-10 in serum may trigger an immune system malfunctioning in challenged animals, the provision of stable levels of this cytokine over time may help to control the disease. This, together with high and timely induction of IFN-γ by the vaccine candidate, could help protect animals from fatal outcomes. Further studies should be conducted in order to support these preliminary results and confirm the role of these two cytokines as potential markers of the evolution of ASFV infection.

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 Antiviral Role of IFITM Proteins in African Swine Fever Virus Infection

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0154366 ◽  
Author(s):  
Raquel Muñoz-Moreno ◽  
Miguel Ángel Cuesta-Geijo ◽  
Carles Martínez-Romero ◽  
Lucía Barrado-Gil ◽  
Inmaculada Galindo ◽  
...  
Keyword(s):  
Virus Infection ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Antiviral Role

scholarly journals African Swine Fever Virus Protein p17 Is Essential for the Progression of Viral Membrane Precursors toward Icosahedral Intermediates

2010 ◽  
Vol 84 (15) ◽  
pp. 7484-7499 ◽  
Author(s):  
Cristina Suárez ◽  
Javier Gutiérrez-Berzal ◽  
Germán Andrés ◽  
María L. Salas ◽  
Javier M. Rodríguez
Keyword(s):  
Early Stage ◽  
African Swine Fever Virus ◽  
Transmembrane Protein ◽  
African Swine Fever ◽  
Integral Membrane Protein ◽  
Proteolytic Processing ◽  
Fever Virus ◽  
Morphological Evidence ◽  
Virus Protein

ABSTRACT The first morphological evidence of African swine fever virus (ASFV) assembly is the appearance of precursor viral membranes, thought to derive from the endoplasmic reticulum, within the assembly sites. We have shown previously that protein p54, a viral structural integral membrane protein, is essential for the generation of the viral precursor membranes. In this report, we study the role of protein p17, an abundant transmembrane protein localized at the viral internal envelope, in these processes. Using an inducible virus for this protein, we show that p17 is essential for virus viability and that its repression blocks the proteolytic processing of polyproteins pp220 and pp62. Electron microscopy analyses demonstrate that when the infection occurs under restrictive conditions, viral morphogenesis is blocked at an early stage, immediately posterior to the formation of the viral precursor membranes, indicating that protein p17 is required to allow their progression toward icosahedral particles. Thus, the absence of this protein leads to an accumulation of these precursors and to the delocalization of the major components of the capsid and core shell domains. The study of ultrathin serial sections from cells infected with BA71V or the inducible virus under permissive conditions revealed the presence of large helicoidal structures from which immature particles are produced, suggesting that these helicoidal structures represent a previously undetected viral intermediate.

scholarly journals Role of African swine fever virus (ASFV) proteins EP153R and EP402R in reducing viral persistence in blood and virulence in pigs infected with BeninΔDP148R

2021 ◽  
Author(s):  
Vlad Petrovan ◽  
Anusyah Rathakrishnan ◽  
Muneeb Islam ◽  
Lynnette C. Goatley ◽  
Katy Moffat ◽  
...  
Keyword(s):  
Vaccine Development ◽  
African Swine Fever Virus ◽  
Clinical Signs ◽  
African Swine Fever ◽  
Fever Virus ◽  
Genotype I ◽  
Virus Persistence ◽  
Challenge Virus

The limited knowledge on the role of many of the approximately 170 proteins encoded by African swine fever virus restricts progress towards vaccine development. Previously, the DP148R gene was deleted from the genome of genotype I virulent Benin 97/1 isolate. This virus, BeninΔDP148R, induced transient moderate clinical signs after immunization and high levels of protection against challenge. However, the BeninΔDP148R virus and genome persisted in blood over a prolonged period. In the current study deletion of either EP402R or EP153R genes individually or in combination from BeninΔDP148R genome was shown not to reduce virus replication in macrophages in vitro. However, deletion of EP402R dramatically reduced the period of infectious virus persistence in blood in immunized pigs from 28 to 14 days and virus genome from 59 to 14 days, 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 did not reduce the period of virus persistence in blood. These results show that EP402R and EP153R have a synergistic role in reducing clinical signs and levels of virus in blood. Importance: African swine fever virus (ASFV) causes a disease of domestic pigs and wild boar which results in death of almost all infected animals. The disease has a high economic impact, and no vaccine is available. We investigated the role of two ASFV proteins, called EP402R and EP153R, in determining the levels and length of time virus persists in blood from infected pigs. EP402R causes ASFV particles and infected cells to bind to red blood cells. Deletion of the EP402R gene dramatically reduced virus persistence in blood but did not reduce the level of virus. Deletion of the EP153R alone did not reduce the period or level of virus persistence in blood. However, deleting both EP153R and EP402R resulted in undetectable levels of virus in blood and no clinical signs showing the proteins act synergistically. Importantly the infected pigs were protected following infection with the wildtype virus that kills pigs.

African swine fever virus-specific cytotoxic T lymphocytes recognize the 32 kDa immediate early protein (vp32)

1997 ◽  
Vol 49 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Fernando Alonso ◽  
Javier Domı́nguez ◽  
Eladio Viñuela ◽  
Yolanda Revilla
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Immediate Early ◽  
Early Protein

scholarly journals In vivo depletion of CD8+ T lymphocytes abrogates protective immunity to African swine fever virus

2005 ◽  
Vol 86 (9) ◽  
pp. 2445-2450 ◽  
Author(s):  
C. A. L. Oura ◽  
M. S. Denyer ◽  
H. Takamatsu ◽  
R. M. E. Parkhouse
Keyword(s):  
Immune Response ◽  
T Lymphocytes ◽  
Protective Immunity ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Protective Immune Response ◽  
Fever Virus ◽  
Specific Role ◽  
Cd8 T Lymphocytes

To understand the mechanisms involved in protective immunity to African swine fever virus (ASFV) infection, the observation that infection with the avirulent Portuguese ASFV isolate OUR/T88/3 protects outbred pigs from challenge with the virulent Portuguese ASFV isolate OUR/T88/1 was exploited. It was demonstrated that pigs exposed to OUR/T88/3 and then depleted of CD8+ lymphocytes were no longer fully protected from OUR/T88/1 challenge. This indicated that CD8+ lymphocytes play an important role in the protective immune response to ASFV infection and that anti-ASFV antibody alone, from OUR/T88/3 infection, was not sufficient to protect pigs from OUR/T88/1 challenge. Inbred pigs of the cc haplotype infected with OUR/T88/3 were not always protected from OUR/T88/1 challenge and developed both viraemia and fever. Such viraemia was always correlated with increased numbers of circulating CD8β + lymphocytes, indicating a specific role for CD8β + lymphocytes in combating viraemia. These experiments indicate an important role for CD8+ lymphocytes, particularly CD8β + lymphocytes, in ASF protective immunity.

scholarly journals Inhibition of Apoptosis by the African Swine Fever Virus Bcl-2 Homologue: Role of the BH1 Domain

Virology ◽  
1997 ◽  
Vol 228 (2) ◽  
pp. 400-404 ◽  
Author(s):  
Yolanda Revilla ◽  
Ana Cebrián ◽  
Elena Baixerás ◽  
Carlos Martı́nez-A ◽  
Eladio Viñuela ◽  
...  
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus

Assembly of African swine fever virus: role of polyprotein pp220.

1997 ◽  
Vol 71 (3) ◽  
pp. 2331-2341 ◽  
Author(s):  
G Andrés ◽  
C Simón-Mateo ◽  
E Viñuela
Keyword(s):  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus

scholarly journals Inhibition of BET family proteins suppresses African swine fever virus infection

2021 ◽  
Author(s):  
Qingli Niu ◽  
Yaru Zhao ◽  
Saixia Yang ◽  
Jifei Yang ◽  
Zhonghui Zhang ◽  
...  
Keyword(s):  
Viral Infection ◽  
Gene Transcription ◽  
Epigenetic Regulation ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Effective Control ◽  
Viral Gene ◽  
And Control

African swine fever (ASF), an acute, severe, highly contagious disease caused by African swine fever virus (ASFV) infection in domestic pigs and boars, has a mortality rate of up to 100%. Because effective vaccines and treatments for ASF are lacking, effective control of the spread of ASF remains a great challenge for the pig industry. Host epigenetic regulation is essential for the viral gene transcription. Bromodomain and extraterminal (BET) family proteins, including BRD2, BRD3, BRD4, and BRDT, are epigenetic "readers" critical for gene transcription regulation. Among these proteins, BRD4 recognizes acetylated histones via its two bromodomains (BD1 and BD2) and recruits transcription factors, thereby playing a pivotal role in transcriptional regulation and chromatin remodeling during viral infection. However, how BET/BRD4 regulates ASFV replication and gene transcription is unknown. Here, we randomly selected 12 representative BET family inhibitors and compared their effects on ASFV infection in pig’s primary alveolar macrophages (PAMs). They were found to inhibit viral infection by interfering with the different stages of viral life cycle (attachment, internalization, desencapsidation and formation of viral factories). The four most effective inhibitors (ARV-825, ZL0580, I-BET-762 and PLX51107) were selected for further antiviral activity analysis. These BET/BRD4 inhibitors dose-dependently decreased the ASFV titer, viral RNA transcription and protein production in PAMs. Collectively?our study reported novel activity of BET/BRD4 inhibitors in inducing suppression of ASFV infection, providing insights into role of BET/BRD4 in epigenetic regulation of ASFV and potential new strategies for ASF prevention and control.

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