scholarly journals Successful Infection of Domestic Pigs by Ingestion of the European Soft Tick O. Erraticus That Fed on African Swine Fever Virus Infected Pig

Viruses ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 300 ◽  
Author(s):  
Rémi Pereira De Oliveira ◽  
Evelyne Hutet ◽  
Maxime Duhayon ◽  
Jean-Marie Guionnet ◽  
Frédéric Paboeuf ◽  
...  

African swine fever is a highly lethal hemorrhagic fever of Suidae, threatening pig production globally. Suidae can be infected by different ways like ingestion of contaminated feed, direct contact with infected animals or fomites, and biting by infected soft tick bites. As already described, European soft ticks (Ornithodoros erraticus and Ornithodoros verrucosus) were not able to transmit African swine fever virus by biting pigs although these ticks maintained the infectious virus during several months; therefore, the possibility for pigs to become infected through the ingestion of infected ticks was questioned but not already explored. To determine if such oral ingestion is an alternative pathway of transmission, O. erraticus ticks were infected by blood-feeding on a viremic pig infected with the European African swine fever virus strain Georgia2007/1, then frozen at zero and two months post-engorgement, then after, were embedded in the food to pigs. Pig infection was successful, with superior efficiency with ticks frozen just after the infectious blood meal. These results confirmed the potential role of O. erraticus ticks as an ASFV reservoir and demonstrated the efficiency of non-conventional pathways of transmission.

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 757
Author(s):  
Sandra Barroso-Arévalo ◽  
Jose A. Barasona ◽  
Estefanía Cadenas-Fernández ◽  
José M. Sánchez-Vizcaíno

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.


2021 ◽  
Author(s):  
Vlad Petrovan ◽  
Anusyah Rathakrishnan ◽  
Muneeb Islam ◽  
Lynnette Goatley ◽  
Katy Moffat ◽  
...  

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.


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 ◽  
...  

2010 ◽  
Vol 84 (15) ◽  
pp. 7484-7499 ◽  
Author(s):  
Cristina Suárez ◽  
Javier Gutiérrez-Berzal ◽  
Germán Andrés ◽  
María L. Salas ◽  
Javier M. Rodríguez

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.


1991 ◽  
Vol 3 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Adilia dos Santos Ribelro ◽  
Mário Passalaqua Arala-Chaves ◽  
Manuel Vilanova ◽  
Maria Teresa Porto ◽  
Antonio Coutinho

2021 ◽  
Author(s):  
Vlad Petrovan ◽  
Anusyah Rathakrishnan ◽  
Muneeb Islam ◽  
Lynnette C. Goatley ◽  
Katy Moffat ◽  
...  

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.


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