scholarly journals No evidence of African swine fever virus replication in hard ticks

2014 ◽  
Vol 5 (5) ◽  
pp. 582-589 ◽  
Author(s):  
Helena C. de Carvalho Ferreira ◽  
Sara Tudela Zúquete ◽  
Michiel Wijnveld ◽  
Eefke Weesendorp ◽  
Frans Jongejan ◽  
...  
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.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Alexandra Hübner ◽  
Bjoern Petersen ◽  
Günther M. Keil ◽  
Heiner Niemann ◽  
Thomas C. Mettenleiter ◽  
...  

2019 ◽  
Vol 270 ◽  
pp. 197667 ◽  
Author(s):  
Margarida Simões ◽  
Ferdinando B. Freitas ◽  
Alexandre Leitão ◽  
Carlos Martins ◽  
Fernando Ferreira

Viruses ◽  
2017 ◽  
Vol 9 (6) ◽  
pp. 133 ◽  
Author(s):  
Miguel Cuesta-Geijo ◽  
Lucía Barrado-Gil ◽  
Inmaculada Galindo ◽  
Raquel Muñoz-Moreno ◽  
Covadonga Alonso

2019 ◽  
Vol 24 (1) ◽  
pp. 180 ◽  
Author(s):  
Ze Chen ◽  
Xiaofeng Xu ◽  
Yufeng Wang ◽  
Jinlong Bei ◽  
Xiufeng Jin ◽  
...  

In this study, we detected African Swine Fever Virus (ASFV) in Dermacentor (Ixodidae) from sheep and bovines using small RNA sequencing. To validate this result, a 235-bp DNA segment was detected in a number of DNA samples from D. silvarum and sheep blood. This 235-bp segment had an identity of 99% to a 235-bp DNA segment of ASFV and contained three single nucleotide mutations (C38T, C76T and A108C). C38T, resulting in a single amino acid mutation G66D, suggests the existence of a new ASFV strain, which is different from all reported ASFV strains in the NCBI GenBank database and the ASFV strain (GenBank: MH713612.1) reported in China in 2018. To further confirm the existence of ASFV in Dermacentor ticks, three DNA segments of ASFV were detected in D. niveus females from bovines and their first generation ticks reared in our lab. These results also proved that transovarian transmission of ASFV occurs in hard ticks. This study revealed for the first time that ASFV has a wider range of hosts (e.g. sheep and bovines) and vectors (e.g. hard ticks), beyond the well-known Suidae family and Argasidae (soft ticks). Our findings pave the way toward further studies on ASFV transmission and the development of prevention and control measures.


Viruses ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 241 ◽  
Author(s):  
Linda Dixon ◽  
Pedro Sánchez-Cordón ◽  
Inmaculada Galindo ◽  
Covadonga Alonso

2018 ◽  
Author(s):  
Ze Chen ◽  
Xiaofeng Xu ◽  
Xiaojun Yang ◽  
Weihao Dou ◽  
Xiufeng Jin ◽  
...  

In this study, we aimed to detect viruses in hard ticks using the small RNA sequencing based method. A 235-bp DNA segment was detected in Dermacentor nuttalli (hard ticks) and D. silvarum (hard ticks) from sheep and bovine, respectively. The detected 235-bp segment had an identity of 99% to a 235-bp DNA segment of African Swine Fever Virus (ASFV) and contained three single nucleotide mutations (C38T, C76T and A108C). C38T, resulting in an single amino acid mutation G66D, suggests the existence of a new ASFV strain, which is different from all reported ASFV strains in NCBI GenBank database. These results also suggest that ASFV could have a wide range of hosts or vectors, beyond the well known Suidae family and soft ticks. Our findings pave the way toward further studies of ASFV transmission and development of prevention and control measures.


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