Reemergence of African Swine Fever in Zimbabwe, 2015.
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ABSTRACT:
SUBMITTER: van Heerden J
PROVIDER: S-EPMC5403036 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:In Poland, African swine fever (ASF) emerged in February 2014; by August 2015, the virus had been detected in >130 wild boar and in pigs in 3 backyard holdings. We evaluated ASF spread in Poland during these 18 months. Phylogenetic analysis indicated repeated incursions of genetically distinct ASF viruses of genotype II; the number of cases positively correlated wild boar density; and disease spread was very slow. More cases were reported during summer than autumn. The 18-month prevalence of ASF in areas under various animal movement restrictions was 18.6% among wild boar found dead or killed by vehicles and only 0.2% in hunted wild boar. Repeated introductions of the virus into the country, the primary role of wild boar in virus maintenance, and the slow spread of the disease indicate a need for enhanced biosecurity at pig holdings and continuous and intensive surveillance for fast detection of ASF.
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Project description:In September 2018, classical swine fever reemerged in Japan after 26 years, affecting domestic pigs and wild boars. The causative virus belongs to the 2.1 subgenotype, which caused repeated outbreaks in eastern and Southeast Asia. Intensive surveillance of swine and vaccination of wild boars will help control and eradicate this disease in Japan.
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Project description:BACKGROUND:African swine fever (ASF) is a highly fatal viral hemorrhagic disease of domestic pigs that threatens livelihoods and food security. In Africa, ASF virus (ASFV) circulates in sylvatic (transmission between warthogs and soft argasid ticks) and domestic (transmission between domestic pigs) cycles, with outbreaks resulting from ASFV spill-over from sylvatic cycle. A number of outbreaks were reported in different parts of Tanzania between 2015 and 2017. The present study investigated ASFV transmission patterns through viral DNA sequencing and phylogenetic analysis. A total of 3120 tissue samples were collected from 2396 domestic pigs during outbreaks at different locations in Tanzania between 2015 and 2017. Partial sequencing of the B646L (p72) gene was conducted for diagnostic confirmation and molecular characterization of ASFV. Phylogenetic analysis to study the relatedness of current ASFV with those that caused previous outbreaks in Tanzania and representatives of all known 24 ASFV was performed using the Maximum Composite Likelihood model with 1000 bootstrap replications in MEGA 6.0. RESULTS:ASFV was confirmed to cause disease in sampled domestic pigs. ASFV genotypes II, IX, and X were detected from reported outbreaks in 2015-2017. The current ASFV isolates were similar to those recently documented in the previous studies in Tanzania. The similarities of these isolates suggests for continuous circulation of ASFV with virus maintenance within the domestic pigs. CONCLUSIONS:Genetic analysis confirmed the circulation of ASFV genotypes II, IX, and X by partial B646L (p72) gene sequencing. The similarities of current isolates to previously isolated Tanzanian isolates and pattern of disease spread suggest for continuous circulation of ASF with virus' maintenance in the domestic pigs. Although certain viral genotypes seem to be geographically restricted into certain zones within Tanzania, genotype II seems to expand its geographical range northwards with the likelihood of spreading to other states of the East African Community. The spread of ASFV is due to breach of quarantine and transportation of infected pigs via major highways. Appropriate control measures including zoosanitary measures and quarantine enforcement are recommended to prevent ASF domestic circulation in Tanzania.
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Project description:In early 2015, a highly fatal haemorrhagic disease of domestic pigs resembling African swine fever (ASF) occurred in North Western, Copperbelt, and Lusaka provinces of Zambia. Molecular diagnosis by polymerase chain reaction targeting specific amplification of p72 (B646L) gene of ASF virus (ASFV) was conducted. Fourteen out of 16 domestic pigs from the affected provinces were found to be positive for ASFV. Phylogenetic analyses based on part of the p72 and the complete p54 (E183L) genes revealed that all the ASFVs detected belonged to genotypes I and Id, respectively. Additionally, epidemiological data suggest that the same ASFV spread from Lusaka to other provinces possibly through uncontrolled and/or illegal pig movements. Although the origin of the ASFV that caused outbreaks in domestic pigs in Zambia could not be ascertained, it appears likely that the virus may have emerged from within the country or region, probably from a sylvatic cycle. It is recommended that surveillance of ASF, strict biosecurity, and quarantine measures be imposed in order to prevent further spread and emergence of new ASF outbreaks in Zambia.
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Project description:Recently moderate-virulence classical swine fever virus (CSFV) strains have been proven capable of generating postnatal persistent infection (PI), defined by the maintenance of viremia and the inability to generate CSFV-specific immune responses in animals. These animals also showed a type I interferon blockade in the absence of clinical signs. In this study, we assessed the infection generated in 7-week-old CSFV PI wild boars after infection with the African swine fever virus (ASFV). The wild boars were divided in two groups and were infected with ASFV. Group A comprised boars who were CSFV PI in a subclinical form and Group B comprised pestivirus-free wild boars. Some relevant parameters related to CSFV replication and the immune response of CSFV PI animals were studied. Additionally, serum soluble factors such as IFN-α, TNF-α, IL-6, IL-10, IFN-γ and sCD163 were analysed before and after ASFV infection to assess their role in disease progression.After ASFV infection, only the CSFV PI wild boars showed progressive acute haemorrhagic disease; however, the survival rates following ASFV infection was similar in both experimental groups. Notwithstanding, the CSFV RNA load of CSFV PI animals remained unaltered over the study; likewise, the ASFV DNA load detected after infection was similar between groups. Interestingly, systemic type I FN-α and IL-10 levels in sera were almost undetectable in CSFV PI animals, yet detectable in Group B, while detectable levels of IFN-γ were found in both groups. Finally, the flow cytometry analysis showed an increase in myelomonocytic cells (CD172a+) and a decrease in CD4+ T cells in the PBMCs from CSFV PI animals after ASFV infection.Our results showed that the immune response plays a role in the progression of disease in CSFV subclinically infected wild boars after ASFV infection, and the immune response comprised the systemic type I interferon blockade. ASFV does not produce any interference with CSFV replication, or vice versa. ASFV infection could be a trigger factor for the disease progression in CSFV PI animals, as their survival after ASFV was similar to that of the pestivirus-free ASFV-infected group. This fact suggests a high resistance in CSFV PI animals even against a virus like ASFV; this may mean that there are relevant implications for CSF control in endemic countries. The diagnosis of ASFV and CSFV co-infection in endemic countries cannot be ruled out and need to be studied in greater depth.
| S-EPMC5540480 | biostudies-other
Project description:In field studies and carefully controlled artificial infections, there is host variation in response to ASF infections. To better understand the mechanisms underlying this diversity and distinguish between resilient and susceptible pigs to African Swine Fever (ASF), the differentially expressed genes (DEGs) were studied between the recovered versus non-recovered pigs before and after an infection challenge and also among non-recovered animals over time. In total, 17 Babraham pigs were sampled. Twelve animals were randomly immunized with low virulent ASFV isolate, and the others received the sham vaccine. All animals were then challenged with the virulent ASFV isolate 18 days after the immunization. Except for five animals, all showed clinical signs and dead between 4 and 6 days later. RNA sequencing was done for whole blood samples collected pre-infection, one day, and one week post-infection.
2023-02-17 | E-MTAB-12608 | biostudies-arrayexpress
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