African swine fever virus (ASFV) was first reported in eastern Europe/Eurasia in 2007. Continued spread of ASFV has placed central European countries at risk, and in 2014, ASFV was detected in Lithuania and Poland. Sequencing showed the isolates are identical to a 2013 ASFV from Belarus but differ from ASFV isolated in Georgia in 2007.
A frican swine fever (ASF) is a complex and lethal viral disease affecting swine and has a significant socioeconomic impact on both the developed and developing world. It has a major negative effect on national, regional, and international trade and constrains pig production in affected areas. The devastating acute form of the disease is characterized, among other features, by functional and congestive-hemorrhagic disorders of the digestive and respiratory systems and causes around 100% mortality in infected pigs (1). Both European wild boars (Sus scrofa) and feral pigs are susceptible and exhibit clinical signs and mortality rates similar to those of domestic pigs. In contrast, African wild pigs (Phacochoerus and Potamochoerus spp.) are resistant to the disease (2-10).The causative agent of the disease, the ASF virus (ASFV), is a large double-stranded DNA virus and the only member of the Asfarviridae family, genus Asfivirus (11, 12). The virus genome is 170 to 192 kb long (13-17). ASF is endemic in sub-Saharan Africa, where it was first described in 1921 (18). Several outbreaks have occurred since then in Europe and South and Central America. In most non-African countries, the disease has been successfully eradicated, the only exception being Sardinia (Italy), where the disease is still endemic (19,20). In April 2007, the disease spread from East Africa to the Republic of Georgia (21), and outbreaks occurred in Armenia, Azerbaijan, and the Russian Federation (22). The ongoing spread of ASFV into adjacent eastern European countries, such as Ukraine (23,24) and Belarus (25), and the situation in Russia affecting both wild boars and domestic pigs placed neighboring areas in the European Union (EU) at risk for the spread of ASFV. The first cases of ASF in wild boars in Lithuania and Poland were reported in early 2014 in areas bordering . According to the World Organisation for Animal Health (OIE), during 2014, nearly 260 ASF cases or outbreaks in wild boars and domestic pigs were detected in EU countries (Latvia, Lithuania, Estonia, and Poland). This situation, combined with the uncertainty present in Belarus, has created a permanent risk of reintroducing ASF into the EU via wild boars or the illegal trade of contaminated pork products and waste (31).No vaccine is available to prevent ASF infection. The control and eradication measures applicable are based on classical disease control methods, including surveillance, epidemiological investigation, tracing of pigs, and stamping out in infected holdings. Citation Gallardo C, Nieto R, Soler A, Pelayo V, Fernández-Pinero J, MarkowskaDaniel I, Pridotkas G, Nurmoja I, Granta R, Simón A, Pérez C, Martín E, Fernández-Pacheco P, Arias M. 2015. Assessment of African swine fever diagnostic techniques as a response to the epidemic outbreaks in eastern European Union countries: how to improve surveillance and control programs.
An experimental infection was conducted to evaluate horizontal transmission, clinical, virological and humoral response induced in domestic pigs infected with African swine fever (ASF) genotype II virus circulating in 2014 into the European Union (EU). Ten naive pigs were placed in contact with eight pigs experimentally inoculated with the Lithuanian LT14/1490 ASF virus (ASFV) responsible for the first ASF case detected in wild boar in Lithuania in January 2014. Clinical examination and rectal temperature were recorded each day. Blood sampling from every animal was carried out twice weekly. Blood samples were examined for presence of ASF virus-specific antibodies and for determining the ASFV viral load. From the obtained results, it was concluded that the Lithuanian ASFV induced an acute disease which resulted in 94, 5% mortality. The disease was easily detected by real-time PCR prior to the onset of clinical signs and 33% of the animals seroconverted. All findings were in accordance with observations previously made in domestic pigs and wild boar when infected with ASF genotype II viruses characterized by a high virulence. One in-contact pig remained asymptomatic and survived the infection. The role of such animals in virus transmission would need further investigation.
African swine fever (ASF) is a lethal haemorrhagic disease of domestic pigs for which there is no vaccine. Strains of the virus with reduced virulence can provide protection against related virulent strains of ASFV, but protection is not 100% and there are concerns about the safety profile of such viruses. However, they provide a useful tool for understanding the immune response to ASFV and previous studies using the low virulent isolate OUR T88/3 have shown that CD8+ cells are crucial for protection. In order to develop a vaccine that stimulates an effective anti-ASFV T-cell response we need to know which of the >150 viral proteins are recognized by the cellular immune response. Therefore, we used a gamma interferon ELIspot assay to screen for viral proteins recognized by lymphocytes from ASF-immune pigs using peptides corresponding to 133 proteins predicted to be encoded by OUR T88/3. Eighteen antigens that were recognized by ASFV-specific lymphocytes were then incorporated into adenovirus and MVA vectors, which were used in immunization and challenge experiments in pigs. We present a systematic characterization of the cellular immune response to this devastating disease and identify proteins capable of inducing ASFV-specific cellular and humoral immune responses in pigs. Pools of viral vectors expressing these genes did not protect animals from severe disease, but did reduce viremia in a proportion of pigs following ASFV challenge.
A non‐haemadsorbing (non‐HAD) ASF virus (ASFV) genotype II, namely Lv17/WB/Rie1, was isolated from a hunted wild boar in Latvia in 2017. Domestic pigs experimentally infected with the non‐HAD ASFV developed a nonspecific or subclinical form of the disease. Two months later, these animals were fully protected when exposed to other domestic pigs infected with a related virulent HAD genotype II ASFV.
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