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Knowledge about African swine fever virus (ASFV) transmission and its survival in the environment is mandatory to develop rational control strategies and combat this serious disease in pigs. In this study, the risk that environmental contamination poses for infection of naïve pigs was investigated. Naïve pigs were introduced as sentinels into contaminated pens kept at ambient temperature (about 18–22˚C) either on the same day or up to 3 days after ASFV-infected pigs were removed. Three experiments were carried out in which four to six pigs per pen were inoculated with virulent ASFV isolates OURT88/1 (genotype I), Georgia 2007/1, or POL/2015/Podlaskie (genotype II), respectively. The majority of the inoculated pigs developed acute disease but with no evident haemorrhagic lesions or haemorrhagic diarrhoea and were culled at the predefined humane endpoint. The levels of ASFV DNA detected in the blood of the infected animals reached 107−9 genome copies/ml before euthanasia. Environmental swabs were taken from different surfaces in the animal rooms, as well as from faeces and urine, close to the time of introduction of the naïve animals. Relatively low quantities of virus DNA were detected in the environmental samples, in the range of 103−7 genome copies per swab or per gram and ml of faeces and urine. No infectious virus was recovered from these environmental samples. Neither clinical signs nor virus genomes were detected in the blood of any of the sentinel pigs over a period of 2 to 3 weeks after exposure, indicating that transmission from the ASFV-contaminated environment did not occur. Interestingly, viral DNA was detected in nasal and oral swabs from some of the sentinel animals at early days of exposure (ranging between 103.7−5.8 genome copies per swab), though none of them developed ASF. The results indicate a relatively low risk of ASFV transmission from a contaminated environment under the conditions provided in these experimental studies and in the absence of b

African swine fever virus (ASFV) is known to be very stable and can remain infectious over long periods of time especially at low temperatures and within different matrices, particularly those containing animal-derived organic material. However, there are some gaps in our knowledge pertaining to the survivability and infectivity of ASFV in groundwater. This study aims to determine the stability and infectivity of the cell culture-adapted ASFV strain BA71V by plaque assay after incubation of the virus within river water samples at three different environmentally relevant temperatures (4 °C, 15 °C, and 21 °C) over the course of 42 days. The results from this study indicate that ASFV can remain stable and infectious when maintained at 4 °C in river water for more than 42 days, but as incubation temperatures are increased, the stability is reduced, and the virus is no longer able to form plaques after 28 days and 14 days, respectively, when stored at 15 °C and 21 °C. Characterizing the survivability of ASFV in groundwater can allow us to develop more appropriate inactivation and disinfection methods to support disease control and mitigate ASFV outbreaks.

Infection with African swine fever virus (ASFV) leads to a short haemorrhagic course of disease that, depending on the virus isolate, results in up to 100% lethality in domestic and Eurasian wild pigs. Consequently, ASFV infection in swine is of considerable economic significance. This chapter explains the basics of antiviral immunity in swine, focusing on the ‘knowns’ and ‘unknowns’ of the response against ASFV. In particular, monocytes and macrophages play an essential role as the main targets of infection and are crucial in viral persistence and dissemination. Furthermore,ASFV has developed several mechanisms to influence the antiviral and cell biological activity of infected monocytes, including down-regulation of cell surface receptors (e.g. CD14 and MHC-I) and modulation of interferon and cytokine/chemokine responses. ASFV infected pigs also develop virus-specific antibodies that can be used diagnostically, and while the neutralising effect of these antibodies has led to their involvement in protective immunity being controversially discussed, they may still exhibit protective functions through complement-mediated lysis and/or antibody dependent cell-mediated cytotoxicity. Indeed, T cells (presumably CD8+) also play a central role in the elimination of the virus, as can be seen in experiments where, after depletion of these cells, pigs previously primed with an avirulent ASFV become ill, while non-depleted animals are protected from highly virulent challenge. Nonetheless, despite these advances in our knowledge, much remains unknown about antiviral immunity generated during the course of a natural ASFV infection, or in response to attenuated virus strains or immunisation. Although such studies would undoubtedly be technically challenging, a deeper understanding of the immunity developed by the natural hosts (i.e. bushpigs and warthogs) against ASFV infection would teach us a lot about an effective protection from ASFV infection, and the involvement of both the

Classical approaches to African swine fever virus (ASFV) vaccine development have not been successful; inactivated virus does not provide protection and use of live attenuated viruses generated by passage in tissue culture had a poor safety profile. Current African swine fever (ASF) vaccine research focuses on the development of modified live viruses by targeted gene deletion or subunit vaccines. The latter approach would be differentiation of vaccinated from infected animals (DIVA)-compliant, but information on which viral proteins to include in a subunit vaccine is lacking. Our previous work used DNA-prime/vaccinia-virus boost to screen 40 ASFV genes for immunogenicity, however this immunization regime did not protect animals after challenge. Here we describe the induction of both antigen and ASFV-specific antibody and cellular immune responses by different viral-vectored pools of antigens selected based on their immunogenicity in pigs. Immunization with one of these pools, comprising eight viral-vectored ASFV genes, protected 100% of pigs from fatal disease after challenge with a normally lethal dose of virulent ASFV. This data provide the basis for the further development of a subunit vaccine against this devastating disease.