ASF -survivors’ sera do not inhibit African swine fever virus replication in vitro
African swine fever virus (ASFV) causes one of the most dangerous diseases of pigs and wild boar - African swine fever (ASF). Since its second introduction into Europe (in 2007), the disease has been spreading consistently, and now ASF-free European countries are at risk. Complex interactions betwee...
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Veröffentlicht in: | Journal of veterinary research 2022-03, Vol.66 (1), p.21-27 |
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Sprache: | eng |
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Zusammenfassung: | African swine fever virus (ASFV) causes one of the most dangerous diseases of pigs and wild boar - African swine fever (ASF). Since its second introduction into Europe (in 2007), the disease has been spreading consistently, and now ASF-free European countries are at risk. Complex interactions between the host's immune system and the virus have long prevented the development of a safe vaccine against ASF. This study analysed the possibility of neutralisation of the ASFV
by sera collected from ASF-survivor animals.
Two pig and three wild boar serum samples were collected from previously selected potential ASF survivors. All sera presented high antibody titres (>5 log
/mL). Primary alveolar macrophages were cultured in growth medium containing 10% and 20% concentrations of selected sera and infected with a haemadsorbing ASFV strain (Pol18_28298_O111, genotype II). The progress of infection was investigated under a light microscope by observing the cytopathic effect (CPE) and the haemadsorption phenomenon. Growth kinetics were investigated using a real-time PCR assay.
Haemadsorption inhibition was detected in the presence of almost all selected sera; however, the inhibition of virus replication
was excluded. In all samples, a CPE and decreasing quantification cycle values of the viral DNA were found.
Anti-ASFV antibodies alone are not able to inhibit virus replication. Interactions between the humoral and cellular immune response which effectively combat the disease are implicated in an ASF-survivor's organism. |
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ISSN: | 2450-7393 2450-8608 2450-8608 |
DOI: | 10.2478/jvetres-2022-0016 |