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Introduction
African Swine Fever (ASF) remains a major threat to wild and domestic
pig populations . The causative agent, ASF virus (ASFV), is a large
dsDNA virus and the only member in the genus Asfivirus of theAsfarviridae family . In its geographic origin in sub-Saharan
Africa, ASFV is transmitted by soft ticks of the Ornithodorosgenus and circulates in other members of the Suidae , warthogs
(Phacochoerus africanus ) and bushpigs (Potamochoerus
larvatus ) . While ASFV infection causes major disease in domestic pigs
and wild boar with profound manifestations and high lethality, it is
clinically inapparent in its reservoir hosts, i.e., African wild suids .
In European and Asian countries, the abundant wild boar populations
serve as a reservoir for ASFV and present a risk for ASFV introduction
into domestic pig holdings . Its near-global panzootic spread already
caused death of millions of pigs in commercial and private farms and
also led to major economic challenges .
At present, little is known about the role of the host’s immune response
against ASFV. Once infection in a mammalian host is established, ASFV
has a distinct cell tropism for myeloid cells. It replicates in
monocytes and macrophages but has also been found in granulocytes . The
pivotal role of lymphocytes, presumably CD8α+ T cells
in particular, has been demonstrated by antibody-dependent depletion of
CD8α+ cells after priming with an avirulent ASFV
strain, which resulted in the loss of protection after homologous
challenge .
Recently, we showed that immune responses of domestic pigs and wild boar
fail to clear an infection with the highly virulent ASFV strain
“Armenia08”, although for different reasons . Wild boar and domestic
pigs showed comparable clinical signs with substantial fatalities within
the first 8 days post infectionem (dpi). However, we found
activated T cells and signs of a cytotoxic response only in wild boar
but not in domestic pigs. Moreover, T-cell proliferation was impaired in
domestic pigs, while CD4+/CD8α+ T
cells in wild boar showed considerable proliferation. Of note, we
detected a significant loss of perforin expression in both subspecies 5
dpi in CD8α+ T cells. Still, neither response was
beneficial for the final disease outcome .
In the present study, we used a similar approach and investigated the
immune responses of domestic pigs and wild boar after infection with the
moderately virulent ASFV strain, “Estonia2014”. ASFV “Estonia2014”
has been shown to cause fatal disease in wild boar whereas different
domestic pigs survived the experimental infection . A comparative
approach with a focus on T-cell responses was used in this study to find
a possible explanation for this phenomenon. Moreover, with these data we
are able to compare immune responses against moderately virulent ASFV
with those against highly virulent ASFV recently published .