African swine fever progresses faster in wild boar than in domestic pigs

Wild boar and domestic pigs respond differently to highly virulent African swine fever virus (ASFV), according to a 2026 doctoral thesis from the Swedish University of Agricultural Sciences. Experimental infections showed that wild boar developed viraemia, clinical disease and systemic viral spread earlier than domestic pigs, yet paradoxically displayed less extensive tissue damage before reaching humane endpoints.

The study compared domestic pigs and European wild boar experimentally infected intranasally with the highly virulent genotype II "Armenia 2007" strain, and then compared those results with naturally infected wild boar collected during field outbreaks.

Wild boar deteriorated more rapidly

Wild boar had shorter incubation periods, earlier clinical signs, earlier viraemia and faster systemic spread of ASFV than domestic pigs. Viral antigen was detected particularly early in the medial retropharyngeal lymph nodes, appearing in wild boar from three days post-infection. The difference in disease progression was striking: wild boar reached humane endpoints at around day 6, compared with approximately day 9 in domestic pigs.

However, wild boar had less severe and less extensive macroscopic and histopathological lesions, together with lower amounts of viral antigen in tissues at the time they reached those endpoints. The authors therefore suggest that wild boar may have lower tolerance to tissue damage, rather than being infected by a less pathogenic virus.

Field cases look different from experimental infections

Naturally infected wild boar showed a broader and often more severe range of lesions than experimentally infected animals. The researchers attribute this partly to the longer and less controlled course of natural infection, as well as concurrent diseases and environmental factors. This distinction is important when interpreting carcasses found during ASF surveillance: pathology observed in the field may not reproduce the relatively uniform picture generated by controlled experimental infection.

The work highlights that domestic pigs and wild boar cannot simply be assumed to develop ASF in the same way, despite belonging to the same species complex. Differences in disease kinetics and pathology may affect how infection is detected and interpreted during surveillance.

These findings are particularly relevant in Europe, where wild boar remain a major reservoir sustaining ASFV circulation and facilitating transmission across affected regions.