ASFV-G-∆I177L vaccine reverts to virulence and impairs reproduction
The ASFV-G-ΔI177L vaccine is a modified-live African swine fever virus (ASFV) strain developed as a vaccination measure against African swine fever (ASF) in pigs. This vaccine strain was created by partially deleting the I177L gene (The I177L gene in ASFV is thought to play a critical role in the virus’s virulence and pathogenicity. It encodes a protein implicated in ASFV virulence. Deletion of this gene, as done in the ASFV-G-ΔI177L vaccine strain, reduces the virus’s pathogenic potential, leading to an attenuated strain that is less harmful to pigs.) and replacing it with the mCherry reporter gene. (The mCherry reporter gene is a commonly used fluorescent protein gene that emits red fluorescence when expressed in cells. In the context of the ASFV-G-ΔI177L vaccine, the mCherry reporter gene serves as a marker to facilitate tracking and studying the behavior of the modified virus within host organisms and experimental setups.)
The ASFV-G-ΔI177L strain has been incorporated into a commercially available vaccine, used to immunize pigs, particularly via intramuscular or oronasal routes. It has shown promise in protecting commercial pigs against ASFV infection. However, concerns regarding its genetic stability emerged following studies indicating that ASFV-G-ΔI177L could revert to virulence during in vivo passaging. Reversion was associated with ASF-specific clinical signs and increased viremia in infected pigs, raising concerns about its safety and effectiveness as a vaccine.
The vaccine was also investigated for its safety in pregnant sows, with findings indicating adverse effects on reproductive outcomes, including litter loss and compromised health of piglets born to vaccinated sows.
Given these findings, the use of ASFV-G-ΔI177L as a vaccine in pregnant animals is not recommended due to concerns over safety and the potential for reversion to a virulent form of the virus. Studies demonstrated that the ASFV-G-ΔI177L strain could regain virulence during in vivo passaging. Specifically, as the virus passed through infected animals, it acquired mutations that restored its pathogenicity. These mutations were linked to increased viremia and the emergence of severe clinical signs in pigs, suggesting that the absence of the I177L protein led to compensatory mechanisms that enabled the virus to regain virulence.
