Thelonevirologist

@thelonevirologist.bsky.social

Virologist. Likes history, hiking, tea, coffee & a good movie.Favourite viruses? Coronavirus, Emerging & Oncogenic Viruses. Favourite country? UK. Dad. Bibliophile.

T
T
T

Potential threats of porcine Getah virus outbreaks and its specific antagonism of host antiviral response through proteasome-dependent degradation of P46 by nsP2 journals.plos.org/plospathogen...

Potential threats of porcine Getah virus outbreaks and its specific antagonism of host antiviral response through proteasome-dependent degradation of P46 by nsP2

Author summary Alphaviruses pose a constant threat to public health, and despite their potential for global emergence, there are currently no approved therapies or vaccines available against most of these viruses. In the past few years (2022–2025), the porcine Getah virus (GETV), a member of genus Alphavirus, has re-emerged in many parts of the world, triggering diarrhea-related disease outbreaks of varying scales within the pig industry. Understanding the pathogenesis of alphaviruses is essential for the developments of effective antiviral therapeutics. This study reports the successful isolation and characterization of a virulent GETV strain, JLY1, from diarrheic piglets in China. Then, we identified P46 as an antiviral host factor against GETV. Interestingly, unlike CHIKV, VEEV, SINV, SFV and RRV, GETV antagonizes P46 through a unique pathway involving Lys48-linked proteasome-dependent degradation. The present study describes a novel role of the GETV nonstructural protein 2 in targeting P46 to counteract host’s antiviral response, and reveals the mechanism by which GETV can antagonize against P46.

journals.plos.org

T
T

Natural immune escape mutations in the envelope proteins of hepatitis B virus (HBV) regulate the assembly and infectivity of human hepatitis delta virus (HDV) journals.asm.org/doi/10.1128/...

Natural immune escape mutations in the envelope proteins of hepatitis B virus (HBV) regulate the assembly and infectivity of human hepatitis delta virus (HDV) | Journal of Virology

The study demonstrated that anti-hepatitis B virus (HBV) immune response via selection for the immune escape mutations (IEMs) in HBV envelope proteins (surface antigen, HBsAg) can considerably reduce the assembly and/or infectivity of hepatitis delta virus (HDV) virions coated with HBsAg. The IEMs could down-regulate concomitant HDV infection mostly via affecting HDV infectivity, which was considerably inhibited by 13 out of 35 IEMs. The HDV spread/super-infection, which are expected to be suppressed by inhibited via HBV-specific IEMs the assembly and/or infectivity of HDV virions, should result in a reduced HDV reservoir in infected livers. The examination of the inhibition of HDV infectivity by IEMs apparently indicated that the major antigenic loop (MAL) of HBsAg could contain the residues primarily involved in viral attachment/entry and also the residues mostly regulating intracellular post-entry trafficking of HDV virions. The data advance our understanding of the MAL functioning during infection and of the indirect regulation of the HDV life cycle through the anti-HBV immune response.

journals.asm.org

T
T
T
T