ABSTRACT The high genetic diversity of porcine reproductive and respiratory syndrome virus (PRRSV) poses a significant challenge to effective vaccination and infection prevention. Recently, NADC30-like PRRSV has become dominant in China. In this study, we characterized a PRRSV isolate XJ2020 from a vaccinated pig. The isolate exhibited moderate pathogenicity in piglets and clustered within the same sub-lineage as NADC30. Sequence analysis identified a unique deletion of the serine residue at position 32 (S32) in the GP5 protein. This deletion was introduced into a highly pathogenic PRRSV (HP-PRRSV) strain, JX2015, to generate the mutant JX2015-ΔS32 using a reverse genetic approach. We found that JX2015-△S32 showed reduced propagation in Marc-145 cells and decreased sensitivity to neutralization by MLV-derived anti-PRRSV positive serum, but exhibited enhance replication in primary porcine alveolar macrophages (PAMs) compared to its parental strain JX2015. Interestingly, the viral load in lung and ileum samples from JX2015-△S32-infected piglets was higher, but the lung injury was milder than in JX2015-infected piglets. Overall, this study highlights the S32 site in the PRRSV GP5 protein as an important factor influencing virus propagation, neutralization, cell tropism and pathogenicity in piglets, and suggests that targeting this residue could lead to the development of more effective PRRSV vaccines.
Xingdong Zhou, Xiaohui Zhang, E. Kan et al.· Virulence· 0 citations
ABSTRACT LiaS is a histidine kinase receptor in two-component systems that senses environmental stress signals. This study investigated the roles of LiaS in Listeria monocytogenes stress resistance and virulence. Phenotypic assays showed that deletion of liaS (ΔliaS) resulted in significantly impaired growth under acidic, alkaline, and osmotic stresses, as well as reduced survival under strong acidic conditions. These defects were partially restored in the complemented strain (CΔliaS). The growth defects were also observed in the ΔliaS under Cu2+ or H2O2 exposure. Furthermore, the ΔliaS strain exhibited impaired invasion and intracellular migration in host cells, along with attenuated colonization in the liver and spleen at 24 h post-infection. Bacterial loads in the spleen of infected mice remained lower at 48 h. The mortality was also delayed in ΔliaS‑infected mice. Transcriptional analysis revealed that compared to neutral conditions, osmotic stress-related genes (except opucB and gbuC) were significantly upregulated in the ΔliaS strain under acidic conditions, indicating that LiaS modulates acid tolerance through transcriptional regulation. Collectively, LiaS is essential for the adaptation of Listeria monocytogenes to acidic, osmotic, and oxidative stresses. Its absence attenuates host cell invasion, intracellular motility, and organ-specific colonization, highlighting its dual role in environmental resilience and pathogenicity. These findings provide a theoretical basis for understanding host–pathogen interactions and offer new strategies against antimicrobial-resistant pathogens.
Yongshu Wu, Jiali Xu, Yifan Wang et al.· Virulence· 0 citations