Summary auto-generated
Rinderpest virus (RPV) isolates of different virulence levels show distinct infection patterns in bovine monocytes and macrophages. Researchers studied three RPV isolates: highly virulent RPV-Saudi, mildly virulent RPV-Egypt, and avirulent vaccine strain RPV-RBOK. All three infected and productively replicated in monocytic cells but differed significantly in infection kinetics. By day 6 post-infection, RPV-Saudi infected approximately 80% of cells, RPV-Egypt infected 50%, and RPV-RBOK infected only 25%. The viruses induced similar cytopathic effects including syncytia formation and stellate cell development, though sizes and frequencies varied by isolate. RPV-Saudi produced the largest syncytia and most progeny virus, while RPV-Egypt was most efficient at forming stellate cells and downregulating MHC class II expression. Notably, all three isolates downregulated MHC class II expression on infected cells but had no effect on MHC class I or LFA-1. These findings establish a relationship between in vivo virulence and in vitro replication characteristics in monocytes/macrophages, suggesting that MHC class II downregulation may help viruses evade immune recognition.
Key findings
- Highly virulent RPV-Saudi infected ~80% of monocytes by day 6, compared to ~50% for mild RPV-Egypt and only ~25% for avirulent RPV-RBOK, showing virulence correlates with infection efficiency
- RPV-Saudi was most efficient at producing infectious progeny virus and large syncytia, while RPV-Egypt was particularly efficient at inducing stellate cell formation and MHC class II downregulation
- All three RPV isolates downregulated MHC class II expression on infected cells but did not affect MHC class I or LFA-1 expression, providing a potential immune evasion mechanism
- Infection progressed more readily in monocytes than in differentiated macrophages, though eventually the latter produced higher infectious titers relative to antigen expression
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Abstract
Three isolates of rinderpest virus (RPV) with different in vivo virulence were able to infect and productively replicate in bovine monocytic cells. They differed in their kinetics of replication and the morphological changes induced in infected cultures. The highly virulent RPV-Saudi infected > 80% of cells within 6 days p.i. (m.o.i. = 0.1 TCID50 per cell). Under identical conditions, > 50% of cells were infected by the 'mild' (causes minimal mortality in vivo) isolate RPV- Egypt, whereas only 25% were infected by the avirulent RPV-RBOK. Infection by all three viruses produced infectious progeny, induced the formation of syncytia and stellate cells with long processes, and down- regulated MHC class II expression; there was no apparent effect on MHC class I nor LFA-1. RPV-Saudi was the most efficient at generating progeny virus and producing syncytia. While RPV-RBOK was the least efficient at inducing syncytia, RPV-Egypt was the least efficient for progeny virus production. In contrast, RPV-Egypt was particularly efficient at inducing stellate cell formation and down-regulating MHC class II expression. These results indicate a relationship between in vivo virulence and the characteristics of replication and induced morphological changes in monocytes/macrophages. The down-regulation of MHC class II expression would offer a means by which the virus could evade immune recognition. This would be particularly useful for the more cell-associated, but less efficient at maturing, RPV-Egypt.