| Autor: |
Turkki, Paula, Laajala, Mira, Stark, Marie, Vandesande, Helena, Sallinen-Dal Maso, Heidi, Shroff, Sailee, Sävneby, Anna, Galitska, Ganna, Lindberg, A. Michael, Marjomäki, Varpu |
| Jazyk: |
angličtina |
| Rok vydání: |
2019 |
| Předmět: |
|
| Popis: |
Enterovirus B species typically cause a rapid cytolytic infection leading to efficient release of progeny viruses. However, they are also capable of persistent infections in tissues, which are suggested to contribute to severe chronic states such as myocardial inflammation and type 1 diabetes. In order to understand the factors contributing to differential infection strategies, we constructed a chimera by combining the capsid proteins from a fast cytolysis causing echovirus 1 (EV1) with non-structural proteins from Coxsackievirus B5 (CVB5) showing persistent infection in RD cells. The results showed that the chimera behaved similar to the parental EV1 leading to efficient cytolysis in both permissive A549 and semi-permissive RD cells. In contrast to EV1 and chimera, CVB5 replicated slower in permissive cells and showed persistent infection in semi-permissive cells. However, there was no difference in the efficiency of uptake of CVB5 in A549 or RD cells in comparison to the chimera or EV1. CVB5 virus batches constantly contained significant amounts of empty capsids, also in comparison to its close relative CVB3. During successive passaging of batch containing only intact CVB5, increasing amounts of empty and decreasing amounts of infective capsids were produced. Our results demonstrate that the increased amounts of empty particles and lowering amounts of infective particles is dictated by the CVB5 structural proteins leading to slowing down the infection between passages. Furthermore, the key factor for persistent infection is the low amount of infective particles produced, not the high number of empty particles accumulating. peerReviewed |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
|
