Capsid-deficient alphaviruses generate propagative infectious microvesicles at the plasma membrane.

ABSTRACT: Alphavirus budding is driven by interactions between nucleocapsids assembled in the cytoplasm and envelope proteins present at the plasma membrane. So far, the expression of capsid and envelope proteins in infected cells has been considered an absolute requirement for alphavirus budding and propagation. In the present study, we show that Semliki Forest virus and Sindbis virus lacking the capsid gene can propagate in mammalian and insect cells. This propagation is mediated by the release of infectious microvesicles (iMVs), which are pleomorphic and have a larger size and density than wild-type virus. iMVs, which contain viral RNA inside and viral envelope proteins on their surface, are released at the plasma membrane and infect cells using the endocytic pathway in a similar way to wild-type

SUBMITTER: Ruiz-Guillen M 

PROVIDER: S-EPMC7079800 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature