Abstract
Structural changes of two patient-derived glioblastoma cell lines after Zika virus infection were investigated using scanning transmission electron tomography on high-pressure-frozen, freeze-substituted samples. In Zika-virus-infected cells, Golgi structures were barely visible under an electron microscope, and viral factories appeared. The cytosol outside of the viral factories resembled the cytosol of uninfected cells. The viral factories contained largely deranged endoplasmic reticulum (ER), filled with many so-called replication organelles consisting of a luminal vesicle surrounded by the ER membrane. Viral capsids were observed in the vicinity of the replication organelles (cell line #12537 GB) or in ER cisternae at large distance from the replication organelles (cell line #15747 GB). Near the replication organelles, we observed many about 100-nm-long filaments that may represent viral ribonucleoprotein complexes (RNPs), which consist of the RNA genome and N protein oligomers. In addition, we compared Zika-virus-infected cells with cells infected with a phlebovirus (sandfly fever Turkey virus). Zika virions are formed in the ER, whereas phlebovirus virions are assembled in the Golgi apparatus. Our findings will help to understand the replication cycle in the virus factories and the building of the replication organelles in glioblastoma cells.
Highlights
Zika virus (ZIKV) is an enveloped flavivirus with a positive-sense, single-stranded RNA genome
As the comparison of the structure of prefixed and non-prefixed controls shows, the Golgi apparatus can still be identified after chemical fixation (Fig. 1)
In ZIKV-infected glioblastoma cells, viral factories consisting of enlarged endoplasmic reticulum (ER) are the main site of virion formation
Summary
Zika virus (ZIKV) is an enveloped flavivirus with a positive-sense, single-stranded RNA genome. The virus can be transmitted to humans by the bite of Aedes mosquitoes, or from human to human by maternal-to-fetal transmission or, in isolated cases, by sexual transmission (Pierson and Graham 2016). On transmission electron microscopy (TEM), The entrance of Zika virions into host cells occurs by virus endocytosis following receptor binding. After endocytosis and vesicle acidification, the approximately 11 kb RNA genome is released into the host cell cytosol. Zika virus infection and replication cause a massive rearrangement of cellular structures (Cortese et al 2017). Foremost, this results in the formation of an area referred to as viral
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
