Viruses can enter cells through a variety of different pathways. Many enter through endocytosis, and there are actually several endocytic pathways: clathrin mediated, caveolin mediated, phago- and pinocytosis, and the rather mysterious “non-clathrin, non-caveolin mediated endocytosis.”
Ebola virus causes a severe hemorrhagic disease with 90% mortality. Its an obviously frightening virus which makes it difficult to study, but knowing the details of its replication cycle may provide important clues on how to treat or prevent the disease. A recent paper demonstrates that Ebola probably uses clathrin-mediated endocytosis. Clathrin is a protein that forms a polyhedral lattice on the inside of the cell membrane helping to form vesicles. Virus attachment induces this vesicle formation, giving the virus access to the cell by entering through these vesicles. Among other experiments, they found that if you use the drug chorpromazine, which inhibits clathrin function, you can block Ebola entry.
The paper raises some interesting questions. First, they didnt actually use Ebola virus. They used a modified HIV that expresses the Ebola virus glycoprotein involved in attachment and entry. Does the natural virus enter in the same way? They used several different cells in culture and found clathrin dependence in all of them, but is it the same in an infected animal? Finally is the drug chlorpromazine one that could be used clinically? Presumably not since disrupting clathrin mediated endocytosis would probably have a broadly toxic effect on the host, but it is an interesting lead compound.