Although we know that bodily fluids are contagious, we still don’t have a definitive picture of how the virus enters the body’s cells. But learning the biology of Ebola infections is necessary for designing and deploying effective drugs and vaccines. Unlike H.I.V., which can only infect a limited set of cell types in the body, Ebola is promiscuous and attacks white blood cells, the cells that line our vessels, and cells that make up our liver, adrenal glands, and airways. Research studies have suggested at least three potential paths that the virus can take to invade our tissues. In one sequence, Ebola attaches to a protein on the surface of a cell that is meant to transport cholesterol. After Ebola has hijacked the surface protein, it sneaks into the cell and rapidly proliferates. (That transport protein is ubiquitous in the body, because all our organs require cholesterol in order to function normally.) Other experiments have indicated that Ebola can commandeer a protein called TIM-1, which is widely distributed in conjunctiva, the insides of our eyelids, and in our cornea. Despite taking precautions with gloves and facemasks, health-care workers who have become infected may have inadvertently brushed a finger near their eye, giving the virus access to TIM-1.
Ebola may have a third, and particularly nefarious, way of overtaking the body. There is a type of white blood cell called a dendritic cell, which normally chews up and destroys invading microbes. When Ebola comes into contact with the mucous membranes of our mouth or a break in the skin, the dendritic cell goes to work against it. But Ebola disarms the cell and uses this crucial bodily defender as a factory to spew out its progeny. We need to understand the mechanisms by which Ebola invades dendritic cells, evades destruction, and then turns the immune system against itself. Deciphering the dendritic pathway could help to alleviate Ebola’s cascading brutality in human hosts.
