Ebola explained

••By attacking the body's first responders, the virus cripples the immune system before it can mount an effective defense

Although it contains only seven genes, Ebola is an exquisitely effective killer of humans and other primates once it enters a body. Unlike the spiky sea urchin that is influenza, or the golf-ball shaped poliovirus, Ebola resembles noosed ropes under the electron microscopes used to capture viral images. 

  

Researchers often describe the battle between the Ebola virus and the humans it occasionally infects as a race—one that people win only if their immune systems manage to pull ahead before the virus destroys too many of their internal defenses. What they may not know is that the virus is a cheat.

The Ebola virus gives itself a head start when it first slips into a human body by disabling parts of the immune system that should be leading the charge against the invader. It hijacks the functions of certain defense warriors known as dendritic cells—whose primary function is to alert the immune system to the incoming threat. Other targets include monocytes and macrophages, types of white blood cells whose job is to absorb and clear away foreign organisms.

These are the first cells Ebola infects and bends to the process of making more Ebola viruses. The maneuver is the viral version of invading a country by hypnotizing the army and turning it against its own people. Then, having kicked the immune system’s feet out from under it, Ebola takes off in a run.

Seven Deadly Genes
Although it contains only seven genes, Ebola is an exquisitely effective killer of humans and other primates once it enters a body. Unlike the spiky sea urchin that is influenza, or the golf-ball shaped poliovirus, Ebola resembles noosed ropes under the electron microscopes used to capture viral 
images.

Classified as a filovirus, Ebola is one of two members of that family; the other is Marburg virus, named after the German city where it was first seen in researchers who caught it from imported non-human primates. Both pathogens are among the most lethal viruses that afflict people, but it is Ebola that has become the recognized and dreaded face of the filovirus family.

>> Scientific American In-Depth Report, Ebola: What You Need to Know

Marburg tends not to provoke the same fear in the general public as Ebola, although it is deserves equal billing. Daniel Bausch, a filovirus expert at Tulane University School of Public Health and Tropical Medicine in New Orleans, La., recalls preparing to head to a Marburg outbreak in the Democratic Republic of Congo in the late 1990s when he was contacted by a journalist. The reporter had heard there was an Ebola outbreak. "And I said 'No, it's Marburg.' And he said 'Oh, thanks anyway' and he hung up the phone.” The outbreak that the journalist had so nonchalantly dismissed 
killed 83 percent of known cases. 

Ebola was previously known as a viral hemorrhagic fever, a description that is falling from use­ because of the erroneous implication that I kills by exsanguination or bleeding out. In fact, most patients do not hemorrhage or ooze blood, at least not externally, Bausch says. Ebola virus disease is now the preferred terminology.

Few autopsies have been performed on people who have died from Ebola virus disease, because of the high risk posed by the procedures. In fact, a scientific review published in October 2014 identified only 30 human cases where an autopsy or post-mortem biopsies were performed. But here is what’s known about the way the disease takes off in the body: The early infection of–or recruitment of—the monocytes, macrophages and dendritic cells is believed to speed spread of the virus to the lymph nodes, liver, spleen and elsewhere in the body. In the liver, the presence of the virus appears to trigger a sharp decline of lymphocytes, white blood cells that help

 fight infections. 

The reason for their decline is unknown, but the result helps the virus; lymphocytes typically would increase in number in the face of an infection.

Decoy Strategy
Meanwhile, Ebola employs a second dastardly trick, another cheat. It releases large amounts of something called secreted glycoprotein – sGP – into the bloodstreams of its victims. A decoy, sGP looks like the glycoprotein on the exterior of the virus, GP, which should be the immune system’s chief target. By tricking the immune system into seeing it, not GP as the invader, sGP undermines the system’s ability to react effectively to stem the infection.