Why is ebola not considered a retrovirus




















He says, on the contrary, that Ebola's evolution towards higher transmissibility though not, of course, towards airborne transmission seems to be "already happening as we speak. It's probably becoming more transmissible.

But that's not the same thing as Ebola becoming more transmissible and maintaining its virulence. That's not the same thing as Ebola finding the conditions necessary for pandemic.

Remember the tradeoff: pathogens that evolve towards higher transmissibility also evolve toward lower virulence, and, says Ewald, "We can look at the numbers to get a sense of that.

If it's evolving towards high transmissibility and low virulence we're going to see the mortality curve flattening off and the case curve [the number of cases] rising.

And, if you look at the data from the last week, that's what seems to be occurring. One of the creepy things about Ebola is that it's a hemorrhagic fever whose "animal reservoir" is bats. But bats live with Ebola without becoming very sick, and even if Ebola evolves into a highly transmissible disease, it is likely that we will adapt, too.

The bad news from Paul Ewald is that one day you might get Ebola from a sneeze. The good news is that if you get Ebola from a sneeze it will probably make you sneeze — and not bleed out from your nipples. United States. Type keyword s to search. Today's Top Stories. Every 'Bond' Film Ever, Ranked. Following the infections as they happen, as well as having an animal model on which to test hypotheses, will likely help us understand how these symbiotic viruses came to play such a powerful role in our own evolution.

The idea that a symbiotic virus or any symbiotic relationship could have such a profound influence on the evolution of a new species is both new and controversial. The late University of Massachusetts researcher believed that cooperation also played a role. Her evidence lurked in every cell of every plant and animal. Beginning in the late s, Margulis argued that our cells contained symbiotic bacteria known as mitochondria and chloroplasts, which earned room and board by either supplying energy or producing food from sunlight.

Receive emails about upcoming NOVA programs and related content, as well as featured reporting about current events through a science lens. By the s, however, enough genetic evidence had accumulated to show that Margulis was right. Symbiosis was responsible for some of the most significant evolutionary leaps in the history of the planet. Margulis, though, saw symbiosis everywhere and believed that this softer, gentler side of evolution was getting short shrift in research.

Although most symbiosis research has focused on the role of the microbiome, the viruses tucked into our DNA can play a similar role in splitting apart two populations, turning one species into two. The first wedge scientists discovered was a protein called syncytin. Boston in the mids was humming with the activity of the Human Genome Project. Sequencing technologies had advanced to the point where scientists were incorporating gene discovery into even the most basic research.

Since the American courts had thus far allowed companies to patent the genes they discovered, companies like the Genetics Institute now a part of Pfizer saw a chance to cash in.

There, molecular biologist John McCoy was looking for proteins secreted by cells since they seemed good targets for developing potential drugs. Before McCoy could go public with his discovery, he needed to figure out exactly what syncytin did, a job he passed to bench scientist Sha Mi, who everyone called Misha.

Syncytin is produced only by certain cells in the placenta, and it directs the formation of the cellular boundary between the placenta and maternal tissue. Approximately one week after fertilization, the egg, now a hollow ball of cells called a blastocyst, implants itself into the uterus, stimulating the formation of the placenta, which provides the fetus with oxygen and nutrients while removing carbon dioxide and other wastes. It also serves as a barrier to prevent infection and keep maternal and fetal blood separate.

Mixing the two could cause a fatal autoimmune response. The cells in the outer layer of the blastocyst form the outer layer of the placenta, and those in direct contact with the uterus are the only ones that made syncytin. When the scientists looked closer at the DNA sequence of syncytin, they found that it was nearly identical to a viral protein called env that caused the virus to fuse with its host cell.

In the placenta, syncytin performed helped the fetus fuse with its mother. At last McCoy, Howe, and Mi knew what syncytin did. The two other retroviral genes next to syncytin, gag and pol , were completely non-functional, McCoy says. Only env remained intact. The team published a paper in Nature in All mammals have placentas, including marsupials and egg-laying mammals.

As of April 4, , a total of 1, people—a quarter under 18 years old—have had confirmed or probable cases of EVD, and have died.

Some 81 cases—and 27 fatalities—are among health-care workers trying to fight the epidemic. Containing the outbreak has proved challenging, in no small part because of community distrust. Reports from on-the-ground media and the World Health Organization say that communities have felt alienated by the heavy-handed approach used by aid groups and the local government. Officials says they are actively working to rebuild trust and stem the tide of infections. All rights reserved.

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