The vast viral universe

For scientists who study the evolution and behaviour of viruses, the Ebola pathogen is performing true to its ancient and diverse kind

By: New York Times | Published:November 2, 2014 12:32 am
An image, created by a scanning electron microscope, of cells infected by HIV virus. An image, created by a scanning electron microscope, of cells infected by HIV virus.

Behind the hellish Ebola epidemic ravaging West Africa lies an agent that fittingly embodies the mad contradictions of a nightmare. It is alive yet dead, simple yet complex, mindless yet prophetic, seemingly able to anticipate our every move.

For scientists who study the evolution and behaviour of viruses, the Ebola pathogen is performing true to its vast, ancient and staggeringly diverse kind. From all available evidence, researchers say, viruses have been parasitising living cells since the first cells arose on earth nearly four billion years ago.

Some researchers go so far as to suggest that viruses predate their hosts. That they essentially invented cells as a reliable and renewable resource they could then exploit for the sake of making new viral particles.

It was the primordial viral “collective”, said Luis P Villarreal, director of the Centre for Virus Research at the University of California, Irvine, “that originated the capacity for life to be self-sustaining.”

“Viruses are not just these threatening or annoying parasitic agents,” he added. “They’re the creative front of biology, where things get figured out, and they always have been.”

Researchers are deeply impressed by the depth and breadth of the viral universe, or virome. Viruses have managed to infiltrate the cells of every life form known to science. They infect animals, plants, bacteria, mould, even larger viruses. They replicate in their host cells so prodigiously and stream out so continuously that if you collected all the viral flotsam afloat in the world’s oceans, the combined tonnage would outweigh that of all the blue whales.

Not that viruses want to float freely. As so-called obligate parasites entirely dependent on host cells to replicate their tiny genomes and fabricate their protein packages newborn viruses, or virions, must find their way to fresh hosts or they will quickly fall apart, especially when exposed to sun, air or salt.

“Drying out is a death knell for viral particles,” said Lynn W Enquist, a virologist at Princeton University.

How long shed virions can persist if kept moist and unbuffeted — for example, in soil or in body excretions like blood or vomit — is not always clear but may be up to a week or two. That is why the sheets and clothing of Ebola patients must be treated as hazardous waste and surfaces hosed down with bleach.

Whenever biologists discover a new way that body cells communicate with one another, sure enough, there’s a virus already tapping into exactly that circuit in its search for new meat.

Reporting recently in Proceedings of the National Academy of Sciences, Karla Kirkegaard, a professor of microbiology and genetics at Stanford University School of Medicine, and her colleagues described a kind of “unconventional secretion” pathway based on so-called autophagy, or self-eating, in which cells digest small parts of themselves and release the pieces into their surroundings as signaling molecules targeted at other cells — telling them, for example, that it’s time for a new round of tissue growth.

The researchers determined that the polio virus can exploit the autophagy conduit to cunning effect. Whereas it was long believed that new polio particles could exit their natal cell only by bursting it open and then seeking new cells to infect, the researchers found that the virions could piggyback to freedom along the autophagy pathway.

In that way, the virus could expand its infectious empire without destroying perfectly good viral factories en route. The researchers suspect that other so-called naked or nonenveloped viruses (like the cold virus and enteroviruses) could likewise spread through unconventional secretion pathways.

For their part, viruses like Ebola have figured out how to slip in and out of cells without kicking up a fuss by cloaking themselves in a layer of greasy lipids stolen from the host cell membrane.

According to Eric O Freed, the head of the virus-cell interaction section at the National Cancer Institute, several recent technological breakthroughs have revolutionised the study of viruses.

Advances in electron microscopy and super-resolved fluorescence microscopy — the subject of this year’s Nobel Prize in chemistry — allow scientists to track the movement of viral particles in and between cells, and to explore the fine atomic structure of a virus embraced by an antibody, or a virus clasped onto the protein lock of a cell.

Through ultrafast gene sequencing and targeted gene silencing techniques, researchers have identified genes critical to viral infection and drug resistance. “We’ve discovered viruses we didn’t even know existed,” Freed said.

Viruses are also notable for what they lack. They have no ribosomes, the cellular components that fabricate the proteins that do all the work of keeping cells alive.

Instead, viruses carry instructions for co-opting the ribosomes of their host, and repurposing them to the job of churning out capsid and other viral proteins. Other host components are enlisted to help copy the instructions for building new viruses, in the form of DNA or RNA, and to install those concise nucleic texts in the newly constructed capsids.

“Viruses are almost miraculously devious,” Freed said. “They’re just bundles of protein and nucleic acid, and they’re able to get into cells and run the show.”

Viruses also work tirelessly to evade the immune system. One of the deadliest features of the Ebola virus is its capacity to cripple the body’s first line of defense against a new pathogen, by blocking the release of interferon.

At the same time, said Aftab Ansari of Emory University School of Medicine, the virus disables the body’s coagulation system, leading to uncontrolled bleeding. By the time the body can rally its second line of defense, the adaptive immune system, it is often too late.
Yet the real lethality of Ebola, Ansari said, stems from a case of mistaken location, a zoonotic jump from wild animal to human being. The normal host for Ebola virus is the fruit bat, in which the virus replicates at a moderate pace without killing or noticeably sickening the bat.

“A perfect parasite is able to replicate and not kill its host,” Ansari said. “The Ebola virus is the perfect parasite for a bat.”

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