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日期:2014-12-05 02:31 作者:王蓓 来源:美亚处

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


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, slime mold, even larger viruses. They replicate in their host cells so prodigiously and stream out into their surroundings 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.


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.


Viruses are masters at making their way from host to host and cell to cell, using every possible channel. 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.

 最近,斯坦福大学医学院(Stanford University School of Medicine)微生物学及基因学教授卡拉?柯克加德(Karla Kirkegaard)和同事在《国家科学院院刊》(Proceedings of the National Academy of Sciences)发表文章描述了一种基于所谓的自噬的“非传统分泌”途径,即细胞消化一部分自身细胞质,然后将它们释放到周围的环境中,充当针对其他细胞的信号分子,比如,告诉它们,现在是进行新一轮组织生长的时候了。

The researchers determined that the poliovirus 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.


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, rather as you might foist a pill down a pet's throat by smearing it in butter.


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

 美国国家癌症研究所(National Cancer Institute)病毒与细胞互动部门的主管埃里克?O?弗里德(Eric O. Freed)表示,最近几项技术突破使病毒研究发生了巨大变革。

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," Dr. Freed said. And that could prove important to detecting the emergence of a new lethal strain.


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 also work tirelessly to evade the immune system that seeks to destroy them. 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,  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, Dr. 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.


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