Thursday, January 21, 2010

MARSEILLEVIRUS, A NEW MEMBER OF THE GIANT VIRUSES

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After Mimivirus, Mamavirus and the virophage, the group of giant viruses now has a new member called Marseillevirus. Discovered in an amoeba by the team led by Didier Raoult at the Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes research group (CNRS/Université Aix-Marseille 2), a description of this new virus was published on the website of the Proceedings of the National Academy of Sciences (PNAS). These findings suggest the exchange of genes in amoebae that may lead to the constitution of different gene repertoires that could be a source of new pathogens.

Amoebae are single-cell, eukaryote (possessing a nucleus) living organisms, some of which are human or animal parasites and may cause a variety of pathologies. Most amoebae live in water, damp soils or mosses. They are mobile and capable of ingesting a wide variety of different organisms (for example, viruses or bacteria with extraordinarily broadly ranging sizes and lifestyles). Thus amoebae provide a site for numerous exchanges of genetic material arising from the many organisms that "colonize" them.

The team led by Didier Raoult at URMITE (CNRS/Université Aix-Marseille 2)1 has recently discovered, in an amoeba, a member of a new family of giant viruses, which it has called the Marseillevirus, smaller than Mimivirus, which is the largest giant virus known at present. With a chimeric genome (containing both DNA and RNA) of 368,000 base pairs, Marseillevirus is indeed the fifth largest viral genome to be sequenced. It has an icosahedral shape and a diameter of about 250 nanometers (or 250 millionths of a millimeter). In addition, the researchers discovered that it contained genes from markedly differing sources, i.e. of bacterial, viral or eukaryote origin, or arising from Archae2. The genome of Marseillevirus, a mosaic of genes from very different organisms, thus demonstrates the exchange of genes between the organisms that "colonize" amoebae. These studies have also revealed the role of amoebae, and more generally phagocytic protists (or single-cell eukaryotes) that feed on microbes in the environment, in the constitution of new gene "repertoires" which may be capable of generating new agents that will be pathogenic to multicellular organisms such as animals, plants or humans.

(Photo: © Raoult / URMITE)

Centre national de la recherche scientique

NEW RESEARCH FINDINGS MAY HELP STOP AGE-RELATED MACULAR DEGENERATION AT THE MOLECULAR LEVEL

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BBSRC-funded researchers at University College London say they have gleaned a key insight into the molecular beginnings of age-related macular degeneration, the number one cause of vision loss in the elderly, by determining how two key proteins interact to naturally prevent the onset of the condition.

In a paper to be published in a forthcoming issue of the Journal of Biological Chemistry, a publication of The American Society of Biochemistry and Molecular Biology (ASBMB), the team reports for the first time how a common blood protein linked to the eye condition reins in another protein that, when produced in vastly increased amounts in the presence of inflammation or infection, can damage the eye.

By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly,” said Zuby Okemefuna, the lead author of the paper.

Age-related macular degeneration, or AMD, is painless but affects the macula, the part of the retina that allows one to see fine detail. One form of the debilitating condition, known as “wet” AMD, occurs when abnormal and fragile blood vessels grow under the macula, leaking blood and fluid and displacing and damaging the macula itself. The second form, “dry” AMD, occurs when light-sensitive cells in the macula slowly break down.

It is believed that both forms start on a common molecular route and then deviate into dry or wet AMD, explained the research leader, Steve Perkins.

The earliest hallmark of AMD is the appearance of protein, lipid and zinc deposits under the retinal pigment epithelial cells,” he said, adding that the yellowish deposits, usually discovered by an ophthalmologist, are commonly known as “drusen.”

The researchers studied two proteins involved in drusen formation - blood protein Factor H and a second blood protein known as C-reactive protein - and showed that Factor H binds to C-reactive protein when C-reactive protein is present in large amounts, as in the case of infection, to reduce the potentially damaging effects of an overactive immune system.

In the eye, during the normal processes of aging, cells will die naturally for all sorts of reasons,” Okemefuna said. “The blood supply to the eye will bring C-reactive protein with it, and a low level of C-reactive protein activity will enable the normal processes of clearance of dead cells at the retina through mild inflammation. In conditions of high inflammation, the levels of C-reactive protein in the retina will increase dramatically.”

Uncontrolled C-reactive protein activity causes damage to the retina, which is followed by more inflammation and then even more damage to the retina, and so forth.

“It’s the debris of broken up retinal cells, some of which is caused by this cycle, that is deposited as drusen,” Okemefuna said.

The team also found that a genetically different form of Factor H does not bind to the C-reactive protein quite as well as the normal one, making people who carry the modified protein more vulnerable to an immune system attack in the eye and, thus, drusen buildup.

“In normal individuals, further damage to the retina by prolonged exposure to high levels of C-reactive protein is prevented by Factor H. C-reactive protein also prevents Factor H from clumping together and initiating the processes that lead to drusen formation,” Perkins said. “Both these ‘good’ activities of Factor H are much reduced in the genetically different form of Factor H.”

While there is no known cure for AMD, existing therapies aim to treat the symptoms and delay progression.

“It is interesting how the interaction of these two blood proteins protects the eye during crisis,” Perkins said. “The two proteins also can be involved in a rare and often fatal cause of kidney failure in children. We now are better positioned to begin to work out preventative strategies for these diseases.”

Bioscience for the future

REDUCING SOME WATER FLOW RATES MAY BRING ENVIRONMENTAL GAINS

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Conservation projects often attempt to enhance the water-based transport of material, energy, and organisms in natural ecosystems. River restoration, for example, commonly includes boosting maximum flow rates. Yet in some highly disturbed landscapes, restoration of natural water flows may cause more harm than good, according to a study published in the January 2010 issue of BioScience.

The study, by C. Rhett Jackson and Catherine M. Pringle of the University of Georgia, analyzes a wide variety of examples in which creating or maintaining reduced flows can create ecological benefits. The presence of nonnative fishes in a river, for example, can argue for maintaining the isolation of some habitats that are separated from the main channel, because the nonnative species may imperil naturally occurring species. In other cases, novel vegetation that has grown up below a dam may be host to terrestrial animal populations, including endangered birds. Restoring natural water flows can lead to a change in the vegetation that is detrimental to the animals.

Awareness of the potential benefits of maintaining low "hydrologic connectivity" has extended to the creation of artificial barriers to protect species at risk. The endangered native greenback cutthroat trout, for example, is protected from nonnative brook trout moving upstream by the placement of small dams in stream headwaters in the Colorado River basin. Expensive attempts are also being made to deter exotic nuisance species such as bighead carp and silver carp from invading Lake Michigan via the Chicago Sanitary and Ship Canal. Experts disagree on whether the multimillion-dollar electric dispersal barriers now being constructed on the canal will succeed, and some authorities have argued that only permanently disconnecting the canal will protect Lake Michigan.

Many urban streams represent particular challenges when attempts are made to restore natural flows. Expensive restoration efforts in streams in Seattle, for example, led to high pre-spawning mortality of salmon, possibly because they were exposed to copper pollution. Maintaining low flows can also mitigate the effects of pollution on ecosystems when ponds and lakes sequester sediments and nutrients that would otherwise be more widely dispersed. The sediments may contain toxic elements that could cause widespread harm to wildlife.

This insight raises another challenge, however: several National Wildlife Refuges have suffered high mortality of fishes and birds as a result of the concentration of toxic substances in lakes. What is clear is that restoring natural flows can bring pros and cons. Jackson and Pringle conclude that "a major challenge is to develop a more predictive understanding of how hydrologic connectivity operates in intensively developed landscapes."

American Institute of Biological Sciences

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