MicrobiologyBytes

From the outside and within, we are constantly bombarded with a myriad of diverse microbial species. However, our bodies are equipped with an evolutionarily conserved innate immune defense system that allows us to thwart potential pathogens. Antimicrobial peptides (AMPs) are a unique and assorted group of molecules produced by living organisms of all types, considered to be part of the host innate immunity. These peptides demonstrate potent antimicrobial activity and are rapidly mobilized to neutralize a broad range of microbes, including viruses, bacteria, protozoa, and fungi. More significantly, the ability of these natural molecules to kill multidrug-resistant microorganisms has gained them considerable attention and clinical interest. With the growing microbial resistance to conventional antimicrobial agents, the need for unconventional therapeutic options has become urgent. This article provides an overview of AMPs, their biological functions, mechanism of action, and applicability as alternative therapeutic agents.

Presently, AMPs represent one of the most promising future strategies for combating infections and microbial drug resistance. This is evident by the increasing number of studies to which these peptides are subjected. As our need for new antimicrobials becomes more pressing, the question remains: can we develop novel drugs based on the design principles of primitive molecules?

Antimicrobial Peptides: Primeval Molecules or Future Drugs? (2010) PLoS Pathog 6(10): e1001067. doi:10.1371/journal.ppat.1001067

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• Antimicrobial Peptides
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Tomato yellow leaf curl virus (TYLCV) poses a serious threat to tomato production throughout the temperate regions of the world. A new analysis suggests that the virus probably arose somewhere in the Middle East between the 1930s and 1950s and that its global spread only began in the 1980s after the emergence of two strains – TYLCV-Mld and -IL. In agreement with other work, it finds that the highly invasive TYLCV-IL strain has jumped at least twice to the Americas – once from the Mediterranean basin in the early 1990s and once from Asia in the early 2000s. Although the results corroborate historical accounts of TYLCV-like symptoms in tomato crops in the Jordan Valley in the late 1920s, they indicate that the region around Iran is both the current center of TYLCV diversity and is the site where the most intensive ongoing TYLCV evolution is taking place. The analysis indicates that this region is epidemiologically isolated suggesting that novel TYLCV variants found there are probably not direct global threats, and identifies the Mediterranean basin as the main launch-pad of global TYLCV movements.

The Spread of Tomato Yellow Leaf Curl Virus from the Middle East to the World. (2010) PLoS Pathog 6(10): e1001164. doi:10.1371/journal.ppat.1001164
The ongoing global spread of Tomato yellow leaf curl virus (TYLCV; Genus Begomovirus, Family Geminiviridae) represents a serious looming threat to tomato production in all temperate parts of the world. Whereas determining where and when TYLCV movements have occurred could help curtail its spread and prevent future movements of related viruses, determining the consequences of past TYLCV movements could reveal the ecological and economic risks associated with similar viral invasions. Towards this end we applied Bayesian phylogeographic inference and recombination analyses to available TYLCV sequences (including those of 15 new Iranian full TYLCV genomes) and reconstructed a plausible history of TYLCV’s diversification and movements throughout the world. In agreement with historical accounts, our results suggest that the first TYLCVs most probably arose somewhere in the Middle East between the 1930s and 1950s (with 95% highest probability density intervals 1905–1972) and that the global spread of TYLCV only began in the 1980s after the evolution of the TYLCV-Mld and -IL strains. Despite the global distribution of TYLCV we found no convincing evidence anywhere other than the Middle East and the Western Mediterranean of epidemiologically relevant TYLCV variants arising through recombination. Although the region around Iran is both the center of present day TYLCV diversity and the site of the most intensive ongoing TYLCV evolution, the evidence indicates that the region is epidemiologically isolated, which suggests that novel TYLCV variants found there are probably not direct global threats. We instead identify the Mediterranean basin as the main launch-pad of global TYLCV movements.

Related:

• Tomato leaf curl virus

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Since the beginning of mankind, human beings have strived to pass on their thoughts and knowledge to other people and to future generations. In this respect, the cultural role played by paper has been immense: paper is used for drawings, books, archival documents, photographs, prints, and so forth. Paper was first made in China around 105 AD, and its history can be roughly divided into two major periods: before the 19th century, when paper was made by hand, cellulose from linen and cotton rags was used as the raw material; from the 19th century onwards, when paper was machine-made from wood pulp, paper has contained several other components in addition to cellulose; these include lignin, hemicellulose and pectin. Furthermore, paper is often coated with sizes (the sizing of paper is a process that renders the sheets impervious to ink) such as gelatine, or with minerals, pigments and other substances to impart desirable properties. Libraries, archives and museums preserve paper material, and such material is at risk of deterioration and needs to be protected from physicochemical and biological agents. In many cases, microbial processes have been implicated in paper deterioration.

Scripta manent? Assessing microbial risk to paper heritage. Trends in Microbiol. Oct 22 2010
Paper, like all other cultural heritage materials, degrades over time, but conservation slows down the rate of its deterioration. There is a long history of cooperation between microbiologists and conservators of libraries and archival materials, but current approaches addressing paper deterioration need urgent reassessment to take full advantage of modern microbiological methodologies. This article discusses what we believe are the current priority research areas in assessing microbial risk to paper heritage, and reports studies on a 13th century Italian manuscript and on Leonardo da Vinci’s Atlantic Codex which illustrate the problems and challenges encountered when dealing with microbial investigations of paper artworks. The potential of using a more advanced microbiological approach is highlighted.

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• The Tomb of the Shroud
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• What have the Romans ever done for us?

I’ve written quite a lot on MicrobiologyBytes about the growing threat from Bluetongue virus. New figures from the European Commission now show that BTV 8, the epidemic strain of the virus, has been virtually eradicated from mainland Europe after an extensive vaccine campaign.

Tens of thousands of cases of bluetongue, predominantly the BTV8 strain, were identified across Europe in 2007 and 2008. The numbers dropped significantly in 2009 and are on course for a further significant decline this year.

The latest figures from the European Commission show incidence of BTV 8 has declined to just two recorded cases, while rare European cases of other strains are also on the way down.

Bluetongue virtually eradicated in Europe. Farmer’s Guardian, 2 November 2010

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• Bluetongue virus
• Midges and the emergence of bluetongue virus in northern Europe
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Dengue virus infection is a growing public health problem with up to 100 million cases annually, and neither vaccines nor effective therapies are available. To search for the ways of preventing and treating dengue infections we need to better understand their molecular mechanisms. As with many other viruses, dengue virus enters cells by fusion between the viral membrane and the membrane of intracellular vesicles (endosomes). In this paper the authors explore the fusion stage of dengue virus entry in different experimental systems ranging from virus fusion to artificial lipid membranes to fusion inside the cells. While earlier work on dengue virus entry has focused on the virus protein that mediates fusion, they found that effective action of this protein requires specific lipid composition of the membrane the virus fuses to. In effect, this lipid dependence allows virus to control intracellular location of the fusion event and, thus, the place of its RNA release by exploiting cell-controlled differences between lipid compositions of different organelles the virus travels through. The essential role of the interactions between dengue virus and its lipid cofactors during virus entry suggests that these interactions may be targeted in drug design.

Dengue Virus Ensures Its Fusion in Late Endosomes Using Compartment-Specific Lipids. PLoS Pathog 6(10): e1001131. doi:10.1371/journal.ppat.1001131
Many enveloped viruses invade cells via endocytosis and use different environmental factors as triggers for virus-endosome fusion that delivers viral genome into cytosol. Intriguingly, dengue virus (DEN), the most prevalent mosquito-borne virus that infects up to 100 million people each year, fuses only in late endosomes, while activation of DEN protein fusogen glycoprotein E is triggered already at pH characteristic for early endosomes. Are there any cofactors that time DEN fusion to virion entry into late endosomes? Here we show that DEN utilizes bis(monoacylglycero)phosphate, a lipid specific to late endosomes, as a co-factor for its endosomal acidification-dependent fusion machinery. Effective virus fusion to plasma- and intracellular- membranes, as well as to protein-free liposomes, requires the target membrane to contain anionic lipids such as bis(monoacylglycero)phosphate and phosphatidylserine. Anionic lipids act downstream of low-pH-dependent fusion stages and promote the advance from the earliest hemifusion intermediates to the fusion pore opening. To reach anionic lipid-enriched late endosomes, DEN travels through acidified early endosomes, but we found that low pH-dependent loss of fusogenic properties of DEN is relatively slow in the presence of anionic lipid-free target membranes. We propose that anionic lipid-dependence of DEN fusion machinery protects it against premature irreversible restructuring and inactivation and ensures viral fusion in late endosomes, where the virus encounters anionic lipids for the first time during entry. Currently there are neither vaccines nor effective therapies for DEN, and the essential role of the newly identified DEN-bis(monoacylglycero)phosphate interactions in viral genome escape from the endosome suggests a novel target for drug design.

Related:

• Dengue Virus
• Pathogenesis and treatment of dengue fever

No.

How do I know? Because the scientists who did the research say so:

The idea that these powerful techniques with undoubted side effects would ever be applied to something as trivial as the common cold is laughable. If only BBC News had kept its head and gone with a sensible headline such as “Is science on the verge of curing Lassa fever?”.

And what happended to the BBC News policy of linking to the original research article?

Several historical epidemic waves of plague have been attributed to Yersinia pestis, the etiologic agent of modern plague. The most famous of these was the second pandemic which was active in Europe from AD 1347 until 1750, and began with the ‘Black Death’. The most informative method to establish the etiological nature of these ancient infections should be the analysis of ancient DNA, but the results of this method have been controversial. By combining ancient DNA analyses and protein-specific detection, this paper demonstrates that Y. pestis caused the Black Death. Furthermore, they show that at least two variants of Y. pestis spread over Europe during the second pandemic. The analysis of up to 20 diagnostic markers reveals that the two variants evolved near the time that phylogenetic branches 1 and 2 separated and may no longer exist. These results resolve a long-standing debate about the etiology of the Black Death and provide key information about the evolution of the plague bacillus and the spread of the disease during the Middle Ages.

Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathog 6(10): e1001134. doi:10.1371/journal.ppat.1001134
From AD 1347 to AD 1353, the Black Death killed tens of millions of people in Europe, leaving misery and devastation in its wake, with successive epidemics ravaging the continent until the 18th century. The etiology of this disease has remained highly controversial, ranging from claims based on genetics and the historical descriptions of symptoms that it was caused by Yersinia pestis to conclusions that it must have been caused by other pathogens. It has also been disputed whether plague had the same etiology in northern and southern Europe. Here we identified DNA and protein signatures specific for Y. pestis in human skeletons from mass graves in northern, central and southern Europe that were associated archaeologically with the Black Death and subsequent resurgences. We confirm that Y. pestis caused the Black Death and later epidemics on the entire European continent over the course of four centuries. Furthermore, on the basis of 17 single nucleotide polymorphisms plus the absence of a deletion in glpD gene, our aDNA results identified two previously unknown but related clades of Y. pestis associated with distinct medieval mass graves. These findings suggest that plague was imported to Europe on two or more occasions, each following a distinct route. These two clades are ancestral to modern isolates of Y. pestis biovars Orientalis and Medievalis. Our results clarify the etiology of the Black Death and provide a paradigm for a detailed historical reconstruction of the infection routes followed by this disease.

Related:

• Ancient Plague
• Plague: Past, Present, and Future
• Plague: From the 14th to the 21st century and still going strong