K
_Kim_
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This study comes from the virology department at Imperial College AND it got published in Science. See, it can be done.
The researchers think that this discovery may explain why some viruses - especially the Human Herpes Viruses - replicate more quickly than expected. The podcast and movies are very informative. Take a look (links below).
ScienceDaily (Feb. 5, 2010) — New video footage of a virus infecting cells is challenging what researchers have long believed about how viruses spread, suggesting that scientists may be able to create new drugs to tackle some viruses.
Repulsion of Superinfecting Virions: A Mechanism for Rapid Virus Spread. Virginie Doceul, Michael Hollinshead, Lonneke van der Linden, Geoffrey L. Smith
Here is a podcast interview with the lead Author Geoffrey L. Smith
And the supplementary material that contains the videos:
The researchers think that this discovery may explain why some viruses - especially the Human Herpes Viruses - replicate more quickly than expected. The podcast and movies are very informative. Take a look (links below).
ScienceDaily (Feb. 5, 2010) — New video footage of a virus infecting cells is challenging what researchers have long believed about how viruses spread, suggesting that scientists may be able to create new drugs to tackle some viruses.
I don't have full text access, but here is the abstract:The researchers believe that other viruses also employ rapid spreading mechanisms. For instance, herpes simplex virus (HSV-1), which causes cold sores, spreads at a faster rate than should be possible given its replication rate. Thus, this phenomenon discovered with vaccinia may be a common feature a viruses.
The discovery may ultimately enable scientists to create new antiviral drugs that target this spreading mechanism. Lead study author Professor Geoffrey L. Smith, a Wellcome Trust Principal Research Fellow from the Section of Virology at Imperial College London, said: "The ability of viruses to spread rapidly is often critical for their ability to cause disease. Therefore, understanding how viruses spread is fundamental to designing strategies to block spread and thereby prevent disease.
"For more than 50 years viruses were thought to spread by an iterative process of infection, replication, release and re-infection, so the rate of spread was limited by the speed of replication. However, my colleagues Virginie Doceul, Mike Hollinshead and Lonnerke van der Linden discovered a novel spreading mechanism that is not limited by virus replication rate and accelerates spread dramatically.
Repulsion of Superinfecting Virions: A Mechanism for Rapid Virus Spread. Virginie Doceul, Michael Hollinshead, Lonneke van der Linden, Geoffrey L. Smith
Here is a podcast interview with the lead Author Geoffrey L. Smith
And the supplementary material that contains the videos:
Also in this issue is an editorial about this article: Greedy Virus Helps Spread Disease. Sverker LundinMovie s1
Movie showing VACV plaque formation. BSC-1 cells were infected with VACV strain WR at low moi and the formation of a plaque was recorded by phase microscopy every h for 16 h after a small plaque first became visible. Note that the motility of infected cells is restricted to within the area showing cytopathic effect (cpe). Virus-induced cell motility is therefore not increasing the rate of spread across the cell monolayer.
Movie s2
Movie showing plaque formation by a VACV strain vEGFPA5L. This virus expresses EGFP fused to the A5 core protein late during infection. BSC-1 cells were infected with vEGFPA5L at low moi and the progression of infection on one side of a plaque was recorded by phase microscopy every h for 16 h.
Movie s3
Movie as for movie 2 except that the growth of the vEGFPA5L plaque was visualized by the EGFP fluorescence.
Movie s4
Movie as for movies 2 and 3 showing merge of phase and fluorescence images. Note that the spread of virus-induced cpe (an early event) precedes that of expression of EGFPA5L, which is made only late during infection.
Movie s5
Movie showing the spread of the edge of a plaque formed by vEGFPA5L at higher rmagnification to show individual virus particles (green dots). Cells were visualised by confocal microscopy using EGFP flourescence. Note cells must express EGFP prior to production of new virus particles and yet there are numerous virus particles on cells distal to those cells expressing EGFP.
Movie s6
Movie showing the formation of actin tails (red) in BSC-1 cells expressing cherryFP-actin that have been infected with vEGFPA5L (green). The movie shows a single focal plane at the periphery of an infected cell where actin tails are formed following the transport of virus particles to the cell periphery (duration, 5 min).
Movie s7
Movie showing green virus particles moving on the tip of red actin tails on a cell expressing cherry-actin and lacking green virus factories. Note that a virus-tipped red actin tail produced by this cell induces the formation of another actin tail after recontacting the cell surface.
Many other viruses, such as herpes simplex virus, appear to employ a similar infection strategy, says Smith. Assuming they utilize the same protein complex as vaccinia, he says, researchers may be able to fight these infections by blocking the interaction of the two proteins.
Cell biologist Michael Way of the London Research Institute agrees that other viruses may also use the vaccinia infection strategy. "I think it may be more general than people realize."