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The herpes simplex virus is one of the herpes, DNA viruses that are important in causing human disease.
It is "composed of an inner core containing linear double-stranded DNA, surrounded concentrically by an icosahedral capsid of approximately 100 nm, an amorphous layer termed the tegument, and an outer envelope composed of lipids and glycoproteins." (Paula W. Using the Baltimore classification (which is based on the mechanism of mRNA production) is a Group 1 virus (dsDNA) from the family Herpesviridae, subfamily Alphaherpesvirinae, Genus Simplexvirus and Species Herpes simplex virus 1. Herpes can be found throughout human history by reading texts from the past that describe the characteristics of the fever blisters.
In addition to affecting the oral and genital areas of the body, HSV can infect other areas. In this research experiment, Becket Feierbach and his associates looked to determine how HSV-1 develops spatial compartments within the host's nucleus where replication takes place. The third research article I found dealt with a possible vaccine that is being developed to prevent being infected with HSV-2.
Feierbach B, Piccinotti S, Bisher M, Denk W, Enquist LW (2006) Alpha-Herpesvirus Infection Induces the Formation of Nuclear Actin Filaments . The bottleneck occurs when HSV-1 particles, which can lie dormant in the cells of the nervous system for decades after initial infection, awaken and invade a nearby skin cell, the first stage in sore formation.
Princeton University research suggests that a common strain of herpes virus causes cold sores with only one or two viral particles, resulting in a bottleneck in which the infection is more vulnerable to medical treatment. This restriction to one or two particles limits the genetic diversity of the virus that spreads to the next individual, Enquist said.


In the case of herpes viruses, Enquist said: "The number of different genomes that infect the cell is remarkably low, so any mutations that weaken the virus are unlikely to survive. Although bottlenecks can ensure that only the most fit viruses are transmitted to the next individual, they also can be points at which the infection is more susceptible to immune system responses and drug treatments, according to Taylor.
Model of herpes virus spread from neuron to skin cell Herpes virus particles move via axonal transport inside a neuron. Julie Pfeiffer, an associate professor of microbiology at the University of Texas Southwestern Medical Center, said the Princeton research is the first to tally how many viral particles are involved in HSV-1 infection — and reveal that as the virus' weak point.
To determine the number of virus particles that infect the skin cell, the researchers constructed three genetically unique viral genomes labeled with either red, green or blue fluorescent tags, and then infected cells with the particles and analyzed them for the presence of the three colors.
Taylor then filmed individual virus particles of pseudorabies virus, a model alpha-herpes virus that infects animals, as the particles exited neurons and entered skin cells.
The video, courtesy of Taylor, reveals a handful of viral particles exiting an axon but only one particle entering a nearby epithelial cell. The paper, "Alphaherpesvirus axon-to-cell spread involves limited virion transmission," was published Oct.
When checked, Shutterstock's safe search screens restricted content and excludes it from your search results. Once inside the skin cell, a single viral particle multiplies and spreads millions of copies to nearby skin cells, creating a visible lesion or "cold sore." The virus can then spread to new individuals through skin-to-skin contact. Viral particles (red dots) move along the narrow interior of a nerve cell, which looks like a black line near the top of the screen. This puts the virus at a disadvantage, he said, because having a variety of distinct genomes enhances the overall chances of the virus surviving and spreading.


He and Enquist worked with co-author Oren Kobiler, a former Princeton postdoctoral researcher now at Tel Aviv University.
Upon exiting the neuron, only one or two viral particles enter the susceptible skin cell, resulting in a bottleneck that restricts viral spread.
They counted the number of cells containing one, two or all three colors and used statistical analysis to determine the number of unique viral genomes expressed in each cell. He found that the bottleneck limiting infection to one or two particles exists for pseudorabies virus as well. Once inside, the virus particle replicates and creates millions of particles that fill up the cell, turning it red in color. A single viral particle exits the nerve cell and moves down toward a cell, enters it and begins replicating to create millions of copies of the viral particle that turn the entire cell red. A well-known example of a virus that relies on genetic diversity to thrive is HIV, which involves large numbers of viral particles with distinct genomes. These viral particles later exit the infected cell and attack surrounding epithelial cells. The work was supported by the National Institutes of Health and the American Cancer Society. Haser of at the University of Pennsylvania School of Medicine discovered such a protein that is produced during latency and its purpose.




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