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Paired fluorescence and "phase" (white light) images of uninfected neurons (top and bottom left) and neurons infected with HSV (top and bottom right). Human herpes virus, commonly known as herpes simplex virus 1 and 2 (HSV-1 and HSV-2), is like that friend who ends up crashing on your couch and never leaves. Most of the time he lurks in the background, relatively innocuous but for the annoying thought of his presence. But unlike your couch-crashing "friend," you can't just put herpes out on the street and be done with it.
And worse yet, the Centers for Disease Control and Prevention estimate that, in the United States alone, herpes infects more than three-quarters of a million new people every year. Moriah Szpara, assistant professor of biochemistry and molecular biology at Penn State and researcher at the Huck Institutes of the Life Sciences, aims to find a cure for the disease.
Beyond being a simple, periodic annoyance, herpes sometimes exhibits hypervirulence: running amok in its host and causing blindness, aseptic meningitis (inflammation of the protective membranes covering the brain and spinal cord), or encephalitis (swelling of the brain).
In fact, HSV-1 is the leading cause of infectious blindness in the United States and is the main cause of sporadic, fatal encephalitis. Early in her career, Szpara (pronounced like the tiny songbird, but ending with an "ah" instead of an "oh") is already leading the way in several important areas of human herpesvirus research. Although a neurobiologist and virologist by training, Szpara has pioneered the use of comparative genomics for analyzing variation in HSVa€”variation that is key both to understanding the genetic factors that contribute to virulence and ultimately to developing a vaccine or a cure for the virus. While pursuing postdoctoral work at Princeton University, Szpara introduced the use of high-throughput DNA sequencing to her field, producing the first new HSV genome sequences in two decades. Building on this work, Szpara applied the same approaches to studying a related animal herpesvirus, pseudorabies virus (PRV), and discovered several key genomic characteristics contributing to virulence and mutability in PRV. At the same time, Szpara pursued the question of how neurons respond to pathogen infection. At Penn State, Szpara is focused on finding causes for the range of virulence observed in human herpesvirus, which is crucial to developing a vaccine or cure with maximum efficacy.


By better understanding how human herpesvirus works and what differentiates the many strains of the virus, Szpara hopes to be able to identify the specific genetic loci that contribute to virulence. An investigational vaccine protected some women against infection from one of the two types of herpes simplex viruses that cause genital herpes, according to findings in the New England Journal of Medicine. In a major breakthrough, scientists at the Gladstone Institutes transformed skin cells into heart cells and brain cells using a combination of chemicals. Age-related changes in the human pancreas govern how our bodies respond to rising and falling blood sugar levels throughout our lifetimes, and could affect whether we develop diabetes as adults. For the first time, scientists studying stool transplants have been able to track which strains of bacteria from a donor take hold in a patient's gut after a transplant. A pair of molecular signals controls skin and hair color in mice and humansa€”and could be targeted by new drugs to treat skin pigment disorders like vitiligo, according to a report by scientists at NYU Langone Medical Center.
When it comes to replicating their DNA so they can propagate, normal cells are perfectionists.
As is clearly visible in the white light images, these neurons form dense networks of connections. But occasionally he comes out of the shadows and ends up in the way in your kitchen at mealtime, uninvited and naturally wanting a little something for himself.
Because the drugs currently available to treat HSV treat only the virus's active, replicating phase and associated symptoms (for example, oral and genital sores), they do not affect its latency in neurons, which is what allows herpes to infect its host for life.
That provided the raw material for the first genome-wide comparative analysis of alpha-herpesviruses (the class of herpesviruses that includes HSV-1 and HSV-2), yielding valuable insights into the diversity of herpesvirus genetic sequences and protein coding ability. Multiple vaccine strains of PRV, including one recently sequenced by Szpara, serve as a model for HSV vaccine development.
In mouse models of HSV-1 and PRV infection, Szpara measured genome-wide transcriptional responses (transcription being the first step in the process of gene expression, which is used by viruses to complete their lifecycles), and discovered over 2,000 significant changes in gene expression.
She is also looking at how HSV infection and latency affect host neurons and neighboring cells, with an eye toward finding intrinsic neuronal features and cellular defense mechanisms that may also provide targets for therapeutics to block the progression of infection.


And by transferring the DNA sequence fragments found at those loci between HSV strainsa€”for example, inserting a candidate gene from a more-virulent strain into a strain that is known to be less virulenta€”Szpara will be able to observe the effects of that gene, in vivo in mouse models and in vitro in cultured neurons, and confirm whether it increases or reduces virulence.
For this research they collect viral strains from different people, different body sites, or from cases with varying extremes of symptoms. Cancer cells, on the other hand, have no problem tolerating mistakes while copying their DNA. Fluorescent dyes can be used to stain and highlight the individual filaments of these networks (top left) as well as to detect a specific viral protein expressed during HSV infection (top right). Later he interrupts an intimate moment with a perfectly timed and inopportune knock at your bedroom door; and as time drags on, he generally spoils your good times by managing to be everywhere you wish he wouldn't be at precisely the wrong moments.
The one on the left has spread a given distance from the center point in 48 hours, while the strain on the right has mutations that cause extremely fast viral spread in the same amount of time. The place where the virus hides is in your neurons, and it doesn't kill those neuronsa€”it will kill your skin cells, but it uses your neurons as its home base.
The viral genes that cause those changes in neuronal gene expression can now be targeted with therapeutics for the development of a vaccine or cure. These viruses are studied using Illumina high-throughput sequencing, and bioinformatics tools that detect the differences between strains.
So that's where I come in: I'm a virologist and a neurobiologist with a toolbox in comparative genomics.




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  • 34, 27.12.2015 at 20:33:24
    Herpes are left to treat themselves ease of use and being in a dialog with HuffPost.
  • xanim_qiz, 27.12.2015 at 14:19:12
    Got the simplex virus illness.
  • Sabishka, 27.12.2015 at 17:28:18
    Lifetime, but until then contaminated.
  • ENRIGUE, 27.12.2015 at 21:44:23
    Virus may have the power to ruin the virus before.