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Virus and bioinformatics articles with some microbiology and immunology thrown in for good measure
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Scientists decode world's most complex human virus

Scientists decode world's most complex human virus | Virology and Bioinformatics from Virology.ca | Scoop.it
Cytomegalovirus – or CMV - is the most complex virus known to man. Most people will in their lives become infected by CMV and, because it is a herpes virus, infection lasts a lifetime. CMV can cause severe disease in immunosuppressed transplant recipients or individuals with HIV/AIDS, and is responsible ...
Chris Upton + helpers's insight:

huh?

...most complex virus known to man??

what's that all about?

 

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Cytomegalovirus load in whole blood is more reliable for predicting and assessing CMV disease than pp65 antigenaemia

Cytomegalovirus load in whole blood is more reliable for predicting and assessing CMV disease than pp65 antigenaemia | Virology and Bioinformatics from Virology.ca | Scoop.it

CMV is a common cause of disease in immunocompromised patients. Because sampling of the diseased organ can be invasive, markers of systemic CMV reactivation such as pp65 and CMV viral load are commonly used to monitor patients at risk of CMV disease. In this retrospective analysis, the performance of these markers was compared in solid organ transplant recipients, patients with haematological malignancies and HIV infection. Both assays were sensitive markers of reactivation, however, the predictive value for disease of a positive result for both was low. Compared to viral load, the pp65 assay was a less sensitive marker of CMV reactivation. It was only positive when the viral load was greater than 3 log (10) copies/ml whole blood and was negative in 10 instances when the viral load was between 3 and 5 logs. In concordantly positive samples, the number of pp65 positive cells varied widely relative to the viral load and the number of positive cells counted could not be used to predict disease likelihood with any certainty. To conclude, CMV viral load provides a more consistent guide to determine likelihood of disease than pp65 count and is a more sensitive marker of CMV reactivation.

 Herpesvirus graphic by Russell Kightley Media

Ed Rybicki's insight:

It gives me great peasure to tout this paper by my Medical School colleagues - for a nice piece of work which should improve C[yto]MV detection.  Because CMV is cucmber mosaic virus, obviously, and no-one cares about that.  Except cucmbers.

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Oyster deaths linked to hot weather

Oyster deaths linked to hot weather | Virology and Bioinformatics from Virology.ca | Scoop.it
A number of oysters have been killed following the outbreak of a virus in Carlingford Lough in County Down, linked to recent hot weather.
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Connecting the Dots: Chicken Pox, Varicella Vaccine and Shingles | Vaccinews Blog

Connecting the Dots: Chicken Pox, Varicella Vaccine and Shingles | Vaccinews Blog | Virology and Bioinformatics from Virology.ca | Scoop.it
“How likely is it that my older 2 kids (who got wild pox and weren’t vaccinated) will get shingles later?”

Via anarchic_teapot
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anarchic_teapot's curator insight, January 13, 2013 11:38 AM

Important stuff. Needs to be read and passed on.

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Pangaea and the Out-of-Africa Model of Varicella-Zoster Virus Evolution and Phylogeography

The goal of this minireview is to provide an overview of varicella-zoster virus (VZV) phylogenetics and phylogeography when placed in the broad context of geologic time.

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CDC - CMV: Homepage

CDC - CMV: Homepage | Virology and Bioinformatics from Virology.ca | Scoop.it
Cytomegalovirus (CMV) and Congenital CMV Infection...
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Viral disease -- particularly from herpes -- gaining interest as possible cause of coral decline

Viral disease -- particularly from herpes -- gaining interest as possible cause of coral decline | Virology and Bioinformatics from Virology.ca | Scoop.it
As corals continue to decline in abundance around the world, researchers are turning their attention to a possible cause that's almost totally unexplored -- viral disease. It appears that corals harbor many different viruses -- particularly herpes.
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Hopeful Genital Herpes Vaccine Misses the Mark

Hopeful Genital Herpes Vaccine Misses the Mark | Virology and Bioinformatics from Virology.ca | Scoop.it
It's back to the drawing board for researchers seeking to develop a vaccine that protects against genital herpes.

Via Sakis Koukouvis
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Biophysicist obtains first experimental evidence of pressure inside the herpes virus

Biophysicist obtains first experimental evidence of pressure inside the herpes virus | Virology and Bioinformatics from Virology.ca | Scoop.it

Herpes viruses are like tiny powder kegs waiting to explode.  For more than 20 years scientists suspected that herpes viruses were packaged so full of genetic material that they built up an internal pressure so strong it could shoot viral DNA into a host cell during infection. No one had been able to prove that theory until now.

Ed Rybicki's insight:

The virus as jack-in-the-box - nice piece of proof!

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Herpes Virus Genome, The Pressure Is On

Abstract

 

Herpes simplex virus type 1 (HSV-1) packages its micrometers-long double-stranded DNA genome into a nanometer-scale protein shell, termed the capsid. Upon confinement within the capsid, neighboring DNA strands experience repulsive electrostatic and hydration forces as well as bending stress associated with the tight curvature required of packaged DNA. By osmotically suppressing DNA release from HSV-1 capsids, we provide the first experimental evidence of a high internal pressure of tens of atmospheres within a eukaryotic human virus, resulting from the confined genome. Furthermore, the ejection is progressively suppressed by increasing external osmotic pressures, which reveals that internal pressure is capable of powering ejection of the entire genome from the viral capsid. Despite billions of years of evolution separating eukaryotic viruses and bacteriophages, pressure-driven DNA ejection has been conserved. This suggests it is a key mechanism for viral infection and thus presents a new target for antiviral therapies.

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Do viruses require the cytoskeleton?

Do viruses require the cytoskeleton? | Virology and Bioinformatics from Virology.ca | Scoop.it
Background

It is generally thought that viruses require the cytoskeleton during their replication cycle. However, recent experiments in our laboratory with rubella virus, a member of the family Togaviridae (genus rubivirus), revealed that replication proceeded in the presence of drugs that inhibit microtubules. This study was done to expand on this observation.

Findings

The replication of three diverse viruses, Sindbis virus (SINV; family Togaviridae family), vesicular stomatitis virus (VSV; family Rhabdoviridae), and Herpes simplex virus (family Herpesviridae), was quantified by the titer (plaque forming units/ml; pfu/ml) produced in cells treated with one of three anti-microtubule drugs (colchicine, noscapine, or paclitaxel) or the anti-actin filament drug, cytochalasin D. None of these drugs affected the replication these viruses. Specific steps in the SINV infection cycle were examined during drug treatment to determine if alterations in specific steps in the virus replication cycle in the absence of a functional cytoskeletal system could be detected, i.e. redistribution of viral proteins and replication complexes or increases/decreases in their abundance. These investigations revealed that the observable impacts were a colchicine-mediated fragmentation of the Golgi apparatus and concomitant intracellular redistribution of the virion structural proteins, along with a reduction in viral genome and sub-genome RNA levels, but not double-stranded RNA or protein levels.

Conclusions

The failure of poisons affecting the cytoskeleton to inhibit the replication of a diverse set of viruses strongly suggests that viruses do not require a functional cytoskeletal system for replication, either because they do not utilize it or are able to utilize alternate pathways when it is not available.

 

Herpesvirus replication graphic from Russell Kightley Media

Ed Rybicki's insight:

Nice review and nice results - rather surprising, too, seeing as I have taught for years that viruses use intracellular transport systems to get around!

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Trends in Microbiology - A cultured affair: HSV latency and reactivation in neurons

After replicating in surface epithelia, herpes simplex virus type-1 (HSV-1) enters the axonal terminals of peripheral neurons. The viral genome translocates to the nucleus, where it establishes a specialized infection known as latency, re-emerging periodically to seed new infections. Studies using cultured neuron models that faithfully recapitulate the molecular hallmarks of latency and reactivation defined in live animal models have provided fresh insight into the control of latency and connections to neuronal physiology. With this comes a growing appreciation for how the life cycles of HSV-1 and other herpesviruses are governed by key host pathways controlling metabolic homeostasis and cell identity.

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PLoS Pathogens: 3D Reconstruction of VZV Infected Cell Nuclei and PML Nuclear Cages by Serial Section Array Scanning Electron Microscopy and Electron Tomography

PLoS Pathogens: 3D Reconstruction of VZV Infected Cell Nuclei and PML Nuclear Cages by Serial Section Array Scanning Electron Microscopy and Electron Tomography | Virology and Bioinformatics from Virology.ca | Scoop.it

"Varicella-zoster virus (VZV) is a human alphaherpesvirus that causes varicella (chickenpox) and herpes zoster (shingles). Like all herpesviruses, the VZV DNA genome is replicated in the nucleus and packaged into nucleocapsids that must egress across the nuclear membrane for incorporation into virus particles in the cytoplasm. Our recent work showed that VZV nucleocapsids are sequestered in nuclear cages formed from promyelocytic leukemia protein (PML) in vitro and in human dorsal root ganglia and skin xenografts in vivo. We sought a method to determine the three-dimensional (3D) distribution of nucleocapsids in the nuclei of herpesvirus-infected cells as well as the 3D shape, volume and ultrastructure of these unique PML subnuclear domains. Here we report the development of a novel 3D imaging and reconstruction strategy that we term Serial Section Array-Scanning Electron Microscopy (SSA-SEM) and its application to the analysis of VZV-infected cells and these nuclear PML cages. We show that SSA-SEM permits large volume imaging and 3D reconstruction at a resolution sufficient to localize, count and distinguish different types of VZV nucleocapsids and to visualize complete PML cages. This method allowed a quantitative determination of how many nucleocapsids can be sequestered within individual PML cages (sequestration capacity), what proportion of nucleocapsids are entrapped in single nuclei (sequestration efficiency) and revealed the ultrastructural detail of the PML cages. More than 98% of all nucleocapsids in reconstructed nuclear volumes were contained in PML cages and single PML cages sequestered up to 2,780 nucleocapsids, which were shown by electron tomography to be embedded and cross-linked by an filamentous electron-dense meshwork within these unique subnuclear domains. This SSA-SEM analysis extends our recent characterization of PML cages and provides a proof of concept for this new strategy to investigate events during virion assembly at the single cell level."

 

This paper is what amounts to a tour de force of structural and cell biology, and represents a very impressive achievement in 3-D image reconstruction at near-cell scale.

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Shingles Vaccine Deemed Safe in Large Study

Shingles Vaccine Deemed Safe in Large Study | Virology and Bioinformatics from Virology.ca | Scoop.it
The shingles vaccine is “generally safe and well tolerated,” according to a study of nearly 200,000 patients.

Shingles, or herpes zoster, is a painful rash caused by reactivation of chickenpox virus that has remained dormant in the body. Up to 1 million Americans, more than half of whom are 60 or older, are diagnosed with shingles every year, the researchers write.

Researchers analyzed data of 193,083 vaccinated patients aged 50 or older for certain side effects that could be related to the shingles vaccine.

The researchers found no increased risk in the first six weeks after vaccination for stroke, heart disease, infections of the brain or spinal cord or other brain diseases, Bell's palsy, or Ramsay-Hunt syndrome, which can occur when the virus that causes shingles affects the facial nerve near an ear.

An increased risk of allergic reaction was found in the first week after receiving the shingles vaccine.

A majority of these reactions involved an inflammatory response at the injection site, involving symptoms such as redness, swelling, and mild pain.


Via Ed Rybicki
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Novel Gene linked to herpes-related cold sores

Novel Gene linked to herpes-related cold sores | Virology and Bioinformatics from Virology.ca | Scoop.it

Researchers have identified a human chromosome containing a specific gene associated with susceptibility to herpes simplex labialis (HSL), the common cold sore. The gene C21ORF91 encodes a cytoplasmic protein with currently unknown function. Cold sores occur when the herpes virus reactivates from its quiescent state within the nerve, infecting the lip, nose, or face.


Via Dr. Stefan Gruenwald
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