How herpesvirus invades nervous system

Northwestern Medicine scientists have identified a component of the herpesvirus that “hijacks” machinery inside human cells, allowing the virus to rapidly and successfully invade the nervous system upon initial exposure.

Led by Gregory Smith, associate professor in immunology and microbiology at Northwestern University Feinberg School of Medicine, researchers found that viral protein 1-2, or VP1/2, allows the herpesvirus to interact with cellular motors, known as dynein. Once the protein has overtaken this motor, the virus can speed along intercellular highways, or microtubules, to move unobstructed from the tips of nerves in skin to the nuclei of neurons within the nervous system.

This is the first time researchers have shown a viral protein directly engaging and subverting the cellular motor; most other viruses passively hitch a ride into the nervous system.

“This protein not only grabs the wheel, it steps on the gas,” says Smith. “Overtaking the cellular motor to invade the nervous system is a complicated accomplishment that most viruses are incapable of achieving. Yet the herpesvirus uses one protein, no others required, to transport its genetic information over long distances without stopping.”

Herpesvirus is widespread in humans and affects more than 90 percent of adults in the United States. It is associated with several types of recurring diseases, including cold sores, genital herpes, chicken pox, and shingles. The virus can live dormant in humans for a lifetime, and most infected people do not know they are disease carriers. The virus can occasionally turn deadly, resulting in encephalitis in some.

Until now, scientists knew that herpesviruses travel quickly to reach neurons located deep inside the body, but the mechanism by which they advance remained a mystery.

Smith’s team conducted a variety of experiments with VP1/2 to demonstrate its important role in transporting the virus, including artificial activation and genetic mutation of the protein. The team studied the herpesvirus in animals, and also in human and animal cells in culture under high-resolution microscopy. In one experiment, scientists mutated the virus with a slower form of the protein dyed red, and raced it against a healthy virus dyed green. They observed that the healthy virus outran the mutated version down nerves to the neuron body to insert DNA and establish infection.

“Remarkably, this viral protein can be artificially activated, and in these conditions it zips around within cells in the absence of any virus. It is striking to watch,” Smith says.

He says that understanding how the viruses move within people, especially from the skin to the nervous system, can help better prevent the virus from spreading.

Additionally, Smith says, “By learning how the virus infects our nervous system, we can mimic this process to treat unrelated neurologic diseases. Even now, laboratories are working on how to use herpesviruses to deliver genes into the nervous system and kill cancer cells.”

Smith’s team will next work to better understand how the protein functions. He notes that many researchers use viruses to learn how neurons are connected to the brain.

“Some of our mutants will advance brain mapping studies by resolving these connections more clearly than was previously possible,” he says.

Apoptosis Triggers Replication of Common Viruses

Researchers from Children’s National Medical Center have found that an alternate, “escape” replication process triggered by apoptosis – the process of cell death or “cell suicide” – appears to be common in human herpesviruses (HHV). The findings have implications for better understanding of viruses and of disease conditions and treatments, like chemotherapy, that stimulate apoptosis. The study was published online, ahead of print, in the Journal of Virology.
“Our findings suggest that most if not all HHV types can sense that the host cell is dying, which prompts them to launch an emergency replication process,” said lead author Alka Prasad, PhD, a post-doctoral fellow in the Center for Cancer and Immunology Research of the Children’s Research Institute at Children’s National. “Herpesviruses have genes that try to prevent apoptosis, but when the viruses cannot block the host cell from undergoing apoptosis, they apparently launch this alternate process to reproduce before the cell dies – suggesting that these herpesviruses are not simply destructive ‘cell-bombs’ but more nuanced organisms that engage in a dialogue with the host cell.”

A. Prasad, J. Remick, S. L. Zeichner. Activation of Human Herpesvirus Replication by Apoptosis. Journal of Virology, 2013; DOI: 10.1128/JVI.01178-13

It’s been a really hard struggle however, I’ve never been in such a good place mentally. I’ve never had such a positive image about myself in my life. I no longer see myself as a slut or a victim and have fully accepted that I have herpes.

How I came in contact with herpes is something I wish no girl has to ever go through. Sadly, it’s a common incident that occurs in today’s society.

I have the most amazing boyfriend to thank for most of this, without his support, I wouldn’t have grown so much.

It’s been about two years since I’ve hit rock bottom.

I’ve never flown so high before.

Herpes: Kuss fürs Baby kann tödlich enden !

Neugeborene sind so süß, dass man sie einfach küssen und herzen will – doch Vorsicht! Durch einen Kuss kann das Herpesvirus auf das Baby übertragen werden, was schlimme Folgen haben kann:

Schwaches Immunsystem

Ein Kuss kann für ein Baby aufgrund des Herpesvirus sehr gefährlich sein. Herpes ist für Erwachsene meist nur lästig, für Neugeborene kann das Virus aber sogar lebensbedrohlich werden. Bei…

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Herpes-Virus: Kommen Babys mit ihm in Kontakt, können Hirnschäden die Folge ...

http://infocontact.de/wp-content/uploads/2015/09/41TiNFnQ3yL._SL160_.jpgHerpes-Virus: Kommen Babys mit ihm in Kontakt, können Hirnschäden die Folge … Kommt ein Baby damit in Kontakt, kann es Leber- und Hirnschäden erleiden und sogar sterben. Ich weiß, das klingt, als würde ich nur Panik machen, aber wenn meine Freundin mir nicht davon erzählt hätte, wäre meine kleine Tochter jetzt ernsthaft Read more at http://bit.ly/1QExAnE

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The Facts about Herpesvirus Infection

The Facts about Herpesvirus Infection

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Herpesvirus infectionsare one of the common sexually transmitted infections among people of all ages. It has been found that one in every six persons in the age group 14 to 49 is prone to the disease. This infection is caused by the herpes simplex virus. There are two types of herpesvirus, HSV-1 mainly causes lesions and blisters around the mouth and HSV 2 mainly causes lesions in the genital…

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Some vaccines support evolution of more-virulent viruses

Some vaccines support evolution of more-virulent viruses #herpesvirus #viruses #leakyvaccines #morevirulentviruses

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Scientific experiments with the herpesvirus such as the one that causes Marek’s disease in poultry have confirmed, for the first time, the highly controversial theory that some vaccines could allow more-virulent versions of a virus to survive, putting unvaccinated individuals at greater risk…

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VirScan: Test que identifica tu historial de infecciones virales

Científicos de la Harvard Medical School de Boston han desarrollado una nueva técnica llamada VirScan que permite mediante una gota de sangre identificar los distintos virus que han infectado a una persona a lo largo de su vida.

La base del funcionamiento de VirScan es posible gracias a que cada virus que entra en contacto con nuestro organismo deja una huella inmunitaria imborrable que modifica…

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Viral Protein Hijacks Cellular Machinery to Invade Nervous System

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Northwestern Medicine® scientists have identified a component of the herpesvirus that “hijacks” machinery inside human cells, allowing the virus to rapidly and successfully invade the nervous system upon initial exposure.

Funding: This work was funded by NIH grant R01 AI056346, R01 EY017809, and by the training program in Immunology and Pathogenesis from the NIH (T32AI07476). It was published in the journal Cell Host & Microbe.

Herpesvirus Bovino tipo 4

Questa immagine al microscopio rappresenta la replicazione in vitro dell’Herpesvirus bovino tipo 4, un membro della famiglia degli Herpesviridae,  sottofamiglia della Gammaherpesvirinae e genere Rhadinovirus. L'infezione è generalmente di tipo sub-clinico, ma può causare la malattia riproduttiva nei bovini, come endometrite, vulvovaginiti e anche mastite. La trasmissione avviene sia verticalmente che orizzontalmente. La distribuzione è in tutto il mondo e il virus infetta una gamma di ruminanti tra bisonti, bufali, pecore e capre. La malattia può essere indicata anche come virus passeggero e virus Moyar. Il virus BHV-4 come si diceva prima è spesso subclinico, senza però segni clinici osservabili. Tuttavia, può provocare l'aborto e conservare membrane fetali, e se un feto infetto è nato vivo, può essere debole. Può anche causare mastiti nelle bovine da latte. Esso può essere isolato da casi di congiuntivite e malattie respiratorie, ma non è noto se la EHV-4 è un patogeno primario o opportunistico in determinati casi. La diagnosi si ottiene tramite l’isolamento del virus da tessuti o secrezioni, tramite PCR, ELISA, e indiretta immunofluorescenza. Poiché l’infezione EHV-4 può essere asintomatica, la presenza del virus non conferma che era la causa dei segni clinici osservati. Il virus può rimanere latente in animali recuperati con spargimento nei momenti di sforzo, permettendo la diffusione della malattia ad altri. Appropriate misure di igiene e di isolamento sono in grado di controllare la malattia. Esistono vaccini negli Stati Uniti, ma non sono molto diffusi. Studi precedenti hanno indicato che i macrofagi splenici sono il principale serbatoio di questa infezione persistente di herpesvirus nei conigli. Ora si segnala l'uso di ibridazione in situ (ISH) e metodi di separazione cellulare per caratterizzare la localizzazione cellulare di persistente BHV-4 nei bovini. 

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This science paper model is the Herpesviridae HSV-1, a large family of DNA viruses that cause diseases in animals, including humans, the papercraft was created by Shinaig. The members of this family are also known as herpesviruses. The family name is derived from the Greek word herpein, referring to the latent, recurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.

Herpesviruses all share a common structure-all herpesviruses are composed of relatively large double-stranded, linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a lipid bilayer membrane called the envelope. This whole particle is known as a virion.

All herpesviruses are nuclear-replicating-the viral DNA is transcribed to mRNA within the infected cell’s nucleus.

Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.

During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency associated transcript accumulate instead. In this fashion the virus can persist in the cell indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.

Reactivation of latent viruses has been implicated in a number of diseases. Following activation, transcription of viral genes transitions from latency-associated LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise, and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.

HSV-1 is Herpes Simplex Virus 1, aka Human herpes virus 1. Symptoms of herpes simplex virus infection include watery blisters in the skin or mucous membranes of the mouth, lips or genitals. Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause very mild or atypical symptoms during outbreaks. However, as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and hiding from the immune system in the cell bodies of neurons. After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron’s axon to the skin, where virus replication and shedding occur and cause new sores. [Source: wiki]

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Herpesvirus canino

Questa immagine al microscopio ritrae un Herpesvirus canino (CHV), un virus della famiglia Herpesviridae che provoca una fatale malattia emorragica nei cuccioli  di meno di 2-3 settimane. E ‘noto esistere negli Stati Uniti, in Canada, in Australia, in Giappone, Inghilterra e in Germania. CHV è stata riconosciuta a metà degli anni 1960 da una malattia mortale nei cuccioli. Il periodo di incubazione è da sei a dieci giorni, e viene trasmessa ai cuccioli nel canale del parto e per il contatto con secrezioni infette orali e nasali della madre o di altri cani infetti, ma non si diffonde attraverso l'aria. Il virus si replica nelle cellule superficiali della mucose nasali, tonsille e della faringe. La bassa temperatura del corpo permette al virus di diffondersi e infettare il resto del corpo. I sintomi includono pianto, debolezza, depressione, scarico dal naso, feci gialle, e una perdita del riflesso di suzione. CHV provoca anche una necrotizzante vasculite che provoca emorragia intorno ai vasi sanguigni. Le lesioni oculari sono cheratite, uveite, neurite ottica, retinite, e displasia della retina. Vi è un alto tasso di mortalità, e si avvicina sull’80% in cuccioli di meno di una settimana di vita, e la morte di solito si verifica in uno o due giorni. Alcuni possono contrarre la malattia neurologica e hanno sintomi come difficoltà di deambulazione e cecità. La riattivazione di un'infezione latente può essere causata da stress o farmaci immunosoppressivi come i corticosteroidi. Il sito di latenza ha dimostrato di essere il ganglio trigeminale ed eventualmente il ganglio lombosacrale. In cani adulti, il virus infetta il tratto riproduttivo, che le permette di essere trasmessa sessualmente o passata ai cuccioli durante il parto. Può causare l'aborto, mortalità neonatale, e la sterilità. E’ anche una causa frequente di tosse dei canili. Tuttavia, il contatto sessuale non è la causa principale di trasmissione. La maggior parte dei cani adulti vengono infettati da inalazione di virus attraverso le particelle sospese nell'aria, diffuse dai colpi di tosse o starnuti. Può anche essere contratta da una ciotola di acqua contaminata, o anche solo dal sniffare o leccare un altro cane che sta spargendo il virus. Il virus non sopravvive al di fuori del corpo ed è facilmente distrutto dalla maggior parte dei detergenti.