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

Australia to destroy alien carp by releasing herpes into rivers
The Australian government has announced a A$15 million plan to release a strain of herpes virus into rivers to kill invasive carp, a notorious pest
By Alice Klein

A carpageddon is coming. The Australian government has announced a A$15 million plan to release a herpes virus into the rivers, in a bid to wipe out the country’s most notorious fish pest.

Carp have decimated native Australian fish populations since their introduction in 1859, particularly in the Murray-Darling river system, where they now make up 80 per cent of fish numbers.

Scientists at CSIRO, Australia’s national research body, have spent the last seven years investigating the potential of a carp-specific herpes strain – cyprinid herpesvirus 3 – to fight off the invaders. Rigorous testing has shown that the virus kills between 70 and 80 per cent of carp populations, but does not harm native fish species or yabbies, eels, chickens, mice, frogs, turtles or water dragons.

The government announced on Sunday that cyprinid herpesvirus 3 will be released into the Murray-Darling river system by the end of 2018.

Continue Reading.


Cancer-fighting viruses win approval

An engineered herpesvirus that provokes an immune response against cancer has become the first treatment of its kind to be approved for use in the United States, paving the way for a long-awaited class of therapies. On 27 October, the US Food and Drug Administration (FDA) approved a genetically engineered virus called talimogene laherparepvec (T-VEC) to treat advanced melanoma. Four days earlier, advisers to the European Medicines Agency had endorsed the drug.

With dozens of ongoing clinical trials of similar ‘oncolytic’ viruses, researchers hope that the approval will generate the enthusiasm and cash needed to spur further development of the approach. “The era of the oncolytic virus is probably here,” says Stephen Russell, a cancer researcher and haematologist at the Mayo Clinic in Rochester, Minnesota. “I expect to see a great deal happening over the next few years.”

Nature 526, 622–623 (29 October 2015) doi:10.1038/526622a

Killer T cells (orange) are recruited to attack malignant cells (mauve) in the viral-based cancer therapy T-VEC. Dr. Andrejs Liepins/SPL

A Very Short Fact: On this day in 1979, the smallpox virus was certified as extinct, making it the first and to date only human disease driven to extinction.

“Jenner’s vaccine works by generating an immune response to a harmless virus (cowpox) that is so closely related to the lethal virus (smallpox) that the immune system cannot distinguish between the two. This same trick was later used to prevent Marek’s disease, a devastating infection of poultry caused by a tumour-associated herpesvirus called Marek’s disease virus. It mainly affects chickens and rapidly kills up to 80% of a domestic flock, causing severe financial loss. The disease, first described by Hungarian pathologist Jozef Marek (1868–1952) in 1907, begins with paralysis of one or more limbs followed by difficulty in breathing leading to death. These symptoms are caused by T cells infiltrating the nerves and producing tumours in vital organs. Once the virus was isolated in 1967, it was soon discovered that a very similar virus, herpesvirus of turkeys, could protect chickens from Marek’s disease virus without ill effect.”

[P.107, Viruses: A Very Short Introduction by Dorothy H. Crawford]

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Image credit: A patient in bed with smallpox, attended by a physician. Col by Wellcome Library, London. CC-BY-4.0 via Wikimedia Commons.

Porcine Respiratory - NAVLE Review #4

Originally posted by dailypiggie

Most common respiratory diseases of Pigs:

Piglets/ Weanlings:


  • Mycoplasma hyopneumoniae: Pneumonia; 3-10 wk old piglets
  • Mycoplasma hyorhinus: Pericarditis, Pleuritis, Peritonitis, Arthritis (all the -itis); 3-10 wk old piglets
  • Pasterurella multocida: Fibrinous pneumonia; seen in association with other diseases (Mycoplasma, APP, SIV)


  • Porcine Reproductive and Respiratory Syndrome Virus (PRRSV): Arterivirus: Focal to diffuse interstitial pneumonia, can progress to bronchopneumonia. 
  • Psudorabies (Herpesvirus): CNS signs in neonates (& sudden death). Piglets > 3 weeks sneezing, coughing, necrotic bronchitis, bronchiolitis, alveolitis. 
  • Porcine Circovirus Virus - 2: Pneumonia, commonly seen as a complex with PMWS. 

Originally posted by 8bitcookies

Grow-Finish Pigs:


Actinobacillus pleuropneumoniae (APP): Pneumonia; Acute death

Atrophic Rhinitis (Bordetella bronchiseptica (+/-) Pasterella multocida): Variable turbinate atrophy, secondary pneumonia. Pigs > 8 weeks. 


Swine Influenza (SIV): high morbidity, low mortality- nasal discharge, coughing. All age groups. 

Oncogenes and RNA splicing of human tumor viruses

Approximately 10.8% of human cancers are associated with infection by an oncogenic virus. These viruses include human papillomavirus (HPV), Epstein–Barr virus (EBV), Merkel cell polyomavirus (MCV), human T-cell leukemia virus 1 (HTLV-1), Kaposi’s sarcoma-associated herpesvirus (KSHV), hepatitis C virus (HCV) and hepatitis B virus (HBV).

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Some vaccines support evolution of more-virulent viruses

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 of severe illness. The research has important implications for food-chain security and food-chain economics, as well as for other diseases that affect humans and agricultural animals.                                

“The challenge for the future is to identify other vaccines that also might allow more-virulent versions of a virus to survive and possibly to become even more harmful,” said Andrew Read, an author of the paper describing the research, which will be published in the July 27, 2015 issue of the scientific journal PLoS Biology. Read is the Evan Pugh Professor of Biology and Entomology and Eberly Professor in Biotechnology at Penn State University.

Chickens in agricultural production. Credit: Andrew Read, Penn State University    

We interrupt our regular program to tell you about this one-eye abandoned kitten that my best friend rescued one night.  

The kitten’s eyes was either underdeveloped in general or atrophied due to a feline herpesvirus and surgery cost $964, bringing the total veterinarian cost to $1,423, which is my friend’s entire monthly income.  She lives in rural New York, off the grid and live off the land.

I’ve donated  here to help my friend recover the cost, if you have any cash you could spare (even just $5) to help with this kitty we would be super grateful. 

Thank you.