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Diagnosis Glitter


News from Penn State: Scientists are starting to study the variations in (and similarities between) various strains of HSV buzzing around different populations, and how they evolve over time.


In a small study, researchers found that the drug — called pritelivir — substantially curbed “viral shedding” in people with genital herpes. That means it decreased the amount of time the virus was active and potentially transmissible to patients’ sexual partners.

The findings, reported in the Jan. 16 issue of the New England Journal of Medicine, are based on 156 patients followed for just four weeks. Experts cautioned that the study is preliminary and offers a “proof of concept.”

Still, they said, the results are important because pritelivir is the first in a new class of drugs that works differently than existing medications for genital herpes. The hope is that pritelivir will be better at preventing transmission of the virus.


talesofdrunkennessandcruelty:

Geneticists Use Herpes to

Confirm Ancient Human

Migration Routes

HERPES = HISTORY.


whoisrichardlevine:

yikes… shivers…

BREAKING NEWS: Immunosuppressive drugs can lead to outbreaks by viruses such as herpes that take advantage of compromised immune systems.

No shit. Glad we spent time and money on that one.

This article is pretty doom and gloom and overly dramatic about herpes, so take it with about a tablespoon of salt. But I do think it’s interesting that there’s evidence the herpes virus can sense when its host cells are about to kick the bucket. Anything that demonstrates the ingenuity and intelligence of the virus is cool to read about.


An international collaboration of researchers including Felicia Goodrum of the University of Arizona’s immunobiology department has studied how a human herpes virus carried by the majority of the population packages its genetic information during infection.
The discoveries improve the chances of developing more targeted therapies in place of existing drugs, which do not always work or come with side effects.

"The human immune system is very sophisticated, and the way this virus has managed to stealthily integrate into our biology to ensure its own survival is no small feat," said Goodrum, also a member of the UA’s BIO5 Institute.

"CMV is a master of human cell biology. From transcribing DNA into blueprints for proteins to the manufacturing of those proteins, from cell division to cellular metabolism, there is not a process this virus has not tweaked," Goodrum also said.

That mastery, she explained, is the reason the virus is so elusive to vaccine, and there currently is no way to eradicate it. Goodrum noted that with other herpes viruses, like Epstein-Barr or chicken pox, the infection is obvious. But that is not the case with CMV.

"From the perspective of a virus, that is the pinnacle of mastery — to infect without ever making its presence known," Goodrum said.

"To develop more effective antiviral strategies, we must understand the biology of the virus infection and how the virus manages to persist for our lifetimes," she said. "We are trying to understand how our cellular mechanisms are being used by this virus and discover targets for drugs to control it."

In which the herpes virus is actually really clever and well developed, and I have to admire it.


medicine-nerd:

Herpes Virus has an internal pressure 8x higher than a car tire. It uses this pressure to literally blast its DNA into human cells. 

Via: https://www.facebook.com/IFeakingLoveScience?ref=stream&hc_location=stream

This is the first “pressure-driven infection mechanism” found in a human virus. More information: http://bit.ly/16bu679

Woah.


earthwindandherpes:

Here’s one of the links I was referring to. I know it’s FOX news but it was more the focus on the antibody cells that I was referring to that I havent found in other articles.

From the article:

Before this study, researchers believed that herpes reactivation was controlled at the ganglion level of the spinal canal area. But by using a technique called laser capture, Corey and his colleagues were able to biopsy and analyze the RNA in pieces of human tissue from the dermal-epidermal junction (DEJ), where the dermis – the outer layer of skin – connects to the epidermis – the layer of tissue just below the skin’s surface.  The team discovered that these CD8αα+ T-cells are located in the DEJ and are responsible for controlling HSV-2 – implying that herpes reactivation is controlled in the skin, not the spine.

Researchers had originally estimated that herpes reactivated once a month, but the discovery of these ever-present T-cells led Corey and his team to believe the virus actually reactivates once a week or every few days.  So when herpes lesions occur, it is because there were not enough CD8αα+ T-cells to suppress the outbreak, Corey said.

CD8αα+ T-cells were previously known to exist in the gut mucosa, but most of the research on CD8+ T-cells focused on studying them in blood circulation.  Corey and his team were the first to find the phenotype of CD8αα+ T-cells to persist in the skin.  He said that a potential herpes vaccine would focus on increasing these cells in the immune system.

“It gives us a marker by which one can test vaccines,” Corey said.

Hm, very cool! Thanks for sharing, anon!

Woah. I wish I could reblog this from notmyphone so the text didn’t crop.


STDs aren’t some fickle god’s punishment for promiscuity — they’re life forms trying to make a living. And it’s not just us. Animals and plants are also plagued by STDs, though in the case of plants the “sex” part gets a little complicated.


A University of Queensland spin-off company is about to start clinical trials that could result in the prevention and treatment of genital herpes, a virus that affects hundreds of thousands of people, threatens newborn babies and is believed to contribute to the development of HIV. 

Coridon Pty Ltd will soon start a Phase I HSV-2 vaccine clinical trial in Brisbane. 

Professor Ian Frazer said the new technology could eventually prevent and cure the herpes simplex virus (HSV-2), and could also lead to other effective vaccinations for incurable diseases such as HIV/AIDS and hepatitis C. 

Professor Frazer, CEO and Director of Research at Brisbane’s Translational Research Institute (TRI) and lead researcher at The University of Queensland Diamantina Institute (UQDI), is leading development of the vaccine. 

The World Health Organisation (WHO) estimates more than half a billion people aged 15–49 years are living with HSV-2 worldwide. 

“HSV-2 genital herpes affects up to one in eight Australians, and there is currently no curative treatment,” Professor Frazer said. 

“The vaccine technology offers the potential of being both a preventative and therapeutic vaccine. 

The vaccine will be injected into the forearms of 20 healthy volunteers in a trial designed to demonstrate its safety and how well it is tolerated, and to determine the effective dose and show that it generates a robust immune response. 

Professor Frazer said HSV-2 was the major cause of genital herpes. 

“The virus causes pain and discomfort, and can have serious health implications for babies born to infected women,” he said. 

“Herpes is also believed to aid in the transmission of HIV. 

“Current herpes treatment involves the use of antiviral drugs which can reduce, but not eliminate, outbreaks and shedding but do not prevent spread of the disease. 

“This is the beginning of an exciting period for our herpes vaccine,” Professor Frazer said. 

“We have seen very encouraging results from animal studies and we expect pivotal data showing that our vaccine, which incorporates our patented optimisation technology, to produce similar immune responses in the clinic.” 

The Phase I clinical trial will be undertaken through Q-Pharm Pty Ltd’s clinical trial site at the Royal Brisbane and Women’s Hospital. 


earthwindandherpes:

bust-the-shades:

Getting closer! *crosses fingers*

URG, I WISH.

According to the lead scientist at Harvard, Dr. Judy Lieberman, the siRNA “could either be administered to a person already infected to reduce viral shedding, pain, and transmission to a sexual partner, or it could be administered to those who are not infected to protect them.” However, before using the microbicide on humans, tests will first need to be done on monkeys.

Not sure I’d call that a cure, but rock on, scientists.



A blog about living with herpes, the glitter of the STD world.

You can talk to me. I don't mind.





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