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From: xcentral13/28/2012 8:37:44 AM
1 Recommendation   of 3484
 
Tomorrow is the meeting:

"NanoViricides, Inc. (OTC BB: NNVC) (the "Company") announced today that March 29th, 2012 has been confirmed by the US FDA as the date for its initial meeting with the Company's scientists....

This clinical drug candidate is expected to be effective against a majority of strains and types of influenzas including novel epidemic influenza strains such as the one encountered in 2009-2010 (so called "swine flu"); seasonal flu such as H1N1, H3N2; highly pathogenic types such as H7N and H9N; as well as the highly lethal type, so called "bird flu" or H5N1. All influenza viruses use the same common receptor to bind to human cells. Therefore the Company believes that its influenza drug candidate should work against most of the influenza viruses.

The market size for anti-influenza drugs is currently estimated to be approximately $4-$7 billion worldwide. The Company believes that if its FluCide(TM) drug becomes available, the influenza drug market size could become substantially larger. "

Cross your fingers ~)

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From: donpat4/1/2012 9:17:35 AM
   of 3484
 
HIV 'Superinfection' Boosts Immune Response

01 Apr 2012 - 0:00 PDT

Women who have been infected by two different strains of HIV from two different sexual partners - a condition known as HIV superinfection - have more potent antibody responses that block the replication of the virus compared to women who've only been infected once. These findings, by researchers at Fred Hutchinson Cancer Research Center in Seattle, are published online March 29 in PLoS Pathogens.
plospathogens.org

"We found that women who had been infected twice not only had more potent antibody responses, but some of these women had 'elite' antibody activity, meaning that they had a broad and potent ability to neutralize a wide variety of strains of HIV over a sustained period of time," said senior author Julie Overbaugh, Ph.D., a member of the Hutchinson Center's Human Biology Division. It is estimated that only about 1 percent of people with HIV are so-called "elite neutralizers" who are able to potently neutralize multiple subtypes of the virus.

"Individuals who become superinfected with a second virus from a different partner represent a unique opportunity for studying the antibody response and may provide insights into the process of developing broad neutralizing antibodies that could inform HIV-vaccine design," she said.

The study suggests that harboring a mixture of different viral strains may be one way to promote a robust antibody response. The findings also suggest that being infected with two different HIV strains not only leads to a strong response, but also a more rapid response that is capable of recognizing many other HIV strains.

The researchers tracked the immune activity of 12 superinfected women from Mombasa, Kenya, over a five-year period and compared each to a control group of three singly infected women. Overbaugh and lead author Valerie Cortez, a doctoral student in her lab, assessed the ability of antibodies present in superinfected and singly infected women to neutralize a spectrum of circulating HIV-1 variants. In doing so they were able to determine whether the presence of two viruses compared to one made a difference in immune response. The researchers controlled for variables such as antibody response prior to superinfection and biomarkers of immunity such as CD4+ T cell count and viral load.

The study found that superinfected women had, on average, 1.68 times more neutralizing antibodies than non-superinfected women, and they scored much higher in their ability to neutralize the virus - superinfected women had 1.46 times greater potency than the singly infected women.

More than 1.1 million Americans are estimated to be living with HIV today, and every nine-and-a-half minutes someone in the U.S. becomes infected, according to the U.S. Department of Health and Human Services. An HIV vaccine is considered the best approach to long-term protection from HIV infection, but attempts to develop such a vaccine so far have meet with limited success.

"The holy grail of an HIV vaccine is to elicit antibodies to the virus because antibodies have been shown to block virus infection. But there has been little progress in determining how to elicit such antibodies with a vaccine. The study of individuals HIV infected who have developed strong antibody responses to the virus may shed light on the best approach to design a vaccine that will induce an effective immune response," Overbaugh said.


medicalnewstoday.com

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From: xcentral14/2/2012 7:58:21 AM
   of 3484
 
NanoViricides Announces Successful Pre-IND Meeting with the US FDA

WEST HAVEN, Conn., Apr 02, 2012 (BUSINESS WIRE) -- NanoViricides, Inc. (OTC BB: NNVC) (the "Company") announced today that its previously announced pre-IND Meeting was held with the USFDA on March 29th, 2012, as scheduled. This pre-IND meeting focused on FluCide™, designated as NV-INF-1, the Company’s novel anti-influenza drug.
The Company received US FDA comments and exchanged a list of questions with the US FDA prior to the Meeting. The Company believes that the US FDA has given us a good roadmap for advancing towards an IND application.

The Company, with guidance from its regulatory consultants at the Biologics Consulting Group, Inc., had previously determined that filing a pre-IND at this stage was important in order to understand potential US FDA required studies that we will need to perform prior to filing an IND. Because of the novelty of the technology and approach, we requested this pre-IND meeting even before performing certain customary safety/toxicological studies.

The Company believes that it has received valuable guidance from the US FDA in this meeting. We believe that the guidance we received goes beyond FDA guidance documents, and is more specific for our drug candidate, NV-INF-1. The Company will now plan and execute the studies identified based on this meeting.

The Company also intends to pursue licensing activities in countries other than the USA. Some of these countries have different procedures that may enable faster regulatory processes than at the US FDA.

The Company also said that its work on enabling cGMP manufacturing capabilities for the nanoviricides drugs for clinical trials is progressing satisfactorily.

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From: donpat4/5/2012 12:08:17 PM
   of 3484
 
Targeted nanoparticles show success in clinical trials

Posted: Apr 5th, 2012

(Nanowerk News) Targeted therapeutic nanoparticles that accumulate in tumors while bypassing healthy cells have shown promising results in an ongoing clinical trial, according to a new paper.

The nanoparticles feature a homing molecule that allows them to specifically attack cancer cells, and are the first such targeted particles to enter human clinical studies. Originally developed by researchers at MIT and Brigham and Women's Hospital in Boston, the particles are designed to carry the chemotherapy drug docetaxel, used to treat lung, prostate and breast cancers, among others.

In the study, which appears April 4 in the journal Science Translational Medicine ("Preclinical Development and Clinical Translation of a PSMA-Targeted Docetaxel Nanoparticle with a Differentiated Pharmacological Profile"), the researchers demonstrate the particles' ability to target a receptor found on cancer cells and accumulate at tumor sites. The particles were also shown to be safe and effective: Many of the patients' tumors shrank as a result of the treatment, even when they received lower doses than those usually administered.
dx.doi.org


An artist's rendering of BIND-014. (Image: Digizyme, Inc.)

"The initial clinical results of tumor regression even at low doses of the drug validates our preclinical findings that actively targeted nanoparticles preferentially accumulate in tumors," says Robert Langer, the David H. Koch Institute Professor in MIT's Department of Chemical Engineering and a senior author of the paper. "Previous attempts to develop targeted nanoparticles have not successfully translated into human clinical studies because of the inherent difficulty of designing and scaling up a particle capable of targeting tumors, evading the immune system and releasing drugs in a controlled way."

The Phase I clinical trial was performed by researchers at BIND Biosciences, a company cofounded by Langer and Omid Farokhzad in 2007.

"This study demonstrates for the first time that it is possible to generate medicines with both targeted and programmable properties that can concentrate the therapeutic effect directly at the site of disease, potentially revolutionizing how complex diseases such as cancer are treated," says Farokhzad, director of the Laboratory of Nanomedicine and Biomaterials at Brigham and Women's Hospital, associate professor of anesthesia at Harvard Medical School and a senior author of the paper.

Researchers at Dana-Farber Cancer Institute, Weill Cornell Medical College, TGen Clinical Research Services in Phoenix and the Karmanos Cancer Institute in Detroit were also involved in the study.

Targeted particles
Langer's lab started working on polymeric nanoparticles in the early 1990s, developing particles made of biodegradable materials. In the early 2000s, Langer and Farokhzad begin collaborating to develop methods to actively target the particles to molecules found on cancer cells. By 2006 they had demonstrated that targeted nanoparticles can shrink tumors in mice, paving the road for the eventual development and evaluation of a targeted nanoparticle called BIND-014, which entered clinical trials in January 2011.

For this study, the researchers coated the nanoparticles with targeting molecules that recognize a protein called PSMA (prostate-specific membrane antigen), found abundantly on the surface of most prostate tumor cells as well as many other types of tumors.

One of the challenges in developing effective drug-delivery nanoparticles, Langer says, is designing them so they can perform two critical functions: evading the body's normal immune response and reaching their intended targets.

"You need exactly the right combination of these properties, because if they don't have the right concentration of targeting molecules, they won't get to the cells you want, and if they don't have the right stealth properties, they'll get taken up by macrophages," says Langer, also a member of the David H. Koch Institute for Integrative Cancer Research at MIT.

The BIND-014 nanoparticles have three components: one that carries the drug, one that targets PSMA, and one that helps evade macrophages and other immune-system cells. A few years ago, Langer and Farokhzad developed a way to manipulate these properties very precisely, creating large collections of diverse particles that could then be tested for the ideal composition.

"They systematically made a set of materials that varied in the properties they thought would matter, and developed a way to screen them. That's not been done in this kind of setting before," says Mark Saltzman, a professor of biomedical engineering at Yale University who was not involved in this study. "They've taken the concept from the lab into clinical trials, which is quite impressive."

All of the particles are made of polymers already approved for medical use by the U.S. Food and Drug Administration.

Clinical results
The Phase I clinical trial involved 17 patients with advanced or metastatic tumors who had already gone through traditional chemotherapy. In Phase I trials, researchers evaluate a potential drug's safety and study its effects in the body. To determine safe dosages, patients were given escalating doses of the nanoparticles. So far, doses of BIND-014 have reached the amount of docetaxel usually given without nanoparticles, with no new side effects. The known side effects of docetaxel have also been milder.

In the 48 hours after treatment, the researchers found that docetaxel concentration in the patients' blood was 100 times higher with the nanoparticles as compared to docetaxel administered in its conventional form. Higher blood concentration of BIND-014 facilitated tumor targeting resulting in tumor shrinkage in patients, in some cases with doses of BIND-014 that correspond to as low as 20 percent of the amount of docetaxel normally given. The nanoparticles were also effective in cancers in which docetaxel usually has little activity, including cervical cancer and cancer of the bile ducts.

The researchers also found that in animals treated with the nanoparticles, the concentration of docetaxel in the tumors was up to tenfold higher than in animals treated with conventional docetaxel injection for the first 24 hours, and that nanoparticle treatment resulted in enhanced tumor reduction.

The Phase I clinical trial is still ongoing and continued dose escalation is underway; BIND Biosciences is now planning Phase II trials, which will further investigate the treatment's effectiveness in a larger number of patients.

Initial development of the particles at MIT and Brigham and Women's Hospital was supported by funding from the National Cancer Institute, the National Institute of Biomedical Imaging and Bioengineering, the David H. Koch Institute for Integrative Cancer Research at MIT, the Prostate Cancer Foundation, a gift from David H. Koch and the Dana-Farber Harvard Cancer Center Prostate Cancer SPORE. Subsequent development by BIND Biosciences was supported by funding from the National Cancer Institute, the National Institute of Standards and Technology, and BIND Biosciences.

Source: By Anne Trafton, MIT


nanowerk.com

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From: donpat4/6/2012 9:43:03 AM
   of 3484
 
Murphy: Keep deadly virus under wraps

Posted: April 6, 2012 - 12:03am

By Mark E. Murphy

A pair of articles published in the March 20 edition of the Annals of Internal Medicine was largely ignored by the lay press. And yet there it was, in black and white.

The possible End of the World As We Know It.

The gist of the articles was this: Two teams of scientists attending a September 2011 conference in Malta announced that they had developed a genetically engineered strain of the currently circulating H5N1 avian (bird) influenza virus that was readily transmissible between ferrets. The results of their research have not yet been published.

So what, right?

The problem here is that most avian flu strains are zoonoses — that is, they are seen primarily in bird populations and are not easily transmissible from birds to humans. Human-to-human transmission is even more rare.

In the case of the current H5N1 bird flu, that is a very good thing. This virus has affected 577 humans thus far. Over 60 percent of those who have contracted the virus have died. That’s a shocking statistic, and here’s why: Seasonal flu affects approximately one billion people each year on this planet. Only a small fraction of people who get the seasonal flu die each year, usually the very young, the very old or the very ill.

Influenza does, however, occasionally cause a pandemic — an infection that spreads through a large community, or even the entire world, affecting a significant proportion of the population. Influenza pandemics occur roughly every 15-30 years.

The most deadly influenza pandemic in modern times was the Spanish Flu of 1918. It resulted in the deaths of between 50 and 100 million people worldwide.

To cause a pandemic, an influenza virus must meet three criteria: Little or no pre-existing population immunity, an ability to cause illness in humans and efficient transmissibility between humans. The current H5N1 avian flu virus meets the first two criteria; it is the third one that it has had trouble with thus far.

But all that could change in a heartbeat.

Ferret models are considered the most reliable surrogate for human influenza transmission. It would be safe, therefore, to assume that a virus transmissible between ferrets would be similarly transmissible among humans. One of the researchers who described his findings at the Malta conference stated that his H5N1 strain was as “easily transmissible as the seasonal flu.”

The deadly 1918 Spanish Flu had a fatality rate of around 2 percent. The current H5N1 avian flu strain has a fatality rate of around 60 percent. If a billion people worldwide were affected, as is usually the case in a seasonal flu epidemic, 600 million people worldwide could die — roughly twice the population of the United States. And if the one-third worldwide infection rate of the Spanish Flu epidemic were seen, that could result in the deaths of over a billion people, or one out of every seven persons on our planet.

That is a sobering statistic.

The World Health Organization issued a statement expressing “concern” about the H5N1 ferret influenza experiments. The U.S. National Science Advisory Board for Biosecurity recommended that the published manuscripts for the influenza research be revised to remove details of the researchers’ methodology and the specific genetic mutations involved.

Dr. Thomas Inglesby of the Center for Biosecurity at UMPC in Baltimore was more blunt, calling for the involved institutions to “restrict dissemination of their experimental results” and stop all further experimentation on the genetically-engineered H5N1 strains.

Historically, free dissemination of knowledge has been at the core of the medical research community. But this instance is a case for restraint. The implications of either an accidental or terroristic release of a genetically-altered influenza virus this lethal are mind-boggling.

The late Michael Crichton’s novel “The Andromeda Strain” was about a highly lethal, extraterrestrial virus being investigated as a potential biological weapon. In that novel, a physician researcher arguing with a government official screamed out, “We did it to ourselves!”

Let’s hope that is not mankind’s epitaph.

Mark Murphy, M.D., is a Savannah physician and writer.

savannahnow.com

No mention of Nanoviricides' cides which could well eliminate such a catastrophe. Now THAT is really sobering. The death of a billion souls when the remedy was available all the time!

Book and movie to follow!!!

Never again!! ;-)

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To: donpat who wrote (2282)4/6/2012 10:09:18 AM
From: donpat
   of 3484
 
And if the virus doesn't get us - this might - imidacloprid


:

Honeybee on knapweed. The likely culprit in sharp worldwide declines in honeybee colonies since 2006 is imidacloprid, one of the most widely used pesticides (Credit: © Elenathewise / Fotolia)

imidacloprid
en.wikipedia.org
Imidacloprid is a systemic insecticide which acts as an insect neurotoxin and belongs to a class of chemicals called the neonicotinoids which act on the central nervous system of insects with much lower toxicity to mammals. The chemical works by interfering with the transmission of stimuli in the insect nervous system. Specifically, it causes a blockage in a type of neuronal pathway (nicotinergic) that is abundant in insects and not in warm-blooded animals (making the chemical selectively toxic to insects and not warm-blooded animals). This blockage leads to the accumulation of acetylcholine, an important insect neurotransmitter, resulting in the insect's paralysis, and eventually death. It is effective on contact and via stomach action. [2]

Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience, (part of Bayer AG). It is sold under many names for many uses. Imidacloprid is one of the most widely used insecticides and can be applied by soil injection, tree injection, application to the skin, broadcast foliar, ground application as a granular or liquid formulation, or as a pesticide-coated seed treatment.

Use of Common Pesticide, Imidacloprid, Linked to Bee Colony Collapse

ScienceDaily (Apr. 5, 2012) — The likely culprit in sharp worldwide declines in honeybee colonies since 2006 is imidacloprid, one of the most widely used pesticides, according to a new study from Harvard School of Public Health (HSPH).

The authors, led by Alex Lu, associate professor of environmental exposure biology in the Department of Environmental Health, write that the new research provides "convincing evidence" of the link between imidacloprid and the phenomenon known as Colony Collapse Disorder (CCD), in which adult bees abandon their hives.

The study will appear in the June issue of the Bulletin of Insectology.

"The significance of bees to agriculture cannot be underestimated," says Lu. "And it apparently doesn't take much of the pesticide to affect the bees. Our experiment included pesticide amounts below what is normally present in the environment."

Pinpointing the cause of the problem is crucial because bees -- beyond producing honey -- are prime pollinators of roughly one-third of the crop species in the U.S., including fruits, vegetables, nuts, and livestock feed such as alfalfa and clover. Massive loss of honeybees could result in billions of dollars in agricultural losses, experts estimate.

Lu and his co-authors hypothesized that the uptick in CCD resulted from the presence of imidacloprid, a neonicotinoid introduced in the early 1990s. Bees can be exposed in two ways: through nectar from plants or through high-fructose corn syrup beekeepers use to feed their bees. (Since most U.S.-grown corn has been treated with imidacloprid, it's also found in corn syrup.)

In the summer of 2010, the researchers conducted an in situ study in Worcester County, Mass. aimed at replicating how imidacloprid may have caused the CCD outbreak. Over a 23-week period, they monitored bees in four different bee yards; each yard had four hives treated with different levels of imidacloprid and one control hive. After 12 weeks of imidacloprid dosing, all the bees were alive. But after 23 weeks, 15 out of 16 of the imidacloprid-treated hives -- 94% -- had died. Those exposed to the highest levels of the pesticide died first.

The characteristics of the dead hives were consistent with CCD, said Lu; the hives were empty except for food stores, some pollen, and young bees, with few dead bees nearby. When other conditions cause hive collapse -- such as disease or pests -- many dead bees are typically found inside and outside the affected hives.

Strikingly, said Lu, it took only low levels of imidacloprid to cause hive collapse -- less than what is typically used in crops or in areas where bees forage.

Scientists, policymakers, farmers, and beekeepers, alarmed at the sudden losses of between 30% and 90% of honeybee colonies since 2006, have posed numerous theories as to the cause of the collapse, such as pests, disease, pesticides, migratory beekeeping, or some combination of these factors.

"In Situ Replication of Honey Bee Colony Collapse Disorder," Chensheng Lu, Kenneth M. Warchol, Richard A. Callahan,Bulletin of Insectology, June 2012

Story Source:

The above story is reprinted from materials provided by Harvard School of Public Health.

MLA
Harvard School of Public Health (2012, April 5). Use of common pesticide, imidacloprid, linked to bee colony collapse. ScienceDaily. Retrieved April 6, 2012, from sciencedaily.com­/releases/2012/04/120405224653.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%2

sciencedaily.com

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From: donpat4/6/2012 11:19:08 AM
   of 3484
 
Could a Mystery Virus be the Culprit in Kawasaki?

By Jennifer Frazer

April 6, 2012

In the Nature podcast interview that went along with my Kawasaki Disease story at Nature ( look for the interview halfway down the page at the story here), I talked about the tantalizing work of Dr. Anne Rowley at the Northwestern Feinberg School of Medicine. She has studied the tissues of Kawasaki Disease patients and believes she has found virus-like particles in their respiratory tissues (hold tight for exciting photos at the bottom of this post). But in describing her research during the interview, I misspoke slightly (forgive me Anne! I was nervous!). Before I correct what I said, a little bit more about her work.

While reporting the KD story, I learned that Rowley was on the trail of a possible virus responsible for Kawasaki Disease from Dr. Jane Burns. I called Dr. Rowley to find out about that, and I found Anne’s work fascinating and included it in my first draft of the story. I was disappointed it didn’t make it into the final version of the story (again, for space reasons). So here’s her story, from the cutting room floor:

Anne Rowley, professor of pediatrics and microbiology/immunology at Northwestern University Feinberg School of Medicine, has been investigating the possibility that Kawasaki disease is caused by a virus.

Rowley has isolated antibodies from the immune cells infiltrating the coronary arteries of children who died from the disease. Her team made synthetic versions of these antibodies and incubated them with the tissues of children that had died of Kawasaki Disease, they found, to their surprise, that they bound to “inclusion bodies” in several of their tissues, including the cells lining the respiratory tract. Many respiratory pathogens – both bacterial and viral — make such inclusion bodies in the bronchial epithelium.

“It fit the hypothesis of a ubiqutious respiratory infectious agent that we were able to see these inclusion bodies in the bronchial epithelium,” she said.

When they looked at these inclusion bodies under electron microscopy, they found no sign of bacteria. But they did find both spherical and rod-shaped virus-like particles nearby.

“If you kind of put all that together you end up concluding the features are not compatible with any known virus family,” Rowley said. “So we suspect that it would represent a new virus family and we think that that’s why it’s been so difficult to identify the causative agent.”

Working with the viral genomics discovery group at Washington University in St. Louis, they are now looking for gene sequences in their tissue samples that have viral homology or that have no match. They hope to assemble the longest possible sequence prevalent among KD patients, and then test living Kawasaki patients to find out if their sequence turns up in those children.

What I meant to say during my interview — but did not in my nervous haze — was that Rowley had found virus-like particles associated with inclusion bodies in the lung tissues of Kawasaki victims. The virus-like particles were not the inclusion bodies themselves (which is what I said in the interview). Mea culpa.

As I mentioned above, the virus-like particles came in two different shapes: spherical and rod-shaped. In support of her hypothesis that the KD pathogen represents a new virus family, I’m not aware of any other virus with such a dimorphic appearance (Readers: Do you know of any?). But perhaps there are two separate viruses at work here? Or some other bizarre possibility? As with so many things Kawasaki, it’s impossible to say right now.

Here’s a photo showing the virus-like particles from KD patients from Rowley’s paper in the Journal of Infectious Disease last year (“ Ultrastructural, immunofluorescence, and RNA evidence support the hypothesis of a “new” virus associated with Kawasaki disease.”). The arrows are pointing to the virus-like particles from Figs. 3 and 5.


Spherical (left) and rod-shaped (right) virus-like particles found in the tissues of Kawasaki victims. From Figs. 3C and 5C of J Infect Dis. 2011 Apr 1;203(7):1021-30. Click for link to paper.


Fascinating! It will be interesting to follow this study and find out if these particles indeed prove to be the culprit. And if so, to find out where these viruses are coming from, and how they survive that impressive trans-oceanic commute!

One other slight amendment: besides the Aspergillus disease of sea fans and Valley Fever in humans, there are two other diseases that are known to be windborne and remain infectious over distances of 1000-or-so kilometers, according to plant pathologist Don Aylor, who I also interviewed for the article: tobacco blue mold, and wheat stem rust, which are both fungal pathogens like Valley Fever and theAspergillus sea fan disease. Neither of those two plant pathogens has ever been shown to cross an ocean.

About the Author: Jennifer Frazer is a AAAS Science Journalism Award-winning science writer who lives in Colorado. She has degrees in biology, plant pathology/mycology, and science writing, and has spent many happy hours studying life in situ.

Follow on Twitter @JenniferFrazer.

blogs.scientificamerican.com

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From: donpat4/7/2012 12:21:18 PM
   of 3484
 
Sci-Fi Level Medical Advances, Part I

Posted on April 6, 2012 | Leave a comment

Thin, tan, and horny.


Ten years ago, in 2002, I read an article in WIRED magazine about an experimental drug called Melanotan. Early test results indicated that the drug could make a pale person tan, without sun exposure. Side effects included reduce appetite and weight loss, and a high frequency of spontaneous erections.

Thin, tan, and horny … WIRED dubbed Melanotan “the Barbie drug.”

(Cont.)

jdmoyer.com

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From: donpat4/12/2012 11:25:49 AM
   of 3484
 
Viral membrane disruption.

Applicants:DREXEL UNIVERSITY

wipo.int@@@false
wipo.int(WO2012048033)&maxRec=1

Abstract:
(EN)The present invention includes a composition comprising a gold nanoparticle compiexed with a cysteine-containing compound. The invention also includes the method of preparing a composition comprising a gold nanoparticle compiexed with a cysteine-containing compound. The invention ftirther includes a method of causing virolysis of a virus using the compositions described therein. The invention ftirther includes a method of inhibiting vims entry using the compositions described therein.



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From: donpat4/13/2012 4:59:59 PM
   of 3484
 
Achilles Heel of Dengue Virus Identified: Target for Future Vaccines

ScienceDaily (Apr. 11, 2012) — A team of scientists from the University of North Carolina at Chapel Hill and Vanderbilt University have pinpointed the region on dengue virus that is neutralized in people who overcome infection with the deadly pathogen. The results challenge the current state of dengue vaccine research, which is based on studies in mice and targets a different region of the virus.

"In the past researchers have relied on mouse studies to understand how the immune system kills dengue virus and assumed that the mouse studies would apply to people as well," said senior study author Aravinda M. de Silva, PhD. associate professor of microbiology and immunology at the UNC School of Medicine.

"Our study for the first time shows what region the immune system of humans target when they are fighting off the virus. The region on the virus targeted by the human immune system is quite different from the region targeted by mice."

The new research, which will appear online during the week of April 11-14, 2012 in the Proceedings of the National Academy of Sciences, was performed using blood cells from local travelers infected with dengue virus.
pnas.org

The global incidence of dengue has grown dramatically in recent decades, putting about half of the world's population at risk. Creation of a vaccine is complicated by the fact that there are four distinct, but closely related forms of the virus that cause dengue. Once people have recovered from infection with one form of the virus, they have lifelong immunity against that form.

But if they become infected with one of the other three forms of the virus, they increase their chances of developing the severe bleeding and sometimes fatal dengue hemorrhagic fever and dengue shock syndrome. The leading theory to explain why some people develop dengue hemorrhagic fever is that under some conditions the human immune response can actually enhance the virus and disease during a second infection.

"This is a huge issue for vaccine development," said lead study author Ruklanthi de Alwis, a graduate student in de Silva's lab. "We have to figure out a way to develop dengue vaccines that induce the good response that protects against infection, at the same time avoiding the bad response that enhances disease."

de Alwis looked at a particular subset of the immune response -- specialized molecules called antibodies. UNC investigators identified 7 local individuals who had contracted dengue during travel to an endemic region and sent blood cells from these individuals to Vanderbilt School of Medicine. Drs. Scott Smith and James Crowe at Vanderbilt were able to isolate dengue antibodies from these cells for further study at UNC. The team found that instead of binding to small fragments of the virus -- like mouse antibodies do -- human antibodies that neutralized the virus bound to a complex structure that was only present on a completely assembled dengue virus.

"Though this is the first time this phenomenon has been shown with dengue, just last year there were a number of studies showing that antibodies recognize similar complex epitopes in both HIV and West Nile Virus," said de Alwis. "New vaccines as well as those already in the pipeline will need to be assessed to see if they bind just a small fragment or the whole virus, which may determine whether or not they work in humans."

The research was funded by the National Institute of Allergy and Infectious Diseases, the Southeastern Regional Center for Biodefense and Emerging Infections and a Pediatric Dengue Vaccine Initiative Targeted Research Grant.

Study co-authors from UNC were Nicholas P. Olivarez; William B. Messer; Jeremy P. Huynh; M. P. B. Wahala; and Ralph S. Baric.

Story Source:

The above story is reprinted from materials provided by University of North Carolina School of Medicine.

sciencedaily.com

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