Biotech / MedicalNNVC - NanoViricides, Inc.

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To: Savant who wrote (2207)2/14/2012 9:12:50 AM
From: xcentral1
   of 10533
NNVC has been working with various Governments for years now,,, "Fast Track" approval has always been our assumption.

In going back through old posts - here are just a few to illustrate same:

1829 - ... remembering that NNVC has consistently received funding and support from the various governments facing major epidemic problems around the world ... such as the rabies challenge in Vietnam and now the dengue fever....

2208 = For Dengue - reports that it has signed a research and development agreement with Dr. Eva Harris's laboratory at the University of California, Berkeley (UC Berkeley).

1831 - Our own Dept. of Defense....""Off balance sheet, Dr. Seymour estimates that the United States government and its various agencies have invested what could be worth 10 to 15 million dollars testing Nanoviricides’ Theracour© technology. These factors should be considered by those who see the company’s low book value per share as well as its approximate 132 million outstanding shares."

2208 - NanoViricides Assigned $5 Million in FY08 Defense Authorization Bill
Funding Focuses R&D on Treatment of Dengue Fever
WEST HAVEN, Conn., Jun 05, 2007 (BUSINESS WIRE) -- The new spending authority Defense authorization bill now making its way through Congress designates $5 million for Connecticut-based NanoViricides, Inc.'s antiviral research, according to an announcement by Senator Joeseph Lieberman.
The funding is designed to explore treatment for dengue fever, an often deadly mosquito-born disease.


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To: xcentral1 who wrote (2209)2/14/2012 10:38:07 AM
From: Savant
   of 10533
Yes, I realize the promise, but still wonder about the possibilities..odds, if you will...and when.
Will it take the start of a pandemic to gain fast track, or just a large outbreak?

I also know govts have provided funding...but the old question arises..what have they done for us lately?

As to the shelf registration...yes, it 'might' provide a more cost effective means of raising capital, however, the terms and funding groups are yet to be determined. And at these levels, the dilution is considerable.

Looking forward, am cautiously optimistic about human trials.


PS..I've grown old awaiting the approval/blessings/whims of the Foot Draggers' Association in regard to other names.

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To: donpat who wrote (2014)2/14/2012 12:46:52 PM
From: donpat
   of 10533
Turmeric-Based Drug Effective On Alzheimer Flies

ScienceDaily (Feb. 14, 2012) — Curcumin, a substance extracted from turmeric, prolongs life and enhances activity of fruit flies with a nervous disorder similar to Alzheimers, according to new research. The study conducted at Linköping University, indicates that it is the initial stages of fibril formation and fragments of the amyloid fibrils that are most toxic to neurons.

Ina Caesar, as the lead author, has published the results of the study in the journal PLoS ONE.

Above left are the survival curves for "Alzheimer flies" treated (dashed line) and those not treated with curcumin. The flies that were administered curcumin lived longer and were more active. The scientists identified an accelerated formation of amyloid plaque in the treated flies, which seemed to protect the nerve cells. On the right we see microscopic images of neurons (blue) and plaque (green) in the fruit fly's brain. The study strengthens the hypothesis that a curcumin-based drug can contribute to toxic fibrils being encapsulated (bottom left of the figure). (Credit: Per Hammarström, Ina Caesar)

For several years curcumin has been studied as a possible drug candidate to combat Alzheimer's disease, which is characterized by the accumulation of sticky amyloid-beta and Tau protein fibres. Linköping researchers wanted to investigate how the substance affected transgenic fruit flies (Drosophila melanogaster), which developed evident Alzheimer's symptoms. The fruit fly is increasingly used as a model for neurodegenerative diseases. Five groups of diseased flies with different genetic manipulations were administered curcumin. They lived up to 75 % longer and maintained their mobility longer than the sick flies that did not receive the substance.

However, the scientists saw no decrease of amyloid in the brain or eyes. Curcumin did not dissolve the amyloid plaque; on the contrary it accelerated the formation of fibres by reducing the amount of their precursor forms, known as oligomers.

"The results confirm our belief that it is the oligomers that are most harmful to the nerve cells," says Professor Per Hammarstrom, who led the study.

"We now see that small molecules in an animal model can influence the amyloid form. To our knowledge the encapsulation of oligomers is a new and exciting treatment strategy," he said.

Several theories have been established about how oligomers can instigate the disease process. According to one hypothesis, they become trapped at synapses, inhibiting nerve impulse signals. Others claim that they cause cell death by puncturing the cell membrane.

Curcumin is extracted from the root of herbaceous plant turmeric and has been used as medicine for thousands of years. More recently, it has been tested against pain, thrombosis and cancer.

Story Source:

The above story is reprinted from materials provided by Linkoeping Universitet, via AlphaGalileo.

Journal Reference:
Ina Caesar, Maria Jonson, K. Peter R. Nilsson, Stefan Thor, Per Hammarström. Curcumin Promotes A-beta Fibrillation and Reduces Neurotoxicity in Transgenic Drosophila. PLoS ONE, 2012; 7 (2): e31424 DOI: 10.1371/journal.pone.0031424

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From: donpat2/14/2012 1:34:54 PM
   of 10533
Scientists tweak fungus to produce anti-virus chemical

IANS | Feb 14, 2012, 06.29PM IST

VIENNA: Scientists have tweaked a fungus commonly found on rotting bread or food stuff to produce a vital drug to fight viral infections.

Biotechnologist Astrid Mach-Aigner and his team made a fungus, Trichoderma, to produce NANA (N-Acetylneuraminic acid), a vital source of drugs to fight viral infections.

However, NANA , which can be obtained from natural sources or synthesized has a major drawback. It is horrendously expensive to produce. Each gram of NANA is 50 times as expensive as a gram of gold, selling for around 2000 Euros.

"We knew that Trichoderma can degrade chitin - that is what the fungus naturally does in soil," says Astrid Mach-Aigner, from the Vienna University of Technology.

In order to get the fungus to produce the desired chemical product, bacterial genes had to be introduced into its genome. "Usually, Trichoderma breaks down chitin to monomer amino sugars", says Mach-Aigner, according to a Vienna statement.

After cellulose, chitin is the most abundant biopolymer on earth. It is found in the carapaces of crustaceans, in the shells of insects, snails and cephalopods and in the cell walls of fungi.

It is estimated that in the sea alone, 10 billion tons of chitin are formed every year - several hundred times more than the cumulative body mass of all the people on earth. This makes chitin a very sustainable resource for chemical synthesis.

The newly developed Trichoderma line can now be cultivated in bio-reactors and produces the precious acid NANA from chitin.

The process has now been patented by the Vienna University of Technology and will be used for the cheap and eco-friendly production of pharmaceuticals on an industrial scale in the near future.

See also:
N-Acetylneuraminic acid

From Wikipedia, the free encyclopedia

N-Acetylneuraminic acid (Neu5Ac or NANA) is the predominant sialic acid found in mammalian cells.

This negatively charged residue is found in complex glycans on mucins and glycoproteins found at the cell membrane. Neu5Ac residues are also found in glycolipids, such as gangliosides, a crucial component of neuronal membranes found in the brain.

Along with involvement in preventing infections ( mucus associated with mucous membranes — mouth, nose, GI, respiratory tract), Neu5Ac acts as a receptor for influenza viruses, allowing attachment to mucous cells via hemagglutinin (an early step in acquiring influenzavirus infection).

Neu5Ac in the biology of bacterial pathogens Neu5Ac is also important in the biology of a number of pathogenic bacteria [1] [2] as it can used either as a nutrient, providing both carbon and nitrogen to the bacterium, or in some pathogens, can be activated and placed on the cell surface. [1] Bacteria have evolved transporters for Neu5Ac to enable them to capture it from their environment and a number of these have been characterised including the NanT protein from Escherichia coli, [3] the SiaPQM TRAP transporter from Haemophilus influenze [4] and the SatABCD ABC transporter from Haemophilus ducreyi. [5]

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From: Savant2/15/2012 11:51:23 AM
   of 10533
NanoViricides Files Quarterly Report

WEST HAVEN, Conn., Feb 15, 2012 (BUSINESS WIRE) -- NanoViricides, Inc. (the
"Company"), has filed its quarterly report with the Securities and Exchange
Commission yesterday, February 14th, in a timely fashion.

The Company reported that it had approximately $12.099M in cash and cash
equivalents, and approximately $322,880 in prepaid expenses as of December 31,
2011, the end of the reporting quarter. The shareholder equity stood at
approximately $12.388M. In comparison, the Company had approximately $10.879M in
cash and cash equivalents, approximately $321,900 in prepaid expenses and other
cash equivalent assets, and $11.386M in shareholder equity as of September 30,
2011. The Company spent approximately $1.012M in Research and Development
expenses (R&D) and approximately $325,600 in General and Administrative expenses
(G&A) in the reported quarter. The Company's rate of cash expenditure was in line
with the Company's budgeted targets.

Subsequently, the Company has raised an additional $2.5M from Seaside 88, LP, a
Florida limited partnership ("Seaside"), upon Seaside's exercise of their option
to purchase the Company's Series B Preferred Stock, as previously disclosed on
February 9, 2012.

The Company estimates that it currently has sufficient cash in hand to support
operations for more than two years from reported period at the current rate of
expenditure. The Company has neither any long term debt, nor any short term debt,
other than small working capital accounts payables.

The Company reports that all of its drug development programs are progressing

The Company has previously announced that it has filed a pre-IND Meeting request
to the US FDA for its clinical drug candidate, namely NV-INF-1, under its
FluCide(TM) anti-influenza nanoviricides program. The Company has reported that
it has also filed certain briefing documents to support this meeting request to
the FDA.

The Company continues to have further discussions with the consultant firm it has
retained for regulatory affairs, Biologics Consulting Group, Inc., to formulate
its national as well as international product development strategy for this
anti-influenza drug candidate.

The Company is in the process of making arrangements to enable the cGMP
manufacture of kilogram quantities of its clinical drug candidates without
capital costs to the Company.

With the current strong cash position, the Company believes that it has
sufficient funding available to perform Toxicology Package studies, and
additional animal efficacy studies, to move at least one of our drug candidates
into an Investigational New Drug Application ("IND") with the US FDA.

The Company currently has five commercially important drug candidates in its
pipeline. These include FluCide(TM), HIVCide(TM), HerpiCide(TM), DengiCide(TM),
and a broad-spectrum nanoviricide eye drop formulation against viral infections
of the eye. These programs are based on the Company's platform technology that
enables specifically targeting a particular type of virus. In addition, the
Company continues its other research and development programs. These include (a)
broad-spectrum nanoviricides against a number of Neglected Tropical Diseases, and
(b) its novel ADIF(TM) ("Accurate Drug In Field"(TM)) technologies which promise
a way to attack novel viruses, whether man-made (bioterrorism) or natural (such
as SARS), before they cause a pandemic.

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From: donpat2/15/2012 9:53:36 PM
   of 10533
Defense Mechanism Against Viruses and Cancer Identified

Fundamentally new mechanism of how our defense system is ramped up when facing a viral intruder. (Credit: Image courtesy of Deutsches Rheuma-Forschungszentrum Berlin)

ScienceDaily (Feb. 15, 2012) — A team of scientists from the Charité and German Rheumatism Research Center Berlin and the University of Geneva has found a fundamentally new mechanism how our defense system is ramped up when facing a viral intruder. Exploitation of this mechanism in vaccines sparks new hope for better prevention and therapy of infectious diseases and cancer.

"T killer cells" (CD8 T cells) represent an important element of our body's defense system. They have the capacity to specifically identify and kill cells, which harbor viruses and bacteria or form a cancer. T killer cells would therefore represent an important component of yet unavailable vaccines against infections like HIV/AIDS, hepatitis C virus and malaria, and also for the treatment of cancer.

It has been a longstanding observation that there is no match to the overwhelming T killer cell armada, which is triggered when a viral infection invades our body. Scientists had generally accredited this observation to "pathogen-associated molecular patterns" (PAMPs) on viruses and other microbes. PAMPs, i.e. the "foreign look" of viruses, alert so-called "dendritic cells," which serve as policemen coordinating the T killer cell response.

In a report now published in the journal Science, researchers led by Prof. Max Löhning (Charité-University Medicine & DRFZ Berlin) and Prof. Daniel Pinschewer (University of Geneva) describe an additional general mechanism by which viral infection triggers potent T killer cells: "Dying virus-infected cells themselves ring the alarm bells to T killer cells.," Löhning says. Viruses cause infected cells to die, resulting in the release of cell components, which normally are not be visible to the outside -- analogous to an injured individual loosing blood. Such substances, heralding injury when released, are referred to as "alarmins." The scientists found that T killer cells can sense an alarmin called "interleukin 33" (IL-33). IL-33 is contained in cells, which form the scaffold of the T killer cells' home, the spleen and lymph nodes, and is released when such scaffold cells die.
[ ]

Mice lacking the gene encoding IL-33 failed to form a large T killer cell army upon viral infection. The few remaining cells had very poor fighting skills. Such mice were therefore exquisitely sensitive to several types of viral infections. Conversely, IL-33 could be used to artificially increase the T killer cell army, which was generated in response to vaccination. As Max Löhning and Daniel Pinschewer explain, PAMPs and alarmins apparently have complementary and non-redundant functions in shaping our T killer cell defense: "The "foreign look" of viruses (PAMPs) activates the "dendritic cell" policemen to engage T killer cells. T killer cells, however, remain lousy fighters unless alerted by a cell death in their neighborhood (alarmins)." These new findings could provide a key to effective vaccination against infectious diseases and cancer.

Story Source: The above story is reprinted from materials provided by Deutsches Rheuma-Forschungszentrum Berlin, via AlphaGalileo.

Journal Reference:
W. V. Bonilla, A. Frohlich, K. Senn, S. Kallert, M. Fernandez, S. Johnson, M. Kreutzfeldt, A. N. Hegazy, C. Schrick, P. G. Fallon, R. Klemenz, S. Nakae, H. Adler, D. Merkler, M. Lohning, D. D. Pinschewer. The Alarmin Interleukin-33 Drives Protective Antiviral CD8 T Cell Responses. Science, 2012; DOI: 10.1126/science.1215418

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From: donpat2/15/2012 10:30:04 PM
   of 10533
BREAD - Basic Research to Enable Agricultural Development - grant research to tackle plant viral diseases

Featured In: Academic Research
Cornell University | Wednesday, February 15, 2012

By Krishna Ramanujan

A team of international researchers is working to tackle the global problem of plant viral diseases that are spread by insects, thanks to close to $1 million from the National Science Foundation (NSF) and the Bill & Melinda Gates Foundation.

The team, headed by Stewart Gray, a U.S. Department of Agriculture-Agricultural Research Service (USDA-ARS) research plant pathologist and Cornell professor of plant pathology, and Michelle Cilia, a USDA-ARS research molecular biologist, received a three-year, Basic Research to Enable Agricultural Development (BREAD) grant of $868,896 to develop protein biomarkers that distinguish insect populations capable of transmitting disease from those that do not.

"One problem with managing viral diseases is there is no cure," said Gray, of the plant diseases that cause an estimated $60 billion in damages worldwide each year. "To control them, you have to develop a resistant crop, or you have to prevent the vector from feeding on and infecting the plant."

Another challenge is that within insect species, such as aphids and whiteflies, that spread these viruses, researchers find populations vary widely in how efficiently they spread a virus. That's because mutations or changes in genes alter specific proteins that viruses use to move through an insect. Slight changes in a gene can drastically alter the way a protein functions, Cilia said.

The researchers have identified protein biomarkers that allow them to determine whether an aphid will efficiently transmit disease or not.

"Finding these biomarkers for virus transmission is an exciting major breakthrough," said Cilia. In medicine, for example, biomarkers for breast cancer and prostate cancer are rare success stories, Cilia added. The researchers are now trying to validate the aphid biomarkers in a range of vector insects.

If successful, the researchers hope to develop a test kit that can be used in the field to identify if an insect population is likely to be a virus vector. Once identified, growers can then target particular insects with pesticides at a certain time in their lifecycle. Currently, growers must spray crops indiscriminately to prevent disease outbreaks.

"Prophylactic spraying of crops to eliminate all potential vectors is not efficient from an economical or environmental standpoint," said Gray.

Common disease-causing viruses include the barley yellow dwarf viruses spread by aphids and Geminiviruses transmitted by white flies. In Africa, viruses commonly destroy entire fields of such staple crops as bananas, cassava, maize and sweet potatoes. In the United States, barley yellow dwarf viruses reduce annual wheat yields by about 5 percent. Last year in Kansas, a severe outbreak of barley yellow dwarf virus caused the highest economic loss from any wheat disease.

The international team also includes researchers from the University of Washington in Seattle, the USDA-ARS U.S. Vegetable Laboratory in Charleston, S.C., and the International Institute of Tropical Agriculture in Nigeria and Cameroon.

BREAD seeks to partner advanced research expertise with the developing world and is jointly funded by the NSF and the Bill & Melinda Gates Foundation.


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From: donpat2/16/2012 3:26:13 PM
1 Recommendation   of 10533
'Signifcant Step' Towards Hep C Vaccine To Be Announced By University Of Alberta Researcher

Article Date: 16 Feb 2012 - 8:00 PST

A University of Alberta researcher and Canada Excellence Research Chair in Virology has made the discovery of a vaccine that will potentially help combat hepatitis C. Michael Houghton, who led the team that discovered the hepatitis C virus in 1989, announced his findings at the Canada Excellence Research Chairs Summit in Vancouver this afternoon. Currently, there are no vaccines against the disease available.

Houghton, also the Li Ka Shing Chair in Virology at the University of Alberta, says the vaccine, developed from a single strain, has shown to be effective against all known strains of the virus. It took more than 10 years to develop and started while he was working for the drug company Novartis. Following previous vaccine tests funded by the National Institutes of Health that yielded promising results, he said there remained two critical questions.

"Did the recipients actually produce antibodies that could neutralize the actual infectious virus," he said, "and if they could, how broad was the neutralizing response?"

The challenge, Houghton said, was that hepatitis C is more virulent than HIV, thus coming up with a vaccine that would neutralize the different strains around the world was believed to be impossible. Using a vaccine developed and tested on humans in his University of Alberta lab, Houghton and his co-investigator John Law discovered that the vaccine was capable of eliciting broad cross-neutralising antibodies against all the different major strains. Houghton says that this finding bodes good news for those with hep C and those who live or travel to areas where the disease is prevalent.

"This tells us that a vaccine made from a single strain can indeed neutralize all the viruses out there," says Houghton. "It really encourages the further development of that vaccine. This is a really a big step forward for the field of HCV vaccinology."

With hundreds of thousands of people being infected with hepatitis C annually, and with between 20 to 30 per cent of those developing some form liver disease, this announcement brings hope. However, Houghton cautions that further testing is required, meaning that it may be five to seven years before the vaccine receives approval. And while it may make some difference in those currently suffering from hepatitis C, it is mainly a preventative measure against acquiring the disease.

The discovery of the vaccine by a University of Alberta researcher, and one of the first appointed Canada Excellence Research Chairs is proud news for both organizations.

"A breakthrough such as this one is exactly the kind of advance we believed would happen here when we created the Li Ka Shing Institute of Virology and recruited internationally renowned researchers such as Michael Houghton and his colleagues," said U of A President Indira Samarasekera.

Chad Gaffield, chair of the steering committee for Canada Excellence Research Chairs program said one of the ambitions of the program was to attract world-class talent to Canada, those whose research would be foremost in making the breakthroughs needed in the 21st century. While it may not be obvious when or where such breakthroughs will occur first, Houghton`s discovery illustrates the impact of this program on a national and international scale.

"The premise of the CERC program is that if you support top minds internationally, good things will happen," he says. "This is a wonderful illustration of how a key problem in the world today becomes much more understandable and solutions are much closer thanks to the work of Michael Houghton."

The breakthrough underscores the benefit of the U of A's Li Ka Shing Institute of Virology.

"This demonstrates that the Li Ka Shing Institute is internationally competitive in important areas of virology research," said Lorne Tyrrell, director of the institute and a leading virologist in his own right. "We are working on topics that are important to patients, and we want to translate discoveries from the lab to patient care. That has been our philosophy since day one. We have a long way to go, but this is a great step."

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From: AllanTrends2/18/2012 6:19:55 PM
   of 10533
This is a potentially powerful chart pattern, suggesting a move up to $1.50 in the next few weeks or months. As the pattern develops, higher targets are likely

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From: donpat2/24/2012 5:12:45 PM
   of 10533
Bacteria-Killing Viruses Wield an Iron Spike

by Michael Bullwinkle on 24 February 2012, 3:55 PM

Viral attack. A handful of P1 phages pierce the membrane of an E. colibacterium, as seen under electron microscopy (left panels) and a 3D reconstruction (right).
Credit: Adapted from J. Liu et al., Virology, 417 (1 September 2011)

Forget needles in haystacks. Try finding the tip of a needle in a virus. Scientists have long known that a group of viruses called bacteriophages have a knack for infiltrating bacteria and that some begin their attack with a protein spike. But the tip of this spike is so small that no one knew what it was made of or exactly how it worked. Now a team of researchers has found a single iron atom at the head of the spike, a discovery that suggests phages enter bacteria in a different way than surmised.

Wherever there are bacteria you will find bacteriophages; digestive tracts, contaminated water, and feces are usually a good start. These viruses begin their dirty work by drilling into the outer membrane of bacteria. Once completely through all of a bug's defenses, the phages inject their DNA, which essentially turns the bacterium into phage-producing factories. Eventually, the microbes become filled with so many viruses that they burst, releasing a new horde of phages into the environment.

Although much is known about phage reproduction, little is understood about how the virus initially gains entry into the bacterium. "We knew ... there must be a special protein that makes the very first opening in the outer cell membrane of the bacterial envelope," says Petr Leiman, a biophysicist at the École Polytechnique Fédérale de Lausanne in Switzerland. "But we didn't know what the very end of the structure, the business end, the tip that attacks the membrane, looks like."

So Leiman and colleagues decided to partially reverse engineer the viral tips. Their new study concerns two bacteriophages known as P2 and F92, viruses that target bacteria such as Salmonella and Escherichia coli. The researchers already knew which gene contained instructions for how to make P2's protein spike. And after a bit of scouring, they discovered an analogous gene in F92. The scientists then produced the proteins those genes encode and turned them into crystals. This allowed them to use a technique called x-ray crystallography, in which they bombard the crystals with x-rays, to get a sense of the proteins' structure.

In theory this should have been enough to give the researchers a glimpse of the elusive tip of the spike. But when they tried to model the spike using the data from the x-ray crystallography work, the tip remained invisible. To get around this problem, the researchers modified the phage's spike genes so that they only produced the portion of the protein tip that was resistant to being viewed. When they crystallized this smaller protein fragment, the x-rays were finally able to resolve its structure, and from this the team had the very first picture of the tip of the spike: a single iron atom held in place by six amino acids, forming a sharp needlelike tip—perfectly suited for piercing the outer membranes of bacteria. The team reports its findings this month in Structure.

Scientists had always assumed that when phages drill their way through the outer membrane, they first have to soften it up a bit in some way, says Mark van Raaij, a biologist and virus expert at the Instituto de Biologia Molecular de Barcelona in Spain, who was not involved in the work. But the discovery of the sharp iron needle, he says, suggests that P2 and F92 don't need any help. "It's like driving a nail or stake through the membrane of the bacteria."

Leiman notes that findings like these could lead to new ways to combat bacteria that make people sick. As scientists reverse engineer phages, he suggests, they can isolate those parts that are most effective at killing bacteria and perhaps produce a new class of antibacterial agents.

PDF 1.90 MB

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Structure, Volume 20, Issue 2, 326-339, 8 February 2012

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