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Showing posts with label could. Show all posts
Showing posts with label could. Show all posts

Tuesday, March 19, 2013

Could you use herpes to empower your life?

Guest author from our community: Lively

Some people feel they are at the effect of life. Others feel they can deal with anything life throws at them. Most of us move between one and the other as we grow and learn. A new challenge can overwhelm us for a time … until we learn how to deal with it. Once we know how to do that, it can be a very short time before we forget how demanding the learning was, and what it took. This may include courage, tenacity, stepping so far outside our comfort zone that we can’t remember where it was before, the willingness to expose ourselves, be vulnerable, accept our imperfection, even (OMG!) allow others to see and accept our imperfection.

So in the midst of dealing with the shadow of herpes, we find this website where some crazy guy is calling it A Gift. An Opportunity. How does that work?

“The first thing to understand is that we have the capacity to either pull away from ourselves or to expand into ourselves.”

I may be able to throw some light on this, as I’ve been around on Planet Earth for a while, have had my share of dramas and challenges, and travel through them pretty smoothly these days. This doesn’t come without much learning and testing, of course, and a commitment to minimizing pain in life … I thought that if I have to have it sometimes (seems that we do), then I may as well learn how to get the most value out of it in the hope of either having less of it in the future, or being less bothered by it in the future, or even both. So you may fancy a shorter learning curve than I had.

That intention has brought me some interesting adventures, but what’s useful to know is that it works so well that I have been known to get excited when a new challenge presents (and I don’t mean just the small ones). It is possible and possibly smart to use every adversity as a learning experience and to milk it to the max. Doing this has made me fearless in some ways and most of the time; it has minimized suffering; it has made processes that were once torturous into fascinating adventures. Even this one. So how do you do it?

The first thing to understand is that we have the capacity to either pull away from ourselves or to expand into ourselves. Mostly we pull away from pain, and expand into pleasure, at least as far as we allow ourselves. (That’s an entirely different article.)

We can learn to expand into pain, confusion — all the emotions — instead of clamping them down or denying them. First we probably will do the automatic pullaway; then we can learn to catch ourselves and ask: What might happen if I just felt this fully? If we breathe as fully as we can, we discover that all emotions pass. Yes, all of them. Emotions are like the weather, they are never permanent … unless we resist. Heard the adage “what you resist persists”? In my experience, it sure does. May as well surrender and let it have its moments. Because they really are moments once we allow space around them and accept them as a legitimate element of ourselves. Resist and they can go on for decades!

First …

Intend to accept the upset of herpes. All of it, the beginning, the middle and the end. At diagnosis time; When we are negotiating the herpes talk and protection in relationships including what if someone gets herpes from us; and when you have become at peace about herpes and all that it entails. Accept it all. Accept the time, the emotion, the learning curve and the crazy things we think about ourselves while we are learning. It is a portal to a higher state of love, compassion, power and freedom. I am asserting that. I know you may not be able to digest that just yet.

Second …

Own this. No one and nothing can make you feel something that wasn’t already within you. So whatever you feel about herpes was already there. Whatever horrible stories you tell yourself that herpes means about you, were already there. It’s how the unconscious works. Google it if you like, a big discussion about that is beyond the scope of this article. Or take it on trust. You already had all those difficult emotions, all those horrible thoughts about yourself. All that herpes does is reveal what’s there. This is part of its gift. Now you know those emotions and thoughts are there, now you can do something about accepting them for now, and then choosing something else you like better for your future. Easier said than done, I know but quite learnable. Not only learnable, but learning it will empower you like nothing else in life, as once you know a way to reconfigure your own emotions and thoughts — and there are MANY ways — you will be able to use that for anything in life that you wish to change or modify.

Here’s something very important to know: We filter experience through what we believe. You’ve probably heard that before. So why would one person say “the glass is half full” and the other “the glass is half empty”?

Well, it may mean nothing at all! And it also may mean that the first one sees life as generous kind and okay, and the second sees life as stingy, limited and tough. Caution applies though! It may not mean that in any individual case. It’s an illustration only.

Although we inherit many beliefs when too young to discern what we are picking up, it’s worth looking at what a belief is. We have a thought; if we continue to choose the same thought it becomes a decision; if we continue to choose the same decision it becomes a belief; once it’s a belief your very own brain will filter out anything that doesn’t fit the belief. Our very own brain will always make us right on our beliefs. So we’d better get cooking on how to change those thoughts we have….we think “no one will ever love me with herpes” even though this site has many stories of those who found an accepting partner. So why do we think that? Oh, perhaps it’s US! We haven’t yet learned to love and accept ourselves yet with herpes, so we think no one else will. This doesn’t look like good news but it is! We can learn to love ourselves with herpes, even to thank herpes for the growth it made unavoidable for us. If that sounds like it will never happen, stay tuned! It already has, to many, many people.

So your job is to transmute the energy of all your upset about herpes into whatever you need and choose: higher levels of self-esteem, self-respect, self-love, compassion, power, choice to grow, choice to become more than your thoughts and feelings, choice to grow beyond whatever you or anyone else has been telling you that herpes means.

As you reclaim the energy of the thoughts /feelings you have about herpes, those filters weaken and you begin to see other possibilities that were literally Invisible thus Unavailable to you before. It feels a magical process…perhaps it is. It requires you to be willing to let go of your opinion, of your feelings, of the thought that you know everything (makes it impossible to grow). Yet feelings pass anyway and more good news: Practice pays off! You can get very fast at doing this. Sometimes our security is that we think some things are set in concrete and never change. It’s a false security.

Learning to flow with life in its ups and downs is the best security you can ever have. You can question yourself:

What are MY values?Is joyous consensual sexuality ever slutty?Did I protect myself before herpes? Will I now?Am I worth the effort of learning? Do others deserve my consideration?Can I forgive myself for letting this happen to me?What can I learn from it that is worth more than my upset about it?Do I matter anyway? Who cares if I do or don’t? (Clue: if not you, then who?)

There are no right answers here, just your authentic truth. As you can see, the depth goes much further than our little skin condition. If you choose, you can make this the springboard for a much clearer, more loving life for YOU. What you will have to offer others will also expand.

The greatest value you can take from herpes or any other challenge is to use the energy of its upset to grow yourself in the way that you choose to do that. The upset will show you what you had within you that you did not know, and now you do. Becoming more conscious is the fuel of power.

Anything less and you are choosing to be a victim of life — not of herpes, not of your “giver”, not of anything but Life itself. Why would you choose that? Remember: thoughts become decisions; decisions become beliefs; once a belief is set your filters stop you seeing your full options; you could get stuck there.

Your mission if you choose to accept it is to allow herpes to be the catalyst of a bigger more loving more compassionate YOU, and yes, a more powerful You. Then you really do have something new to offer yourself and others you invite into your life; as well as a roadmap of how to leverage any upset that you have in your body, not just as a good idea, as a physical fact.

Yes it takes time and can be emotionally overwrought at times; but that’s just life isn’t it? Once life has given you the herpes pathway to growth, there’s no giving it back. So kindly, lovingly, in rage and fury and sadness and shame, and all the emotions you discover within you, take the journey on. Take it on willingly, with certainty that you can make this the pivotal point of discovering your own power. There is no better place than this community to do this. There is nothing else to do.

herpes forum


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Thursday, January 24, 2013

Chicken Pox in Children Could Lead to the Much Painful Herpes Zoster; VyGone Introduces the Ultimate Zoster Vaccine

Children that suffer from chicken pox get infected with the herpes zoster virus according to a study published on The Lawton Constitution and the virus is known to cause shingles later on in life which is credited with forming painful blisters on the body. VyGone provides the ultimate zoster vaccine on http://www.ultimatecoldsoretreatment.com/.

Boise, Idaho (PRWEB) December 26, 2012

On the 25th of November, The Lawton Constitution posted an article about the main cause of shingles, also known as the herpes zoster. The article (http://www.swoknews.com/styles-new/health) informed readers that chicken pox is to be blamed for this as it causes the herpes zoster virus to enter and settle into the body. Dr. Robert Hay was interviewed about the virus and he said, “When a child gets chickenpox and it's treated, this virus remains dormant in a nerve root,” and, “It can be anywhere in the system. We don't know what makes it come out of dormancy, but, if it does, it travels along the nerve, creating the issue known as shingles.” The article also warned those who have suffered from chicken pox to be aware of shingles so that they are not alarmed if it does in fact infect them at some point in life.

Shingles, or herpes zoster, is more commonly known as the painful blisters that form on the skin in large patches. They are caused by the herpes virus which forever remains in the body of those infected with it, even after treatment for shingles has been done. The virus may remain in its dormant state for years on end, becoming active only when any particular thing triggers the virus cells to multiply rapidly, such as weather changes, stress, weakened immunities, etc. It is found in the nerve cells of the human body. VyGone is an online based company which helps educate individuals about Shingles and has introduced an ultimate vaccine.

VyGone is the company to visit to find out about the best treatment for shingles and herpes zoster. Other than that, it also provides reliable information about not only shingles, but other various diseases and infections such as syphilis, warts, cold sores, herpes and many others. Visit the website at http://www.ultimatecoldsoretreatment.com/ to look up the zoster vaccine and other remedies. More information about the vaccine can be availed on http://www.ultimatecoldsoretreatment.com/.

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Saturday, September 8, 2012

New way to target viruses could make antiviral drugs more effective

ScienceDaily (July 21, 2010) — Scientists have developed a new way to target viruses which could increase the effectiveness of antiviral drugs.

Instead of attacking the virus itself, the method developed at the University of Edinburgh alters the conditions which viruses need to survive and multiply.

By making the site of infection less hospitable for the virus, the virus becomes less able to mutate and build up resistance to drugs. The researchers were also able to target more than one virus at the same time.

Viruses take up residence in host cells within our body, which produce proteins that enable the virus to multiply and survive.

The study, published in the journal Proceedings of the National Academy of Sciences (PNAS), analysed molecules known as microRNAs, which regulate how much of these proteins are made.

The scientists were able to manipulate the microRNA levels, which enabled them to control a network of proteins and stop viruses from growing.

Most existing antiviral therapies only work against one virus. However, by adapting the virus host environment the researchers were able to target different types of viruses.

It is hoped that the research could lead to new treatments for patients suffering from a range of infections.

Dr Amy Buck, of the University's Centre for Immunity, Infection & Evolution, said: "A problem with current antiviral therapies, which generally target the virus, is that viruses can mutate to become resistant. Since new viral strains emerge frequently, and many infections are difficult to diagnose and treat, it is important to find new ways of targeting infection. Our hope is that we will be able to use host-directed therapies to supplement the natural immune response and disable viruses by taking away what they need to survive."

Scientists studied the herpes family of viruses, which can also cause cancer with the Epstein-Barr virus, and the Semliki Forest virus, which is mainly spread by mosquitoes.

Both viruses have different characteristics. Viruses from the herpes family replicate inside the nuclei of cells, while the Semliki Forest multiplies outside the nucleus of a cell.

Further research has begun to look at how this method could be used to target influenza.

The study was funded by the Wellcome Trust and the Biotechnology and Biological Sciences Research Council.

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The above story is reprinted from materials provided by University of Edinburgh.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Diwakar Santhakumar, Thorsten Forster, Nouf N. Laqtom, Rennos Fragkoudis, Paul Dickinson, Cei Abreu-Goodger, Sergei A. Manakov, Nila Roy Choudhury, Samantha J. Griffiths, Annaleen Vermeulen, Anton J. Enright, Bernadette Dutia, Alain Kohl, Peter Ghazal, and Amy H. Buck. Combined agonist-antagonist genome-wide functional screening identifies broadly active antiviral microRNAs. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1008861107

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


View the original article here

Wednesday, August 29, 2012

Drug against AIDS could be effective against herpesvirus

ScienceDaily (Sep. 24, 2010) — Scientists at the Institute for Research in Biomedicine (IRB Barcelona) headed by the coordinator of the Structural and Computational Biology Programme, Miquel Coll, have published a new study that demonstrates that raltegravir, the drug approved in 2007 for the treatment of AIDS that is sold by Merck under the name Isentress, cancels the function of an essential protein for the replication of one kind of herpes virus. This study, published in the journal Proceedings of the National Academies of Sciences (PNAS), is the first step towards the development of a drug against the entire herpesvirus family.

"These results have a clear medical impact for three reasons," explains Miquel Coll, also a CSIC research professor. "First, humans do not have the viral protein that is affected, thus this would allow a highly specific drug that does not show the secondary effects that other drugs may have. Second, the inhibitor is not toxic for humans when administered at therapeutic concentrations because it is already on the market and thus toxicity tests are facilitated; and third, we have data that indicate that all herpes viruses have this protein. Therefore, it could be a valid target against all Herpesviridae."

Herpesviruses include pathogens such as herpes simplex 1 and 2, the virus that causes chickenpox otherwise known as zoster virus, the Epstein-Barr virus -associated with several types of cancer -, the roseola virus, the cytomegalovirus and the herpes virus associated with Kaposi sarcoma -in AIDS patients -. The human cytomegalovirus (HCMV), on which the study was performed, causes neurological defects in 1% of neonates in developed countries. It also produces retinitis that deteriorates into blindness in 25% of subjects with AIDS, defects in the brains and central nervous systems of young adults, inflammation of the colon -also in those with AIDS -, mononucleosis and serious diseases of the throat. Although 90% of adults carry HCMV, this virus is opportunistic, acting in people with weakened immune systems such as in cancer and AIDS patients, recipients of organ transplants and neonates.

Blocking viral replication

To replicate, the herpes virus enters the nucleus of a cell where it uses the cell machinery to copy its DNA several times into a single large chain. Once this copy has been made, acts a complex called terminase, formed by three protein subunits. The terminase cuts the new DNA into small fragments, the size of a single viral genome, and introduces these into empty shells (capsids) that have developed in the cell nucleus. Then, the new viruses leave the cell to continue infection. The researchers resolved the 3D structure of one part of the terminase and when they observed that it resembled the integrase of the AIDS virus, for which drugs are available, they tested it against the herpes virus protein. Thus they discovered that raltegravir acts on the subunit UL89 of the terminase and cancels the scissor function, which is required for viral replication.

The assays were performed directly on the protein in test tubes. "Now we must do the assays on whole infected cells, improve the effect of the drug and validate that it is also effective for other kinds of herpes viruses," explains Miquel Coll, whose lab has patented this second application for raltegravir. To resolve the 3D structure of the target protein, the scientists have used a state-of-the-art high-performance protein expression technique, with the collaboration with Darren Hart's group at EMBL in Grenoble, where 18,000 clones or different fragments of the protein have been tested. They have also used the Grenoble synchrotron to obtain the structural data. The study has lasted five years and forms part of the European project SPINE-2 complexes.

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Story Source:

The above story is reprinted from materials provided by Institute for Research in Biomedicine-IRB.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

M. Nadal, P. J. Mas, A. G. Blanco, C. Arnan, M. Sola, D. J. Hart, M. Coll. Structure and inhibition of herpesvirus DNA packaging terminase nuclease domain. Proceedings of the National Academy of Sciences, 2010; 107 (37): 16078 DOI: 10.1073/pnas.1007144107

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


View the original article here

Thursday, August 9, 2012

Recurring genital problems could be herpes, Swedish study suggests

ScienceDaily (Apr. 11, 2011) — A study of patients attending sexual health clinics in Gothenburg found that just four out of ten patients with genital herpes actually knew that they had the disorder. However, a third of those who did not realise that they had been infected reported typical symptoms at a follow-up visit, reveals a thesis from the University of Gothenburg, Sweden.

In her thesis Matilda Berntsson, a specialist in skin and sexually transmitted infections at the Frölunda Specialist Hospital's skin clinic and researcher at the Sahlgrenska Academy, investigated the prevalence of genital herpes type 2 among patients attending sexual health clinics in Gothenburg. Her investigation included more than 1,000 patients, both male and female.

Genital herpes caused by herpes simplex virus type 2 infects the genital membranes before moving to the nerve ganglia alongside the spinal cord, where it remains for the rest of a patient's life. Although many people who have been infected do not experience any discomfort, the virus can be activated and spread further through sexual contact. The disorder can also result in recurring genital problems.

"1,014 patients who attended sexual health clinics, the Sahlgrenska University Hospital skin clinic and the Sesam sexual health clinic were tested for herpes simplex virus type 2," says Matilda Berntsson. "The presence of antibodies in the blood shows that a person is infected with the virus."

The test results revealed that more than one in five women and one in ten men were infected with genital herpes type 2. Just four out of ten patients with herpes type 2 antibodies actually knew that they were infected. However, a third of those patients who did not know that they were infected reported typical symptoms in the form of recurring genital blisters and sores at a follow-up visit.

"The study reinforces our perception that genital herpes is common and that most people carrying it are unaware that they have it," says Berntsson. "Non-specific recurring genital symptoms could be undiagnosed herpes, which can be detected with a simple test at the doctor's."

She therefore suggests that people with non-specific genital symptoms who are worried about genital herpes should see a doctor for an examination.

"If the symptoms and/or findings suggest herpes, there are good methods for testing for the disorder," says Berntsson. "Pronounced symptoms can be treated with medicines that alleviate discomfort, and a daily preventative treatment can be given for longer periods where recurrences are frequent."

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Story Source:

The above story is reprinted from materials provided by University of Gothenburg, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


View the original article here

Sunday, May 6, 2012

Recurring genital problems could be herpes, Swedish study suggests

ScienceDaily (Apr. 11, 2011) — A study of patients attending sexual health clinics in Gothenburg found that just four out of ten patients with genital herpes actually knew that they had the disorder. However, a third of those who did not realise that they had been infected reported typical symptoms at a follow-up visit, reveals a thesis from the University of Gothenburg, Sweden.

In her thesis Matilda Berntsson, a specialist in skin and sexually transmitted infections at the Frölunda Specialist Hospital's skin clinic and researcher at the Sahlgrenska Academy, investigated the prevalence of genital herpes type 2 among patients attending sexual health clinics in Gothenburg. Her investigation included more than 1,000 patients, both male and female.

Genital herpes caused by herpes simplex virus type 2 infects the genital membranes before moving to the nerve ganglia alongside the spinal cord, where it remains for the rest of a patient's life. Although many people who have been infected do not experience any discomfort, the virus can be activated and spread further through sexual contact. The disorder can also result in recurring genital problems.

"1,014 patients who attended sexual health clinics, the Sahlgrenska University Hospital skin clinic and the Sesam sexual health clinic were tested for herpes simplex virus type 2," says Matilda Berntsson. "The presence of antibodies in the blood shows that a person is infected with the virus."

The test results revealed that more than one in five women and one in ten men were infected with genital herpes type 2. Just four out of ten patients with herpes type 2 antibodies actually knew that they were infected. However, a third of those patients who did not know that they were infected reported typical symptoms in the form of recurring genital blisters and sores at a follow-up visit.

"The study reinforces our perception that genital herpes is common and that most people carrying it are unaware that they have it," says Berntsson. "Non-specific recurring genital symptoms could be undiagnosed herpes, which can be detected with a simple test at the doctor's."

She therefore suggests that people with non-specific genital symptoms who are worried about genital herpes should see a doctor for an examination.

"If the symptoms and/or findings suggest herpes, there are good methods for testing for the disorder," says Berntsson. "Pronounced symptoms can be treated with medicines that alleviate discomfort, and a daily preventative treatment can be given for longer periods where recurrences are frequent."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Gothenburg, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


View the original article here

Saturday, May 5, 2012

Drug against AIDS could be effective against herpesvirus

ScienceDaily (Sep. 23, 2010) — Scientists at the Institute for Research in Biomedicine (IRB Barcelona) headed by the coordinator of the Structural and Computational Biology Programme, Miquel Coll, have published a new study that demonstrates that raltegravir, the drug approved in 2007 for the treatment of AIDS that is sold by Merck under the name Isentress, cancels the function of an essential protein for the replication of one kind of herpes virus. This study, published in the journal Proceedings of the National Academies of Sciences (PNAS), is the first step towards the development of a drug against the entire herpesvirus family.

"These results have a clear medical impact for three reasons," explains Miquel Coll, also a CSIC research professor. "First, humans do not have the viral protein that is affected, thus this would allow a highly specific drug that does not show the secondary effects that other drugs may have. Second, the inhibitor is not toxic for humans when administered at therapeutic concentrations because it is already on the market and thus toxicity tests are facilitated; and third, we have data that indicate that all herpes viruses have this protein. Therefore, it could be a valid target against all Herpesviridae."

Herpesviruses include pathogens such as herpes simplex 1 and 2, the virus that causes chickenpox otherwise known as zoster virus, the Epstein-Barr virus -associated with several types of cancer -, the roseola virus, the cytomegalovirus and the herpes virus associated with Kaposi sarcoma -in AIDS patients -. The human cytomegalovirus (HCMV), on which the study was performed, causes neurological defects in 1% of neonates in developed countries. It also produces retinitis that deteriorates into blindness in 25% of subjects with AIDS, defects in the brains and central nervous systems of young adults, inflammation of the colon -also in those with AIDS -, mononucleosis and serious diseases of the throat. Although 90% of adults carry HCMV, this virus is opportunistic, acting in people with weakened immune systems such as in cancer and AIDS patients, recipients of organ transplants and neonates.

Blocking viral replication

To replicate, the herpes virus enters the nucleus of a cell where it uses the cell machinery to copy its DNA several times into a single large chain. Once this copy has been made, acts a complex called terminase, formed by three protein subunits. The terminase cuts the new DNA into small fragments, the size of a single viral genome, and introduces these into empty shells (capsids) that have developed in the cell nucleus. Then, the new viruses leave the cell to continue infection. The researchers resolved the 3D structure of one part of the terminase and when they observed that it resembled the integrase of the AIDS virus, for which drugs are available, they tested it against the herpes virus protein. Thus they discovered that raltegravir acts on the subunit UL89 of the terminase and cancels the scissor function, which is required for viral replication.

The assays were performed directly on the protein in test tubes. "Now we must do the assays on whole infected cells, improve the effect of the drug and validate that it is also effective for other kinds of herpes viruses," explains Miquel Coll, whose lab has patented this second application for raltegravir. To resolve the 3D structure of the target protein, the scientists have used a state-of-the-art high-performance protein expression technique, with the collaboration with Darren Hart's group at EMBL in Grenoble, where 18,000 clones or different fragments of the protein have been tested. They have also used the Grenoble synchrotron to obtain the structural data. The study has lasted five years and forms part of the European project SPINE-2 complexes.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Institute for Research in Biomedicine-IRB, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

M. Nadal, P. J. Mas, A. G. Blanco, C. Arnan, M. Sola, D. J. Hart, M. Coll. Structure and inhibition of herpesvirus DNA packaging terminase nuclease domain. Proceedings of the National Academy of Sciences, 2010; 107 (37): 16078 DOI: 10.1073/pnas.1007144107

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.


View the original article here

Sunday, October 30, 2011

Herpes Virus Could Kill Aggressive Breast Cancer

A genetically engineered version of the virus that causes herpes shows promise as a treatment for a particularly aggressive type of breast cancer, according to a new study in animals.

The virus targeted and killed triple-negative breast cancer cells in mice. Triple-negative breast cancer is a form of breast cancer that cannot be treated with hormone therapies, such as tamoxifen and Herceptin.

The results are preliminary, and it's not clear whether the therapy will have the same effect on tumors growing in people. Much more research is needed to determine this. If a treatment is developed, it will likely be used in conjunction with other cancer therapies, including chemotherapy and radiation, the researchers said.

The study will be presented today (Oct. 24) at the meeting of the American College of Surgeons in San Francisco.

Herpes therapy

Triple-negative breast cancer accounts for about 20 percent of all breast cancer cases. It disproportionally effects young, African-American women and is usually treated with chemotherapy. (Triple-negative breast cancers are not fueled by the hormone estrogen, so they do no respond to treatments designed to block the hormone.)

Study researcher Dr. Sepideh Gholami, a research fellow in the at Memorial Sloan-Kettering Cancer Center in New York City. and colleagues infected breast cancer cells in a dish with a herpes virus called NV1066. Within a week, the virus killed up to 90 percent of the tumor cells.

The researchers then injected breast cancer cells into mice. After treating the mice with the virus for 20 days, they saw the tumors had largely disappeared, Gholami said.

The dramatic response may be due to the fact that triple-negative breast cancer cells have high levels of a protein called p-MAPK. The herpes virus specifically targets cells with high levels of this protein, the researchers said.

The therapy is just one of many in recent years to explore the use of viruses as a means to target and destroy cancer cells. The herpes virus has been tested in people as a treatment for head and neck cancer, but not for breast cancer, the researchers said.

More research

The study is an "extremely exciting step" in the pursuit of a cancer therapy that uses the herpes virus, said Dr. Stefan Gluck, a medical oncologist at the University of Miami's Sylvester Comprehensive Cancer Center.

However, the researchers still need to show that this herpes virus is safe to use in patients. After all, the herpes virus is known to cause infection in humans, including infections in the brain. Proving the therapy's safety will likely be a lengthy process, and will involve testing it on other animals first, such as dogs and primates, Gluck said.

The researchers plan to figure out exactly how the virus works to kill the breast cancer cells, and try to bolster its effect.

Pass it on: The herpes virus can infect and kill breast cancer cells in a dish and in mice.

This story was provided by MyHealthNewsDaily, a sister site to LiveScience. Follow MyHealthNewsDaily staff writer Rachael Rettner on Twitter @RachaelRettner. Find us on Facebook.


View the original article here

Monday, September 26, 2011

Discovery could lead ways to prevent herpes spread

Discovery could lead ways to prevent herpes spread

Enlarge

Recently enveloped herpes simplex virion in the perinuclear space of an infected cell.

(Medical Xpress) -- Herpesviruses are thrifty reproducers -- they only send off their most infectious progeny to invade new cells. Two Cornell virologists recently have discovered how these viruses determine which progeny to release.

The College of Veterinary Medicine researchers report in the Aug. 23 (108:34) issue I of the Proceedings of the National Academy of Sciences on the mechanisms of this quality-control system, which helps streamline viral reproduction to optimize its spreading.

The virologists identified proteins in the nuclear membranes of infected cells that control which viral products exit. This map could be used to identify new targets for future drugs that would hamper viral reproduction by clogging inspection pathways to trap viruses in the cells they first infect.

"When a herpesvirus hijacks a cell, it turns the nucleus into a viral production factory," said Joel Baines, the James Law Professor of Virology, who co-authored the study with postdoctoral research associate Kui Yang. "It makes protein shells called capsids, stuffs them with viral DNA and ships them out of the nuclear membrane to infect new cells. But errors in the assembly line leave some capsids empty, without DNA, and shipping these is a waste of resources."

When capsids bud from the nuclear membrane, they take pieces of it with them, forming protective lipid envelopes that let them move to new cells. Empty capsids can't reproduce, so the virus only allows capsids with DNA through. How the membrane could determine whether the capsid had DNA or not was a mystery until Yang and Baines mapped its method.

"We found clamplike proteins on the surface of herpesvirus capsids that hold them together and keep them from bursting when they're stuffed full of DNA," said Baines. "Those with DNA have far more of these than empty capsids. We also found a protein complex living in the host cell's nuclear membrane that binds to these structural support proteins, selecting DNA-filled capsids to pull through the membrane. Thus the virus releases only its most infectious particles."

Discovery could lead ways to prevent herpes spread Various species of herpesvirus.

This streamlining process has helped herpesvirus species spread prevalently and permanently across all animal species. Eight of the 25 known viruses in the herpes family regularly infect humans, posing a leading cause of human viral infection.

Once in a body, herpesvirus stays for life. It can flare up at any time, causing symptoms and diseases, ranging from infected sores to brain inflammation, birth defects and cancers of the nose, throat and lymphatic system. Though usually not fatal, herpes can prove dangerous to patients with weak immune systems, such as those with HIV/AIDS or infants who contract HIV/AIDS from their mothers.

There is no cure for herpes, but Baines' map illustrates a viral reproduction system that can be subverted.

"Take away either component, the capsid's clamplike proteins or the membrane's inspector proteins, and nothing escapes the host cell," said Baines. "This opens the door to developing drugs that could block the interactions between these protein complexes, covering the binding sites to clog the system so that no viral particles get through. This would significantly slow or even stop the virus's spread between cells. Our lab is now working on even more detailed maps of these proteins' exact interaction sites that will help drug developers pinpoint precise targets to thwart viral reproduction."

The research was supported, in part, by the National Institutes of Health.

Provided by Cornell University (news : web)


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