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Posted by john on July 9th, 2007 — in Aldara Top News
Scientists have told a conference in Switzerland that a genetically engineered herpes virus has shown early promise in clinical tests.
They say researchers believe viruses - which are experts at killing cells - could one day become a valuable addition to the medical armoury against cancer.
The latest progress has been made in a small study using MediGene AG’s virus NV1020 and was presented at the annual European Society for Medical Oncology conference in Lugano, Switzerland.
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NV1020 is a modified version of the herpes simplex virus, which causes cold sores.
Its genetic make-up has been altered that so it only replicates in cancer cells, killing them in the process and leaving ordinary cells alone
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Posted by john on July 6th, 2007 — in Aldara Top News
Hansa, Woodland Park Zoo’s 6 1/2-year-old elephant, died of a previously undiscovered herpes virus, Zoo officials announced Monday.
Related content
- Photo gallery of Hansa’s life
The as-yet unnamed virus is different on a genetic level than the more familiar types of herpes viruses that are known to affect Asian and African elephants, both in captivity and in the wild, Zoo Deputy Director Bruce Bohmke said.
Herpes is especially deadly for elephants younger than 10, Zoo veterinarian Kelly Helmick said. Of 21 known cases among elephants of all ages in North American zoos since 1983, only three survived herpes. Scientists do not know how any of the herpes strains are transmitted among elephants, although it is known that they can harbor the virus for many years and never appear ill.
There is no known cure for herpes in elephants, she said. A vaccine is still many years away. Elephants can be treated with the same antiviral drug used to treat human herpes, but the results to date have not been very successful, based on the survival rates.
Hansa was tested for the known herpes viruses when she fell ill in late May, and the test was negative, Zoo officials said. In hindsight, the negative finding occurred because the existing test could not detect the new type of herpes. Scientists are in the process of developing a genetic test that can detect the new type of herpes in elephants, as well as an antibody test that can detect whether an elephant already had the virus.
Herpes viruses infect most species, and typically are species specific, meaning they don’t cross over among different types of animals. For example, nine types of herpes viruses are known to attack humans. The human virus is genetically different than the elephant virus.
The newly discovered herpes virus that killed Hansa attacked the blood vessels throughout her body, Helmick said. Hansa did not exhibit the typical symptoms for a known herpes infection, which include development of a swollen, purplish tongue and rapid death.
Hansa, an Asian elephant that was born and raised at the Zoo, was found dead June 7 after a brief illness. The popular young elephant had shown signs of reduced activity and appetite, and “coliclike” symptoms in the week or so before her death. Lab tests and clinical examination showed no signs of disease, however, and she appeared to be improving just before her death.
After her death, a team of veterinarians and pathologists from three institutions performed a necropsy.
According to early test results released June 22, the team ruled out sand colic, gastric torsion, foreign-body obstruction, salmonellosis, cancer or any form of genetic or nutritional disease.
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The Zoo then began sending tissue samples to a half-dozen institutions, including Johns Hopkins University, the Smithsonian National Zoo and the University of California, Davis.
The virus eventually was identified by Dr. Laura Richman, a research scientist at the National Elephant Herpesvirus Laboratory at the Smithsonian zoo in Washington, D.C.
“The most closely related viruses are the Asian and African elephant endotheliotropic herpesviruses, known collectively as EEHV,” Richman said Monday. “But this newly identified virus is not the same as EEHV. Its genetic difference is why it could not have been detected previously.”
Woodland Park Zoo is in the process of notifying elephant keepers around the country of the findings, Bohmke said. Zoo is monitoring its other elephants, which all appear healthy.
Although the mode of transmission of this particular virus is unknown, other herpes viruses are transmitted through close contact from animal to animal, Richman said. Some may be transmitted from mother to offspring through the birthing process.
It’s also not understood why the virus causes some animals to get sicker than others.
The Smithsonian lab plans to go back and look at previous elephant deaths around the country to determine whether the newly identified virus may have been a factor, Richman said.
Maria French, president of the Northwest Animal Rights Network, said she hoped the United States Department of Agriculture would investigate Hansa’s death and shed additional light on what happened.
Mark French, the network’s treasurer, said he doubted that herpes was the sole cause of Hansa’s death, citing her habit of eating sand. He criticized the Zoo’s investigation for not allowing scientists from activist groups to participate.
“We’re really mourning the loss of Hansa,” Maria French said, adding that the group advocates the release of the Zoo’s remaining elephants to a sanctuary in Tennessee.
The Zoo’s elephant keepers and veterinary staff also continue to mourn Hansa’s death, but the outpouring of sympathy and support from around the country has been some solace, said Nancy Hawkes, who curates the Zoo’s elephant exhibit.
“I can’t tell you what a help it has been for the staff,” she said.
The Zoo’s three remaining elephants have resumed their normal routines after a brief period in which they appeared to acknowledge Hansa’s passing, she said.
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Posted by john on July 2nd, 2007 — in Aldara Top News
SEATTLE (AP) - The Woodland Park Zoo in Seattle says the 6-year-old elephant who died last month had herpes.
Hansa (HAHN’-suh) died June eighth after her handlers noted a drop in activity and appetite.
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Hansa was born at the zoo in November 2000 to an elephant named Chai (chy) who remains at the zoo with two other elephants.
Copyright 2007 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
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Posted by john on June 30th, 2007 — in Aldara Top News
Generic drug developer Teva Pharmaceutical Industries Ltd. said Friday the Food and Drug Administration approved the company’s generic version of Pfizer Inc.’s Norvasc treatment for hypertension and angina.
The generic approval covers amlodipine besylate tablets in 2.5-milligram, 5-milligram and 10-milligram doses.
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Mylan Laboratories Inc. (nyse: MYL - news - people ) also markets a generic version of Norvasc. Sales of Norvasc totaled $1.07 billion in the first quarter, marking a 10 percent drop from the prior year, mainly because of increased generic competition.
Shares of Israel-based Teva were up a penny at $41.04 in afternoon trading, while shares of Pfizer (nyse: PFE - news - people ) fell 15 cents to $25.48. Shares of Mylan fell 22 cents to $18.15.
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Posted by john on June 25th, 2007 — in Aldara Top News
U.S. researchers have patented a strategy for developing a human vaccine to prevent Human cytomegalovirus infection and disease.
Cytomegalovirus, or CMV, is a type of herpes virus that’s the leading viral cause of birth defects and a serious problem in patients with compromised immune systems. The body’s natural immunity doesn’t protect against infection by the virus, estimated to be present in up to 75 percent of all adults.
“Until now, scientists haven’t been able to develop a vaccine to protect against CMV,” said University of California-San Diego Professor Deborah Spector. “Using a two-pronged approach, we successfully created and tested a vaccine in a mouse model with CMV that shows enormous promise for redirecting the body’s immune system, enabling it to fight the virus.”
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She said the mouse vaccine generates an immune response by disarming the virus’s ability to replicate and establish a persistent infection.
The research is to appear in the July issue of the Journal of Virology.
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Posted by john on June 23rd, 2007 — in Aldara Top News
Q. I’m a 47-year-old man and my wife is 49. We got married four years ago. Two days ago, she came back from the doctor and told me she has genital herpes. I am floored. She said she just found out. She said she must have contracted it years ago and never had an outbreak until 10 days ago. She has been to the doctor countless times over the last 20 years. I don’t know what to think. Is it really possible she didn’t know? I know she needs me to be a loving husband now, but it’s hard when I can’t believe she just found out about this. If she knew about it and lied to me, my trust is destroyed. Also, how can our marriage survive when I can’t bring myself to have sex with her? What do you think? —MARRIAGE IN SERIOUS TROUBLE
A. I think you’re being a douche, MIST. But, hey, everyone’s entitled to a little douchebaggery now and then. The wife’s got a sexually transmitted infection—that’s upsetting and you’re freaked. Understandable. You’re also overreacting and misinformed, MIST, and continued douchebaggery on your part may end your marriage. So let’s set down the douchebag and start getting informed, OK? “His wife could have been exposed to the herpes virus decades ago,” says Karen J. Pataky, a nurse practitioner and clinician at Planned Parenthood of Metropolitan Washington. Which means it’s possible that your wife didn’t know, MIST—believe it. Why would she suddenly have an outbreak? “Her immune system could have kept it contained all this time,” says Pataky. “As we near 50, our immune systems become a little less competent to deal with certain things.” As for all those trips to the doctor? “None of the medical situations that MIST describes would lead a physician to check for herpes antibodies; she would not know through routine blood tests, either.” (MIST included some details about his wife’s medical history that I shared with Pataky.) And guess what, MIST? If your wife could have been infected for years without knowing, then you could have been infected for years without knowing. Pataky connects the suppurating dots: “It’s possible that he is the one who infected her and he has not had an outbreak. Or he had a small outbreak and it went away quickly and he didn’t think twice about it.”
If it turns out that you’re not already exposed, MIST, you can use condoms at all times to protect yourself—but condoms don’t provide 100 percent protection against herpes. So why not do the decent, loving thing and just assume you’re already infected and refuse to let a piddling thing like herpes destroy your marriage?
“Cancer, HIV, heart attacks—that’s horrible news,” says Pataky. “This is not horrible news. Herpes is not something to ruin a marriage over, medically speaking. It’s never life-threatening and it’s possible to go years without any outbreaks.”
So, MIST, do you love your wife more than you fear a relatively mild STI that you’ve probably already been exposed to and may have exposed your wife to in the first place? If the answer to that question isn’t “yes,” MIST, you’re a bigger douche than I thought.
Q. I’m dating again after taking a break due to a spate of bad relationships. Four weeks ago, I met a guy I felt a genuine interest in and he let things develop. Then he told me that he would be moving to Las Vegas at the end of July, but wanted to date until he left. With Pride Weekend coming up and plenty of opportunities to find someone who may actually be living in Seattle for more than a few weeks, I declined. After bouncing back, I met someone even more wonderful. We share this electricity and he’s someone I could see myself with long-term. Then he tells me that he, too, is moving at the end of the month! Am I the goodbye committee for the gay scene in Seattle? Any wise words to help a lost little ‘mo? —Left Behind
A. Yeah, LB: Stop whining. In four weeks, you’ve met two guys you could see yourself with long-term. There are fags out there having a hard time meeting guys they can see themselves with through happy hour. Keep going out, keep meeting guys, and, again, stop whining.
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Oh, and speaking of lost little ‘mos . . . Tyler Whitney is an up-and-coming conservative activist. Just 18 years old, Whitney is working for the GOP’s most rabidly antigay presidential candidate, Tom Tancredo, as webmaster; he heads up a rabidly antigay political group on his college campus; and he carried a “Go Back in the Closet!” sign at an antigay protest. Which is odd, since Whitney is gay and has recently been outed.
Well, not outed, exactly. Whitney had begun quietly coming out to a few friends when a blog, the Michigan Conservative Dossier, posted an item about him that hurried the process along. Between the Lines, Michigan’s gay newspaper, published a story, which was then picked up by national gay bloggers.
Predictably, conservatives are rallying around their pet self-hating homo. Bay Buchanan, senior adviser to Tancredo, says Whitney’s “sexual preference is a personal matter” and that it should have “nothing to do with the campaign.”
Sorry, Bay, but gay-bashing thugs—people like you, your horrible brother Pat, your vile candidate—can’t have it both ways. If Whitney’s sexual preference is a personal matter, then so is mine. If Whitney’s sexual preference shouldn’t have anything to do with the campaign, then neither should mine—nor should the sexual preference of any other American. So long as the GOP insists on attacking gay and lesbian Americans, Whitney’s sexual orientation—to say nothing of his hypocrisy—is relevant to a debate that the GOP started. Some stupid homos, of course, are saying that we should feel compassion for poor Tyler Whitney. Oh, he’s just a kid, too young to be outed, have a little sympathy, blah blah blah. Uh . . . nope.
Someone who’s 18 and gay is old enough to drive, join the army, vote, and come out. Someone who’s 18 and gay and not ready to come out is old enough to know better than to march with assholes carrying “Straight Power” signs at antigay rallies. And someone who’s 18 and gay and politically active, as Whitney is, is politically savvy enough to know that working for antigay politicians makes him a prime outing candidate.
I say this as someone who doesn’t support outing in all instances. Hell, I recently talked someone out of outing a public figure. A Savage Love reader was contemplating outing an innocuous celeb back in April. I advised him against it, because outing is brutal and it should be reserved for brutes. Whitney more than qualifies. Want to feel sorry for someone? Feel sorry for Sean William Kennedy, a 20-year-old gay man who was beaten to death outside a bar in South Carolina. If Kennedy was old enough to die at the hands of a thug who, without a doubt, votes for the same assholes Whitney does, then Whitney is old enough to be outed.
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Posted by john on June 17th, 2007 — in Aldara Top News
The DNA damage response normally fixes DNA errors caused by radiation or other environmental factors, or mistakes accidentally introduced when cells copy their genetic material prior to dividing.
In the murine (or mouse-infecting) herpes virus they studied, researchers at Washington University School of Medicine in St. Louis identified a protein that can trick the mouse cell into turning on the DNA damage response. They also showed that Epstein-Barr virus, a human herpes virus, has a similar protein. Scientists found that blocking murine herpes virus from activating the DNA damage response caused viral replication rates to plummet.
“We don’t want to treat viral infection by blocking DNA damage response systemically because this process is used constantly throughout the body and is very important to preventing cancer,” says lead author Vera Tarakanova, Ph.D., a postdoctoral fellow. “However, by targeting the viral protein responsible for activating the DNA damage response, we may be able to block viral replication. In addition, determining how the DNA repair response helps viral replication may enable us to develop novel strategies to treat infection.”
The paper appears online this week in Cell Host & Microbe. Scientists have known for some time that viral infection of cells activates the DNA damage response. But researchers had assumed that this activation occurred because repair mechanisms were mistaking replicating viral DNA for damaged or dysfunctional cellular DNA.
“Viruses sometimes structure their own DNA differently than cellular DNA,” Tarakanova notes. “Many of us thought that such differences might be triggering the DNA damage response.” Working in the laboratory of Herbert W. “Skip” Virgin, M.D., Ph.D., Edward Mallinckrodt Professor and head of the Department of Pathology and Immunology, Tarakanova found that murine herpes virus, rather than the host cell, was triggering the DNA damage response. She showed that introducing just one viral protein into cells led to activation of two cellular proteins involved in the damage response, ATM and H2AX.
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The viral protein that triggered this inappropriate activation, orf36, is a kinase, a type of protein that chemically modifies other molecules to activate different processes or transmit signals. Genetic comparisons with several human herpes viruses revealed kinases similar to orf36 in the human viruses. Scientists then took a similar kinase from human Epstein-Barr virus and showed that introducing it into cells also activated the DNA damage response.
When the research team genetically disabled orf36 in the murine herpes virus and infected mouse cells with it, the virus no longer activated the DNA damage response. The virus’s ability to replicate also dramatically decreased.
Kinases are versatile proteins that sometimes play multiple roles. To ensure that enhanced viral replication wasn’t linked to orf36’s interactions with other molecules, researchers turned to mice lacking the genes for ATM and H2AX, the damage response proteins activated by infection. When they infected cells from these mice with murine herpes virus, its ability to reproduce was again curtailed. How DNA damage response benefits viral replication is still a mystery and a topic of continuing investigation in the Virgin lab.
“The discovery that induction of the cells’ DNA damage response is an intentional viral strategy, rather than a passive cellular response to viral invasion, means that we should look into whether other DNA viruses use a similar approach to enhance their growth,” says Virgin.
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Posted by john on June 13th, 2007 — in Aldara Top News
Therapy with valacyclovir (Valtrex, GlaxoSmithKline), started within three months of infection with either herpes simplex virus type 1 (HSV-1) or HSV type 2 (HSV-2), reduces the rate of symptomatic outbreaks compared with placebo, Seattle investigators report in the Journal of Sexually Transmitted Diseases.
However, the response rate to valacyclovir in this study was somewhat lower than rates seen in other studies, in which treatment wasn’t started for a year or more after the onset of infection, according to Dr. H. Hunter Handsfield of the Batelle Center for Research and Evaluation and the University of Washington’s Center for AIDS and STDs and colleagues.
“All the studies to this point were in patients who had been infected for at least a year before treatment,” Handsfield told Reuters Health. “That’s what FDA approval of valacyclovir is based on.”
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Handsfield and colleagues conducted a pilot study of 119 patients with early HSV infection who were randomly assigned to valacyclovir or placebo daily for six months.
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The average patient age was 28.7 years, 66 percent were women, 63 percent had HSV-1 infection and 18 percent had HSV-2 infection. The maximum duration of infection was three months for eligibility in the trial.
At follow-up, the investigators found that the valacyclovir-treated patients had an average of 1.7 outbreaks of HSV infection per year compared with 3.4 episodes per years with placebo.
The average time to first recurrence of symptoms was 80 days with valacyclovir and 54 days with placebo. Eighteen patients (47 percent) on valacyclovir were recurrence-free at the end of the study period compared with 10 patients (27 percent) on placebo.
Handsfield said that although the response rate is somewhat lower with early compared with delayed antiviral treatment, “there is every reason to suppose, based on the pattern of response seen in other studies, that the response rate will continue to improve over time…and reach that seen in previous studies.”
“One important public health message here is that HSV infection…doubles the risk of HIV infection…Patients should be offered early therapy and also counseled about the risk of transmission to uninfected sexual partners,” and the importance of abstaining from intercourse during outbreaks and always using condoms.
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Posted by john on June 10th, 2007 — in Aldara Top News
Hansa, whose Thai name meant “Supreme Happiness,” left Seattle supremely sad Friday after her sudden death during the night.
Related content
Hansa paints
The life of Hansa in photos
Learn more:
- No pattern in deaths at zoo (May 31, 2006)
- Death renews debate about zoos
- The zoo has a Web page for visitors to express condolences
Hansa, Woodland Park Zoo’s 6 1/2-year-old elephant, was found dead Friday morning, closing the elephant exhibit for the day, according to zoo officials.
“She was a little princess,” said an emotional Kelly Helmick, the zoo’s director of animal health, at a news conference Friday afternoon. “She was definitely a little spoiled.”
Hansa had been a favorite since her birth on Nov. 3, 2000.
Zoogoers immediately took to the little elephant with the big personality. Her cavorting made her an unofficial mascot, often drawing long lines at the elephant exhibit where she grew quickly, packing on 2 pounds a day.
The year she was born, attendance, which normally runs about 1 million visits a year, spiked by 200,000, Deputy Director Bruce Bohmke said.
“She was special because she was the first one born,” said Linda Stemler of Bothell, pausing at the closed entry to the elephant exhibit. Stemler had hoped to show her son and two grandsons, who were visiting from Colorado Springs, the zoo’s elephant, but was instead sharing her loss with them.
Hansa had been under the weather since May 31, when zoo staff noticed a decline in appetite, coliclike symptoms and a decrease in her activity level.
Recent tests were “inconclusive,” and she was being monitored and given antibiotics, zookeepers said. The young elephant, which wouldn’t have reached adult size until about age 12, weighed between 5,000 and 6,000 pounds. Her diet of grain, hay, fruits and vegetables was the same as that fed to the other elephants. She had showed no previous signs of illness, Helmick said. The elephants undergo annual exams to check their health. Their normal life expectancy in captivity is about 46 years.
The zoo performed a necropsy this afternoon, but definitive results won’t be known for several weeks.
The elephant barn was closed Friday. And zoogoers were told at main gates what had happened.
Early in the day, however, many visitors first got the news at the entrance to the trail that led to the elephant barn, where a notice of the death was posted next to the “Path Closed” sign.
“It’s just so sad,” said Lawrie Lillie of Bainbridge, who was making her first pilgrimage to the zoo after 20 years living back East. She had been hoping to see the little elephant she’d heard so much about.
For 9-year-old Zachary Osborn, the news was almost too much to absorb. Stunned and sad-looking, he had no words.
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“He has a connection to the elephants,” said his mom, Dalene Osborn. “We need to go have a discussion now about life and death, and the suddenness of it all.”
Osborn and Zachary had been coming to see the elephant since she was born, Osborn said. “They kind of grew up alongside each other.”
Zoo officials said people who want to leave memorials to Hansa can do so at the wall at 50th Avenue North and North Fremont Avenue.
Hansa was the first elephant born at the zoo and in the state. Her mother is Chai, 28.
Her name came from Madison Gordon, a Redmond girl. Hers was among 30,000 suggestions the zoo received. Madison was out of the country Friday, but zoo staff left a message for her and her family notifying them of the death.
Hansa was a popular celebrity as soon as she was born, charming zoogoers with her antics. Her first steps, her first swim and her first birthday cake of cornmeal mush and mashed potatoes made the news. Sometimes called a “miracle baby,” she was conceived after years of unsuccessful artificial insemination. Her conception was finally accomplished when Chai was shipped to a Missouri zoo to mate with an elephant named Onyx. Twenty-two months later, the bouncing 235-pound baby was born in the wee hours of the morning. She stood barely taller than a yardstick.
For several years, she could still scoot under her mother’s belly when she wanted extra protection, a coy trick she employed when evading her keepers, or entertaining visitors.
Hansa’s death was discovered by one of her keepers at 7:40 a.m. The animals had all been inside in their usual, separate sleeping quarters during the night. Hansa and her mother usually slept together in the herd room.
She was found lying in the stall with her mother. The other elephants — Watoto, 38, and Bamboo, 40, were allowed to visit with her body for a while “to pay respects,” Bohmke said.
Elephants are known in the wild to exhibit mourning behavior, often standing vigil for hours or days when a member of the herd is lost. Some elephants also will revisit and appear to remember the bones of those left behind.
Zoo officials still hope to add to the herd. They are waiting to see whether Chai, who recently was inseminated a fourth time, is pregnant. An ultrasound test should yield a result by the end of the summer. Previous efforts at artificial insemination ultimately have failed.
Around the country, there has been a recent boomlet in elephant births, with eight born in 2006 and 2007, according to Mike Keele, who keeps statistics on the Asian elephant population for the North American Region of the Association of Zoos and Aquariums. Currently, there are 150 Asian elephants in 78 zoos that belong to the association. There have been 37 births over the last decade, but only 17 of those elephants are still alive, he said. Forty-eight died in the same time frame.
Of elephants in Hansa’s age range, there have been six deaths — four male and two females, he said.
“I was very surprised, he said. “It’s pretty unusual for an elephant to die once they are past the age of 1.”
The herpes virus is a frequent cause of death in young elephants in captivity, he said, although it’s not possible to say yet whether that was a factor.
Keele, who is also deputy director of the Oregon Zoo, was shocked and saddened when he heard of Hansa’s death. “It’s a tough one,” he said. “You really become attached to them.”
After the necropsy is completed, Hansa’s remains will be cremated, Bohmke said.
Zoo staff were still deciding about plans for some way to memorialize the little elephant.
But elephant-lovers are unlikely to ever forget.
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Posted by john on June 5th, 2007 — in Aldara Top News
Rats with erectile dysfunction, or ED, that were injected with a gene therapy vector containing either of two nerve growth factors were able to regain normal function after four weeks, according to a study conducted by University of Pittsburgh School of Medicine researchers. These findings are being presented at the 10th annual meeting of the American Society of Gene Therapy, which is convening May 30 to June 3 at the Washington State Convention & Trade Center, Seattle.
ED is the repeated inability to achieve or maintain an erection necessary for sexual intercourse. Because of the variability of symptoms, estimates of the incidence of ED vary but range from 15 million to 30 million affected men in the United States. ED is frequently associated with damage to the cavernous nerve that results from surgery for prostate cancer. Even if a patient receives a nerve-sparing procedure during surgery, recovery from ED after radical prostatectomy may take a long time.
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In this study, which was led by Joseph C. Glorioso, III, Ph.D., chair of the department of biochemistry and molecular genetics, and Joel Nelson, M.D., chair of the department of urology, University of Pittsburgh School of Medicine, researchers inserted either the gene for the glial cell line derived neurotrophic factor (GDNF) or the GDNF family ligand (neurturin) into a genetically engineered herpes simplex virus (HSV). They then injected either of the recombinant viruses into the damaged cavernous nerve of rats. GDNF is an important nerve growth promoter and has been shown in other studies to contribute to survival and regeneration of penile nerves. Neurturin also is a nerve growth factor closely related to GDNF. Control mice received only the virus without the GDNF or neurterin genes inserted.
Four weeks after the treatment, rats administered HSV-GDNF exhibited significant recovery of intracavernous pressure (ICP) and systemic arterial pressure (AP) compared with rats treated with the control virus or untreated mice with ED. Rats treated with HSV-neurturin also exhibited significant recovery of ICP and AP compared with the control or untreated mice at four weeks after treatment. Fluorescent protein studies also showed that the delivered genes had been effectively incorporated into the target nerve cells.
According to Dr. Glorioso, HSV delivery of GDNF or neurturin presents a potentially important new approach for the treatment of ED. “Because the herpes virus persists in the nerve cell for as long as it is alive and nerve cells typically do not reproduce, this represents the first-ever demonstration of a long-term treatment for ED that does not rely on the chronic administration of drugs that can have potentially harmful side effects,” he explained.
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