Science nod to family of unwitting medical heroine

Sixty-two years ago, scientists harvested cancer cells from an African American tobacco farmer which were used for some of the biggest breakthroughs in medical science -- without her knowledge or consent.

The abnormally resilient cells were taken from Henrietta Lacks shortly before she died and used for decades without her family's knowledge, spawning Nobel-winning discoveries and a multi-million-dollar industry that yielded the polio vaccine, cloning, in-vitro fertilisation and many medicines.

It became the most widely used human cell line used by researchers and made Lacks a giant contributor to medical science, albeit unwittingly.

Now, six decades after her death, Lacks' descendents are paving the way yet again -- this time helping to lay the groundwork for ethical use of genetic data obtained in the name of research.

On Wednesday, authorities announced they had finally reached an agreement with Lacks' family for the continued, though controlled, use of the cells' genomic data, which was published on the same occasion.

"It is truly fitting, given the priceless contributions that Henrietta Lacks has made to science and medicine, that her story is now catalysing enduring changes in policy," Francis Collins, director of the US National Institutes of Health (NIH), told journalists.

"We should all count Henrietta Lacks and her family among the greatest philanthropists of our time if we consider how they have contributed to the advancement of science and human health."

Lacks, a mother of five, was 31 when she died of an aggressive cervical cancer at Johns Hopkins Hospital in Baltimore, Maryland in 1951.

At the time, US regulations did not require doctors to obtain a patient's consent to harvest cell specimens.

The cells taken from Lacks, dubbed HeLa for the first letters of her first and last names, caused great excitement in scientific circles: they were the first-ever human cells to grow endlessly in the lab -- all others harvested up to this point eventually died.

"HeLa cells... are considered one of the biggest medical miracles in the last century," said a statement from the University of Washington in Seattle, which on Wednesday published a genome sequence of the cells in the journal Nature under the terms of the new agreement.

"The cells allowed scientists to perform experiments without using a living human and led to major medical breakthroughs", including a vaccine for certain types of cervical cancer and drugs for herpes, leukemia, influenza and Parkinson's disease.

Lacks' identity was revealed in a scientific journal in 1971, followed by a television documentary in 1997 and the publication in 2010 of a book, "The Immortal Life of Henrietta Lacks", now being made into a film.

Then in March this year, scientists from the European Molecular Biology Laboratory in Germany published a full genome of the cell line -- including data that could divulge certain heritable traits of Lacks' descendents.

Such information, which may point to a propensity for diseases like alcoholism, Alzheimer's disease or bipolar disorder, could be used to deny people life insurance or disability coverage, and the data was removed from public fora within days after the family protested.

The incident resulted in talks between the Lacks family and the NIH, which in turn yielded Wednesday's deal in terms of which researchers must apply to the NIH to use the HeLa genomic data in a study, agree to terms defined by a panel that will include two Lacks family members, and contribute their findings to a database.

"Today's release of the human genome sequencing is a historic, game-changing event," granddaughter and family spokeswoman Jeri Lacks Whye told a telephone conference.

"In the past, the Lacks family has been left in the dark... For more than 60 years our family has been pulled into science without our consent and researchers had never stopped to talk to us... or to give us a voice in the conversation about HeLa cells, until now."

Whye said the decision had been a complicated one, seeking to balance the needs of science with protecting her family's privacy.

"We are proud of what HeLa cells have done for science," she said, and welcomed a stipulation that will require researchers to recognise Henrietta Lacks and her cells' contribution to science.

The agreement covered only researchers funded by the NIH, and would not prevent others from "piecing together" large parts of the HeLa genome from data already in the public domain, or even sequencing it from scratch.

"Such actions would not be right and would not be respectful of the Lacks family," said NIH deputy director for science, outreach and policy, Kathy Hudson.

Collins stressed the agreement was not precedent-setting, and was necessary only because the HeLa cells were in such widespread use and the Lacks family was by now so widely known.

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Discovery Of Protein That Reactivates Herpes Simplex Virus Helps Solve Medical Mystery

ScienceDaily (Mar. 26, 2009) — Research in PLoS Pathogens appears to solve a long standing medical mystery by identifying a viral protein, VP16, as the molecular key that prompts herpes simplex virus (HSV) to exit latency and cause recurrent disease.

Led by researchers at Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, the landmark study points to a molecular target for designing improved HSV vaccines and treatments. It also could direct refined engineering of HSV viruses used in cancer therapy, the investigators said.

The study was conducted in collaboration with the Medical Research Council Virology Unit of Glasgow, Scotland.

The two distinct lifestyles of HSV – active and latent – were first proposed 80 years ago. The virus replicates itself at the body surface, producing thousands of copies that can be transmitted to other people. In neurons, however, the virus can enter a silent state, where the viral genetic code can be maintained for the lifetime of the infected person.

"Our current findings show that, in elegant simplicity, the herpes simplex virus regulates this complex lifecycle through the expression of VP16," said Nancy Sawtell, Ph.D., author and researcher in the Division of Infectious Diseases at Cincinnati Children's Hospital Medical Center.

The study points to what causes the virus to periodically reactivate in latently infected neurons, prompting new rounds of virus replication at the body surface. By understanding how HSV achieves this complex interaction inside the human nervous system, researchers can gain crucial insight into how to control the spread of the virus. At present, there is no way to eliminate latent virus or prevent the virus from exiting latency. There also are no effective vaccines to protect people who are uninfected and transmission rates remain high, the researchers said.

In the study, the research team simulated high fever in a mouse model of HSV infection, demonstrating that VP16 must be produced before the virus can exit the latent state in neurons. Fever has long been known to induce HSV reactivation, and recurrent lesions are often called cold sores or fever blisters because of this association. In the vast majority of neurons, the virus remains latent. In a few neurons, however, the scientists observed that fever in the mice led to a stochastic, or random de-repression of VP16, causing the virus to exit latency and reactivate.

"This completely changes our thinking about how this virus reactivates from latency," said Richard Thompson, Ph.D., co-author and researcher in the Department of Molecular Genetics, Biochemistry and Microbiology at UC. "Instead of a simple positive switch that turns the virus on following stress, it appears instead to be a random de-repression of the VP16 gene that results in reactivation."

The leading infectious cause of blindness and acute sporadic encephalitis in the United States, HSV-1 is usually acquired during childhood. Both HSV-1 and HSV-2 can be sexually transmitted diseases that when passed to newborns during birth causes a severe and often fatal infection. As many as 80 percent or more of people are infected with HSV. Most of the time, people carrying the virus do not have symptoms, although they can still transmit the virus.

The researchers hypothesize that HSV usually remains latent because VP16, which normally enters the cell with the virus particle, does not make the long trip the virus takes through the nervous system and isn't transported efficiently to the nerve cell nucleus.

Future studies will use this new information to develop strategies to prevent or control herpetic disease, said Dr. Sawtell, who also is an associate professor of Pediatrics at UC.

Funding support for the study came from National Institutes of Health.

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Tenofovir Vaginal Gel Protects Against Herpes - Medical News Today

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Main Category: Sexual Health / STDs
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Anti-HIV drug, tenofovir, when formulated as a vaginal gel, was found to reduce herpes simplex risk in females, researchers from the USA, Belgium and Italy reported in the journal Cell Host & Microbe. The scientists explained that this is because of the higher concentrations that reach vaginal cells in the vaginal gel formulation, compared to the drug when taken orally.

The authors explained that tenofovir disables a DNA enzyme of the herpes virus - reverse transcriptase - thus stopping its spread.

This study was a collaboration between researchers from the Catholic University of Leuven (Belgium), the University of Rome (Italy), the National Institute of Child Health and Human Development (NICHD) (USA), and Gilead Sciences Inc.

A 2010 clinical trial found that tenofovir in vaginal gel form reduced the risk of HSV (herpes simplex virus) infections, as well as HIV infections in females. In this latest report, scientists say they can explain why.

Oral Tenofovir had been shown to undermine the reproduction of HIV. However, nobody knew it could block the genital herpes virus.

Leonid Margolis, Ph.D., NICHD, said:

"HIV infection is closely associated with herpes viral infection. When people with genital herpes are exposed to HIV, they are more likely to become infected than are people who do not carry the herpes virus. Human tissues convert tenofovir to a form that suppresses HIV. We found that this form of tenofovir also suppresses HSV. This discovery may help to identify drugs to treat the two viruses even more effectively."

Dr. Margolis explained that previously approved drugs which are found to have other therapeutic benefits, apart from those they were approved for, can save millions of dollars. A new compound has to undergo extensive testing for efficacy and safety before eventually coming onto the market several years and millions of dollars later. In the case of an already existing drug, most of the safety and other testing has already been done.

The scientist studied individual cells and groups of cells that had been infected with HSV. They found that tenofovir, in high concentrations blocked the virus' ability to reproduce.

Their study also showed that tenofovir does not damage cells, such as those that line the vagina. Vaginal cells are targeted by HIV and HSV.

Cellular enzymes convert tenofovir into another chemical form which suppresses both HIV and HSV. The new chemical form deactivates an enzyme that is crucial for the virus' reproduction.

They tested tenofovir in tissue samples, including tonsils and cervix. After 12 days they found that tenofovir-treated samples only had from 1% to 13% of viral levels compared to untreated samples. They also found that tenofovir blocked viral reproduction of both HIV and HSV simultaneously in infected tissue.

In laboratory experiments, they found that mice infected with the herpes virus had no herpes symptoms and lived longer when treated with tenofovir.

When tenofovir is taken orally, concentration levels in target cells are not high enough to affect HSV in any significant way, the authors explained.

Dr. Morgolis said:

"When using the gel, the amount of tenofovir on the affected tissues is about 100 times the amount in the body when taking tenofovir in pill form. That explains why its anti-herpes activity wasn't noticed before. Thus, under proper conditions, an anti-HIV drug becomes an anti-HSV drug."

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our sexual health / stds section for the latest news on this subject. "Topical Tenofovir, a Microbicide Effective against HIV, Inhibits Herpes Simplex Virus-2 Replication"
Graciela Andrei, Robert Snoeck, and Jan Balzarini (senior author), Joost van den Oord, Catholic University of Leuven; Emanuela Balestra, Carlo-Federico Perno (senior author), University of Rome; Tomas Cihlar, Gilead Sciences; and Andrea Lisco, Christophe Vanpouille, Andrea Introini, and Leonid Margolis (senior author) NICHD.
Cell Host & Microbe, Volume 10, Issue 4, 379-389, 20 October 2011 (10.1016/j.chom.2011.08.015) Please use one of the following formats to cite this article in your essay, paper or report:

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Christian Nordqvist. "Tenofovir Vaginal Gel Protects Against Herpes." Medical News Today. MediLexicon, Intl., 21 Oct. 2011. Web.
30 Oct. 2011. APA

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posted by Sammy on 25 Oct 2011 at 9:51 pm

Women with herpes are unlucky to have herpes because it brings much trouble to their life; they are lucky at the same time because the virus will make them have less chance to have breast cancer.

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