Tag Archives: rhesus macaque

From Macaques to Humans: UK regulator gives cautious thumbs up to advanced IVF techniques to prevent mitochondrial disease

Yesterday the UK’s Human Fertilisation and Embryology Authority (HFEA) advised the government that there is no evidence the two advanced forms of IVF developed to prevent mitochondrial diseases are unsafe, recommending that research using human embryos should continue, with close monitoring of the  health of children born through these two techniques, which are known as maternal spindle transfer and pronuclear transfer. At the same time the HFEA announced that a public consultation undertake last year had found broad support for the techniques.

The UK parliament will need to make the final decision on whether these techniques – somewhat misleadingly dubbed “three person embryos” - should be allowed, and it’s important to note that even if they give their approval the HFEA stressed in its assessment that further studies of human embryos in the lab will need to take place over the next 3 to 5 years before they can move into the clinic. These further studies will help to minimize any risks associated with the procedures, though Professor Robin Lovell Badge, a member of the HFEA panel that undertook a thorough scientific review of the science underpinning the techniques, did stress in a statement to the BBC that the ultimate test of the techniques would only cone then they were tried in the clinic.

Safety is absolutely not a black and white issue. In reproductive medicine in particular it is not possible to be absolutely certain about the consequences of any new treatment until children are born.

“Someone at some point is going to have to take the brave decision to go ahead with it.”

This announcement demonstrates that 35 years after the birth of the first IVF baby, the UK still leads the way in pioneering reproductive medicine. The UK did not get here alone though, as scientists in other countries – particularly the USA – have played a vital role in the development of these techniques.

In particular just a few months ago we discussed how Professor Shoukhrat Mitalipov of the Oregon National Primate Research Center  had developed the technique of spindle–chromosomal complex transfer – a.k.a. maternal spindle transfer, and one of the two techniques that the HFEA assessed  – through studies of Rhesus macaque monkeys. These studies included one where the health of four monkeys created using these techniques was followed closely for three years, with no ill effects observed.

Mitochondrial Gene Therapy. Source Mitalipov Lab/OSHU

Mitochondrial Gene Therapy. Source Mitalipov Lab/OSHU

The development of offspring born through the technique of pronuclear transfer, which was originally developed through research in mice, has not yet been studied in primates. Professor Douglass Turnbull of Newcastle University , who has demonstrated the technique is viable in human embryos in vitro, has cited the Rhesus macaque studies undertaken by Professor Mitalipov as evidence for the safety of the approach.

It is good to see the positive but cautious approach being adopted by the HFEA  as these techniques developed through a synergy of in vivo research on mice and monkeys and in vitro research on human embryonic cells in vitro move closer to becoming a clinical reality for the many parents who are waiting for them.

Speaking of Research

Not Difficult To Grasp

Paralysis can have tremendous negative consequences for a person’s quality of life.  In the US alone, there are more than 200 thousand people living with chronic spinal cord injury, which is a cause of immense suffering to them and their families.  The disease generates economic burden for society as well.   Thus, there has been a lot of interest in using our knowledge of how movement is coded in the brain to allow patients to bypass nerve injuries and communicate directly with the environment.  Moreover, when asked about their priorities in terms of regaining motor function the vast majority of patients rank regaining arm and hand function as most important.

It is thus encouraging to read in Nature today an update on how these efforts by scientists have allowed a paralyzed patient to reach for a cup, bring it to her lips, and drink from it.

Critical milestones in the development of motor prosthesis for paralyzed patients

As explained in a nice News and Views piece by Andrew Jackson that accompanies the article, this type of work builds on decades of previous research on the neural mechanisms that control arm movements (here, here and here) (blue on the Fig above), on the development of chronic multi-electrode arrays (orange), their recording properties in animals, and on feasibility studies of neural interfaces in monkeys (here, here, here and here) (green), which opened the way to clinical studies in humans (here and here) (purple).

The value of animal research should not be difficult to grasp. The knowledge that allows us to “read out” the planned movements of the patient from different brain regions in order to guide the movement of the robot is critical in the design of the system.  And it is an indisputable fact that such knowledge has been (and continues to be) obtained by experiments in awake, behaving monkeys.

And for those that doubt the true motivation of scientists for doing their work, it is worth noting what Dr. Leigh Hochberg (one of the leading authors of the study) had to say about their results – “The smile on her face … was just a wonderful thing to see.”   Do you want to see her smile too?  Watch this:

Of course the BrainGate system used by Dr. Hochberg and Dr. John Donoghue - director of the Institute for Brain Science at Brown University - is not the only brain-machine interface system under development to restore function in paralysis. In 2008 we wrote about a similar brain implant developed by Dr. Andy Schwartz at the University of Pittsburgh which enabled monkeys to manipulate robotic hands with unprecedented dexterity. Last year we wrote about how Dr. Schwartz’s team had used a different technology known as electrocorticography to enable a paralysed man to manipulate a robotic arm, while Dr. Chet Moritz and colleagues at Wachington National Primate Research Centre, have coupled readings from individual nerve cells to a technology called functional electrical stimulation to restore control to temporarily paralysed muscles in monkeys, an approach that may eventually supersede the use of robotic arms in some patients. It will be fascinating to watch this technology progress into more widespread clinical use over the next decade, and thrilling to think that, impressive as it appears today, we have barely begun to tap the potential of brain-machine interface technology to change lives.

OHSU Rhesus macaque embryo research to improve Preimplantation Genetic Diagnosis

Preimplantation Genetic Diagnosis is used by parents to screen embryos produced through in-vitro fertilization (IVF) in order to ensure that the baby will be free of specific genetic diseases.  New research from Oregon Health and Science University on the inheritance of the mitochondrial genome indicates that screening for genetic mutations that are located in the genome of the mitochondria – which is outside the nucleus of the cell where the much larger chromosomal genome id found, and is inherited only from the mother – can be made more accurate by carrying out the screening procedure slightly later than is now the practice.

Dr. Shoukhrat Mitalipov, who led this research project, explains what the project involved and its implications

A press release from OHSU highlights the importance of the Rhesus macaque to this discovery about the inheritance of mitochondial genomes:

“This latest breakthrough, which was conducted in rhesus macaque monkeys because of their similarity to humans, demonstrates the specific stage of early embryonic development when genetic mutations are passed from mother to fetus. This stage, referred to by scientists as “the bottleneck,” occurs when an early embryo called blastocyst, transitions into a fetus.

To conduct the research, Mitalipov and colleagues needed to design a way to mark and track specific mitochondrial genes as they transitioned from egg, through fertilization, to embryo and then to fetus. This was accomplished by combining two separate mitochondrial genomes into one egg cell. More specifically, one-half of an egg cell from a species of Indian-continent rhesus macaque monkey was merged with one-half of an egg cell from a Chinese-continent monkey. Because these animal species have distinct mitochondrial gene sequences (like breeding two distinct species of dogs), their genetics could be tracked closely.

The microscopic manipulation of splitting and uniting two halved egg cells takes specialized skills and expertise, which the Mitalipov lab has developed over a period of several years.

By studying the development of these joined and then fertilized eggs, scientists were surprised to see that eggs transitioned from containing a 50/50 split of genetics to a fetus that contained a nearly 100 percent either Indian or Chinese-based genome.

 We discovered that during early development, each individual cell in the eight-cell embryo would contain varying percentages of the Indian and Chinese rhesus genes. Some would be a 50/50 split. But others would be 90/10 and so on,” explained Mitalipov. “When these percentages were combined as a whole embryo, the average genetic split between the two species was about equal as initially created. However, later during the transition from a blastocyst to fetus, the genetics would swing one way or another. The resulting offspring would have always a genome that is predominantly Chinese or Indian. Our study tells us precisely when this mitochondrial gene switch occurs and how this can lead to disease.”

This finding raises significant questions about validity of currently methods for genetic diagnosis in early embryos, when a woman is known to carry a mitochondrial gene mutation may pass a disease to her children.

The current pre-implantation genetic diagnosis method is to examine genetic disease risk is by taking one cell from an early eight-cell embryo, and then looking for mutations in that one particular cell. This is done to predict if the remaining embryo is mutation-free,” explained Mitalipov.

The problem with this approach is that you may choose a cell that may not have mutations. But that does not mean the remaining cells in an embryo are mutation-free. Our research suggests that such approach could be flawed because diagnosis takes place prior to the stage when an offspring’s mitochondrial genetics is truly established.”

With this new information and with additional data gathered through further research, Mitalipov and colleagues believe that new methods for genetic diagnosis for mitochondrial disease should be located. The research also demonstrates that the Mitalipov lab’s previously developed method for preventing the passing of mitochondrial mutations from mother to child is highly successful.”

It’s an important discovery, one with important implications for preimplantation genetic diagnosis, and we congratulate Dr. Mitalipov and his colleagues at OHSU on their success!

Lee, H., Ma, H., Juanes, R., Tachibana, M., Sparman, M., Woodward, J., Ramsey, C., Xu, J., Kang, E., Amato, P., Mair, G., Steinborn, R., & Mitalipov, S. (2012). Rapid Mitochondrial DNA Segregation in Primate Preimplantation Embryos Precedes Somatic and Germline Bottleneck Cell Reports DOI: 10.1016/j.celrep.2012.03.011

Professor Doudet vindicated as investigation rejects animal rights allegations.

Two weeks ago we discussed the targeting by Canadian animal rights group Stop UBC Animal Research (STOP) of University of British Columbia scientist Professor Doris Doudet. STOP alleged that Prof. Doudet had performed experiments on monkeys without the approval of the UBC Animal Care Committee, and then lied in a scientific paper to cover her tracks, though as we reported at the time their allegations of professional misconduct against her were based on a deliberate misrepresentation of the facts. We are now happy – though in the circumstances not very surprised – to learn that an independent investigation of Prof. Doudet’s work has dismissed the allegations made against her.

According to today’s report in the Vancouver Sun, the Canadian Council on Animal Care (CCAC) carried out a detailed review of the research undertaken by Prof. Doudet’s team, and found:

no evidence to support allegations of animal cruelty against a University of British Columbia research team related to the deaths of four macaque monkeys.”

An earlier report on CTV news adds that the CCAC investigation:

found no evidence to support allegations that UBC was subjecting monkeys to cruel research experiments that were not overseen by the UBC Animal Care Committee.”

The letter from the CCAC to STOP detailing the conclusions of their investigation can be read here.

We asked Prof Doudet her views about this week’s developments, welcoming the news she said:

It is distressing to be wrongly accused, but the truth prevailed and we are all grateful for it.  MPTP always had unexpected effects, not only in monkeys but in the humans who unknowingly injected themselves with it: Out of the more than 100 people who were exposed to the drug in the early 80s, only a handful developed severe parkinsonism and there is no way to predict who will have such a severe negative response. But the MPTP primate model and the knowledge gained from it have played an important part in the basic understanding of physiological mechanisms involved in the disease, and this has been key to the development of many therapies for Parkinson’s disease, including DBS and the current testing of many gene therapies.”

We too welcome this news, though we wonder whether a formal investigation was really required to confirm what had been patently obvious right from the start.

Speaking of Research

Merry Christmas for Patients with Hemophilia B

That was the headline of an editorial in the New England Journal of Medicine (NEJM) which discussed the very promising results of a small clinical trial of gene therapy to treat hemophilia B – also known as Christmas Disease*. Patients with haemophilia B suffer bleeding in the joints and muscles due to deficiency in a coagulation factor IX, which blocks the coagulation cascade that normally leads to blood clots forming and prevents bleeding. Hemophilia B can be successfully managed by intravenous infusion of factor IX several times a week, but this therapy is very expensive – it has to be isolated from donated human blood plasma – and causes allergic reactions at the injection site in some patients.

Studies in mice were key to developing gene therapy for hemophilia B

Clearly a more permanent solution to factor IX deficiency is highly desirable, and to develop one scientists at University College London and the St Jude Children’s Research Hospital in Memphis turned to a technology that we have discussed on several occasions on this blog in recent years – gene therapy. The results of their clinical trial, published in NEJM, were impressive, all the patients were able to stop regular factor IX injections to maintain adequate factor IX levels, or to greatly reduce the frequency of injections.

As the NEJM editorial points out, this therapy has the potential to not only improve the lives of people with hemophilia B, but also to save millions of dollars over their lifetime.

In an excellent post discussing the clinical trial science blogger ERV notes that:

This treatment is not perfect yet– but its a huge step in a right direction, and only possible because of viruses.”

A very good point, in medicine we usually think of viruses as the enemy, but when it comes to gene therapy they are an ally.

But they are not always the easiest of allies to campaign alongside, and that is where another scientific technique without which this advance would not have been possible comes in – animal research!

A key choice when developing any virus-based gene therapy is the vector used to deliver the replacement gene to the cells of the body.  The vector must deliver enough copies of the gene to the target tissue to be effective, enable the gene to express in sufficient quantity to ameliorate the condition, and do so safely. Adenoviruses are often chosen for this task, with the serotype AAV 2 being the most widely studied in animals and humans. But there is a serious problem with AAV2, roughly half the population have been exposed to AAV2 naturally, and mount an immune response that clears the vector from the bloodstream before it can deliver its gene cargo to the target tissue.

The researchers addressed this problem by turning to another adenovirus serotype AAV8, which was isolated from rhesus monkeys a decade ago.  They chose AAV8 for three reasons, firstly earlier studies in mice showed that AAV8 injected into a peripheral vein delivered genes to the liver – the natural site of factor IX production – much more efficiently than AAV2, secondly the mouse studies also showed that AAV8 uncoats and delivers its  gene payload to cells more swiftly that AAV2, helping to ensure that the gene is delivered before the body can mount an immune response, and thirdly prior immunity is far less common in the human population than immunity to AAV8.

The AAV8 vector wasn’t perfect though, it would still require a large number of virus particles to be injected – potentially enough to trigger liver damage or stimulate a larger and more rapid immune response – so they designed a modified AAV8 vector known as a self-complementary (SC) vector that delivers the gene to liver cells even more efficiently.  Injection of mice with an SC vector containing the factor IX gene was found to lead to a 20-fold increase in liver of factor IX expression compared to the same amount of standard AAV8 vector, with no increase in toxicity. Since the ability of vectors developed from different adenovirus serotypes to target gene expression to particular tissues can vary between mice and primates, they then evaluated this vector in rhesus monkeys, finding that the SC vector could drive safely therapeutic levels of factor IX production in the monkey liver, and that prior immunity to one adenovirus serotype did not diminish the efficiency of factor IX production by a vector based on another serotype.

These studies paved the way for the clinical trial that caused so much excitement in the scientific and popular press earlier this month. Hopefully further development and larger clinical trials in people with hemophilia B will confirm the potential of this exciting new therapy, a therapy that was developed thanks to viruses and to animal research!

* after a patient named Stephen Christmas from whom factor IX was first isolated.

Paul Browne

Mice and macaques pave the way for effective HIV vaccines

There is encouraging news this week on the prospects for an effective vaccine against HIV. A  research team led by Professor Mariano Esteban at the Spanish Superior Scientific Research Council (CSIC) have announced that the vaccine MVA-B elicited a persistent immune response against HIV in  85% of volunteers in a phase 1 clinical trial. MVA-B is a therapeutic vaccine, it is not intended to block infection but rather to keep HIV levels in the body at levels well below those at which the virus can cause illness.

As a CSIC press release published online on EureakAlert! notes the MVA-B vaccine, created by inserting four HIV genes from the B subtype of HIV – the subtype accounting for most HIV infections in Europe and North America – into a vector derived from the Modified Ankara Vaccinia virus (a smallpox vaccine and shown to be safe in both animal studies and extensive human use), notes that:

In 2008, MVA-B already showed very high efficiency in mice as well as macaque monkeys against Simian’s immunodeficiency virus (SIV). Due to it’s high immunological response in humans, Phase I clinic trials will be conducted with HIV infected volunteers, to test its efficiency as a therapeutic vaccine.”

This is indeed true, a 2007 study in mice revealed that the MVA-B vaccine induced a strong immune response , while a paper published in 2008 by the same group demonstrated that a very similar MVA vaccine was able to induce a robust response involving both the HIV-1-specific CD4+ helper T-cells  and CD8+ cytotoxic T cells in Rhesus macaques, and was able to control virus levels in macaques infected with the SHIV 89.6P hybrid virus whereas in unvaccinated monkeys the levels of virus rose and most developed an AIDS-like illness.

There is a question over whether the immune response generated by the MVA-B vaccine will be able to restrict HIV in humans, after all the MRK-Ad5 vaccine which failed to restrict the HIV virus in human trials and the pathogenic SIV MAC239 – considered a better model for HIV infection than SHIV 89.6p – in macaque monkeys had successfully controlled SHIV 89.6P in earlier studies.

Some reassurance on this issue comes from a study at Oregon Health and Science University (OHSU) that was announced earlier this year, where a group led by Dr. Louis Picker used a different vaccine vector – one based on Cytomegalovirus – to elicit a very similar broad immune response , with strong memory T-cell involvement, to that induced by MVA-B, and found that it induced long-term control the highly pathogenic SIV MAC239 strain. This was the highest degree of control demonstrated to date against this SIV strain, and indeed the cytomegalovirus vaccine is one of the first to demonstrate any ability to control SIV MAC239 levels.

Professor Esteban and his colleagues are certainly not resting on their laurels either, further clinical trials of the MVA-B vaccine are planned, to determine whether it can protect against HIV.  In the meantime they are also seeking to improve on this vaccine.  Earlier this year they published a paper in the open-access journal PloS One where they deleted a gene in the MVA vector to yield a new MVA-B  vaccine that showed in mice a substantial increase in the magnitude and breath of the immune response compared with their original MVA-B vaccine, and an even better  memory T-cell response. They now plan to evaluate this improved vaccine in a non-human primate model of HIV infection, and it will be interesting to see if they choose to use a more stringent model of infection such as SIV MAC239 rather than SHIV-89.6P.

Despite the setbacks and disappointments over the past two decades, it is clear from the work being done at the CSIC and OHSU that real progress is being made towards the development of both prophylactic and therapeutic  vaccines against HIV, and it is just as clear that animal research continues to play a vital role in that progress.

Paul Browne

Albert Sabin and the monkeys who gave summer back to the children.

Albert Sabin has been called “the doctor who gave summer back to the children.”*

Because of his decades of research to develop the oral polio vaccine, children today know nothing of the fear that polio brought to the United States every summer well into the 20th century.  Swimming pools and movie theaters were closed and children were kept inside their homes by frightened parents.  Worldwide, the disease killed millions of people and left legions of others permanently disabled.

Albert Sabin administering the vaccine that saved millions from polio.

We’ve just celebrated the 50th anniversary of the introduction of Dr. Sabin’s vaccine. Estimates suggest that in just its first two years of worldwide use, the vaccine prevented nearly 500,000 deaths and five million cases of polio.  Today, the world is on the brink of realizing Dr. Sabin’s lifetime dream: the eradication of polio from the planet.

The development of the oral polio vaccine required years of extensive research with rabbits, monkeys and rodents.

Animal rights activists long ago seized on a single phrase by Dr. Albert Sabin, and have been using it ever since to try to support their outrageous claim that the developer of the oral polio vaccine(OPV) opposed the use of animals in research.

That phrase, “The work on prevention (of polio) was long delayed by an erroneous conception of the nature of the human disease based on misleading experimental models of disease in monkeys” spoken by Dr. Sabin during a congressional hearing in 1984, has been used in animal rights publications and comments for over two decades.

Dr. Sabin, a member of the Board of Directors of the pro-research Americans for Medical Progress until his death in 1993, spent years working to correct the record.  Here is a letter he wrote to the editor of the Winston Salem Journal, published in 1992.

Winston-Salem Journal

March 20, 1992

The Correct Conclusion

In a recent letter to the Journal (“Misrepresenting Research,” Feb. 20), Dr. Stephen R. Kaufman, the chairman of the Medical Research Modernization Committee, correctly quoted my 1984 testimony before Congress but he drew wrong conclusions from it.  Dr. Kaufman was also wrong when the said “the polio vaccine was based on a tissue culture preparation … not animal experimentation.”

On the contrary, my own experience of more than 60 years in biomedical research amply demonstrated that without the use of animals and of human beings, it would have been impossible to acquire the important knowledge needed to prevent much suffering and premature death not only among humans but also among animals.

In my 1956 paper in the Journal of the American Medical Association (Vol. 162, p. 1589), I stated that during the preceding four years “approximately 9,000 monkeys, 150 chimpanzees and 133 human volunteers were used thus far in studies of various characteristics of different poliovirus strains.”  These studies were necessary to solve many problems before an oral polio-virus vaccine could become a reality.

Albert B. Sabin, M.D.

Washington”

It is true that in the early years of polio research some lines of inquiry eventually proved unsuccessful. An overreliance on a strain of the virus known as the MV strain that had become adapted to survive only in nervous tissue, and the fact that the Rhesus macaque, while a good model for many aspects of polio, cannot be infected through ingestion via the mouth, led to the incorrect assumption that polio could only infect nerve cells (despite evidence to the contrary from both clinical studies and laboratory studies with other polio strains and monkey species).   These mistakes were unfortunate, though understandable given the fact that virology as a science was in its infancy.

However, these failed attempts do not cancel out the fact that animal research, and research using monkeys in particular, was absolutely crucial to the development of vaccines for polio.  Without it the polio vaccine would certainly not have been developed by the end of the 1950’s, and we might even still be waiting for it.

These vital contributions made by animal research to the development of polio vaccines were not limited to the work of Albert Sabin, and include:

  • The discovery by Karl Landsteiner and Erwin Popper in 1908 that polio was caused by a virus, a discovery made by inoculating macaque monkeys with an extract of nervous tissue from polio victims that was shown to be free of other infectious agents.
  • The subsequent discovery by Simon Flexner  that blood serum from infected macaque monkeys could protect against polio infection.
  • The discovery by Carl Kling and colleagues in 1911, following an earlier discovery that polio virus could be isolated from the lymph nodes of the small intestine of monkeys, that polio virus was present in the throat and intestinal tissues of people who dies from polio. Soon afterwards they isolated virus from the intestines of patients suffering from acute polio, and importantly from family members who did not display the symptoms of polio, establishing that healthy carriers played an important role in spreading the disease. In these studies the presence of polio was demonstrated by injecting filtered fluid from the patients into monkeys, the only method then available to confirm the presence of polio (Introduction to Epidemiology, fifth edition, by Ray M, Merill, Jones and Bartlett Learning).
  • The discovery in the early 1930’s by the Australian scientists Macfarlane Burnet and Jean Macnamara that antibodies against one strain of polio did not always protect macaque monkeys against infection with another strain.
  • The discovery by John Enders, Thomas Weller and Frederick Robbins that the polio virus could be grown in a number of tissue types, not just nerve tissue as previously assumed, a discovery that required the use of mice and monkeys to prove that the cultured virus was indeed polio and still capable of causing paralysis.
  • The determination in 1949 by David Bodian and colleagues at Johns Hopkins University that there were three major families of polio virus, referred to as types 1, 2, and 3, and that a separate vaccine would be necessary for each to give broad protection against polio.
  • The discovery by David Bodian and colleagues in the late 1940’s and early 1950’s that the polio virus entered the body through the mouth, and then needed to pass into the blood stream before it could infect nervous tissue, and that if you could block the infection in the blood you could prevent the virus from entering nerve tissue and causing paralysis. The work of Enders and Bodian paved the way for the development of vaccines by Salk and Sabin.
  • The evaluation by Jonas Salk and his colleagues at the University of Pittsburgh  of vaccine candidates produced by inactivating the virus with formalin under a range of conditions, until a vaccine was identified that was effective and safe enough for human trials.
  • The evaluation by Albert Sabin of hundreds of polio virus strains in hundreds of monkeys and scores of chimps before identifying attenuated strains that were capable of efficiently entering the body through the digestive system and provoking an adequate immune response to protect against the different pathogenic strains of polio while not causing the disease themselves.

It is hardly surprising that those close to Albert Sabin are disgusted with the way in which his views are misrepresented by animal rights activists. Writing for the Wall Street Journal two years after his death Albert Sabin’s widow, Heloisa Sabin, discussed the value of animals to his research.

ANIMAL RESEARCH SAVES HUMAN LIVES

The Wall Street Journal, October 18, 1995

by Heloisa Sabin

Mrs. Sabin is honorary director of Americans for Medical Progress.

That scene in “Forrest Gump,” in which young Forrest runs from his schoolmate tormentors so fast that his leg braces fly apart and his strong legs carry him to safety may be the only image of the polio epidemic of the 1950s etched in the minds of those too young to remember the actual devastation the disease caused. Hollywood created a scene of triumph far removed from the reality of the disease.

Some who have benefited directly from polio research, including the work of my late husband, Albert Sabin, think winning the real war against polio was just as simple. They have embraced a movement that denounces the very process that enables them to look forward to continued good health and promising futures. This “animal rights” ideology — espoused by groups such as People for the Ethical Treatment of Animals, the Humane Society of the U.S. and the Fund for Animals — rejects the use of laboratory animals in medical research and denies the role such research played in the victory over polio.

The leaders of this movement seem to have forgotten that year after year in the early ’50s, the very words “infantile paralysis” and “poliomyelitis” struck great fear among young parents that the disease would snatch their children as they slept. Each summer public beaches, playgrounds and movie theaters were places to be avoided. Polio epidemics condemned millions of children and young adults to lives in which debilitated lungs could no longer breathe on their own and young limbs were left forever wilted and frail. The disease drafted tiny armies of children on crutches and in wheelchairs who were unable to walk, run or jump. In the U.S., polio struck down nearly 58,000 children in 1952 alone.

Unlike the braces on Forrest Gump’s legs, real ones would be replaced only as the children’s misshapened legs grew. Other children and young adults were entombed in iron lungs. The only view of the world these patients had was through mirrors over their heads. These, however, are no longer part of our collective cultural memory.

Albert was on the front line of polio research. In 1961, thirty years after he began studying polio, his oral vaccine was introduced in the U.S. and distributed widely. In the nearly 40 years since, polio has been eradicated in the Western hemisphere, the World Health Organization reports, adding that with a full-scale effort, polio could be eliminated from the rest of the world by the year 2000.

Without animal research, polio would still be claiming thousands of lives each year. “There could have been no oral polio vaccine without the use of innumerable animals, a very large number of animals,” Albert told a reporter shortly before his death in 1993. Animals are still needed to test every new batch of vaccine that is produced for today’s children.

Animal activists claim that vaccines really didn’t end the epidemics — that, with improvements in social hygiene, polio was dying out anyway, before the vaccines were developed. This is untrue. In fact, advanced sanitation was responsible in part for the dramatic rise in the number of paralytic polio cases in the ’50s. Improvements in sanitation practices reduced the rate of infection, so that the average age of those infected by the polio virus went up. Older children and young adults were more likely than infants to develop paralysis from their exposure to the polio virus.

Every child who has tasted the sweet sugar cube or received the drops containing the Sabin Vaccine over the past four decades knows polio only as a word, or an obscure reference in a popular film. Thank heavens it’s not part of their reality.

These polio-free generations have grown up to be doctors, teachers, business leaders, government officials, and parents. They have their own concerns and struggles. Cancer, heart disease, strokes and AIDS are far more lethal realities to them now than polio. Yet, those who support an “animal rights” agenda that would cripple research and halt medical science in its tracks are slamming the door on the possibilities of new treatments and cures.

My husband was a kind man, but he was impatient with those who refused to acknowledge reality or to seek reasoned answers to the questions of life.

The pioneers of polio research included not only the scientists but also the laboratory animals that played a critical role in bringing about the end of polio and a host of other diseases for which we now have vaccines and cures. Animals will continue to be as vital as the scientists who study them in the battle to eliminate pain, suffering and disease from our lives.

That is the reality of medical progress.”

 

Animal rights activists are free to express their opposition to the use of animals in research, but they cannot do so by blatantly robbing society of scientific achievements.  This one fact is clear — if our critics had their way, today millions of children would be dead or disabled from polio and other infectious diseases.

* Of course Jonas Salk is equally, if not more, deserving of this accolade.