Rockefeller University

Rockefeller University is an American private graduate university in New York City. It focuses primarily on the biological and medical sciences and provides doctoral and postdoctoral education. Rockefeller is the oldest biomedical research institute in the United States of America, and has dominated its medical life since 1901.¹⁾

The university's first director of laboratories Simon Flexner was the brother of Abraham Flexner, the author of the Flexner Report to Congress. The report was the decisive part of the Rockefeller family's offensive to take over the American medical system.

The Rockefeller University was founded in June 1901 as The Rockefeller Institute for Medical Research by John D. Rockefeller, who had founded the University of Chicago in 1889, upon advice by his advisor Frederick T. Gates and action taken in March 1901 by his son, John D. Rockefeller Jr.^{2) 3)}

Greatly elevating the prestige of American science and medicine, it was America's first biomedical institute, like France's Pasteur Institute and Germany's Robert Koch Institute. The Rockefeller Foundation, a philanthropic organization founded in 1913, is a separate entity, but has close connections mediated by prominent figures holding dual positions.⁴⁾

The first director of laboratories was Simon Flexner, who supervised the development of research capacity at the Institute, and whose staff made major discoveries in basic research and medicine. While a student at Johns Hopkins University, Flexner had studied under the Institute's first scientific director, William H. Welch, first dean of Hopkins' medical school and known as “the dean of American medicine.” Flexner retired in 1935 and was succeeded by Herbert Gasser.⁵⁾ He was succeeded in 1953 by Detlev Bronk, who broadened The Rockefeller Institute into a university that began awarding the PhD degree in 1954. In 1965, The Rockefeller Institute's name was changed to The Rockefeller University.

It was the site of the 2009 Good Club meeting, a secret get-together of some of the world's most powerful billionaires including Bill Gates, Oprah Winfrey, George Soros, Warren Buffett, and Ted Turner, discussing the problem of how to solve overpopulation.⁶⁾

For its first six decades, the Institute focused on research to develop basic science, applied research as biomedical engineering, and clinical science. The Rockefeller Hospital's first director Rufus Cole retired in 1937 and was succeeded by Thomas Milton Rivers.⁷⁾ As director of The Rockefeller Institute's virology laboratory, he established virology as an independent field apart from bacteriology.

While working at the Rockefeller Institute for Medical Research, French surgeon and biologist Alexis Carrel suggested the use of gas to euthanize lawbreakers, and in a later edition endorsed the German “suppression” of “the defective.”⁸⁾

The school has received 25 grants from the Bill & Melinda Gates Foundation from 2006-2021.⁹⁾ Funded activities include research into tuberculosis, monoclonal antibodies, diagnostic testing and “novel” vaccines for HIV, ZMapp manufacturing for Ebola prevention, vaccine adjuvants, the microbiome, mother-child transfer of IgG antibodies, gene editing, artificial olfactory receptors, COVID-19 testing assays, evaluating cellular and molecular events post-mRNA vaccine, and monoclonal antibodies against SARS-CoV-2.

David Rockefeller joined the board of trustees in 1940, was its chairman from 1950 to 1975, chaired the board's executive committee from 1975 to 1995, became honorary chairman and life trustee, and remained active until his death in 2017.¹⁰⁾

=== Charles M. Rice === When experiments keep failing, is there a time to call it quits? Meet the scientist who spent decades of his life chasing after hepatitis C before his efforts helped produce a cure. By Jessica Wapner - April 1, 2017

harlie rice first began work on the hepatitis C virus in 1989, when it seemed like a straightforward project. The hope was that a vaccine could be modeled after one that had successfully eradicated yellow fever from much of the world.

But the virus proved inscrutable. The vaccine never materialized, and it took decades of study before an effective treatment could be created—a combination of antiviral drugs that became available in 2013 and are credited with saving hundreds of thousands of lives.

For his pivotal role in the development of this therapy, Rice, Maurice R. and Corinne P. Greenberg Professor in Virology, was awarded the Lasker-DeBakey Clinical Medical Research Award last fall alongside two other scientists. We spoke with him about the highs and lows of his 30-year quest to cajole the virus into a form scientists could work with.

When you first began researching the hepatitis C virus, did you know what a vexing foe it would prove to be?

Yes and no. Certainly the mystery of identifying the virus in the first place hinted at the complicated future to come. For many years, we knew that there existed some entity in blood that was neither hepatitis A nor hepatitis B. But until that entity was found, we could only refer to it as non-A, non-B hepatitis. That cumbersome name really foreshadows how hard this virus would be to pin down.

Yet there were reasons to think we could readily stop the virus in those early years, too. When the hepatitis C virus (HCV) was finally identified, in 1989, scientists saw that it was a member of the same family as the virus that causes yellow fever. The yellow fever vaccine is one of the safest and most effective immunizations available, so it was easy to imagine that creating a vaccine for HCV would not be too arduous.

n fact, back in the late 1980s, when I was at the Washington University in St. Louis, my lab was working on a molecular clone of the strain of the yellow fever virus that was used in the vaccine, and my group, in concert with others, tried to use that clone to create an HCV vaccine. It seemed like a logical approach, considering the similarity between these two pathogens.

So what happened?

As it turned out, the features that distinguish HCV from yellow fever and other viruses also make it a challenging target for a vaccine. More than 20 years later, we are still waiting for an HCV vaccine.

When did you turn your attention to searching for a cure?

We realized that if we wanted any chance at finding a treatment for HCV, we needed to be able to study it outside of people—in cell cultures and animal models. But when we tried to coax the virus to replicate in cells in the lab or in animals, it mostly didn’t work. We used all the classic techniques, which used the genome of the virus to initiate replication, but failed.

Eventually we started to wonder: Were we actually working with the correct genome sequence for the virus? RNA viruses like HCV won’t replicate if a portion of the genetic sequence is missing. And indeed, when we reevaluated the sequence, it turned out we’d been missing a portion that was essential for replication. A Japanese group working on the same problem came to the same conclusion at around the same time.

Was that realization enough to clear the way toward finding a treatment?

No. The shifty nature of HCV proved to be another significant hurdle. The replication mechanism of the virus is prone to error. That tendency constantly gives rise to new versions of the virus, enabling it to avoid attacks by the immune system, which may not recognize a particular mutant as an invader. And creating a treatment that works on all versions of the virus was a daunting proposition. How do you know that the genetic target you home in on is exactly the same in all strains of the virus?

Does the diversity of the virus mean that people living with hepatitis C could be housing a virus whose genome differs from the one you were studying in the lab?

Yes, and that was yet another problem we needed to solve. To overcome this issue, we created our own version of the genome, in which each building block of the RNA genome was the one most commonly found in a person infected with the virus. This lab-created version of the virus proved capable of replicating in the liver, just like natural HCV.

This was a critical breakthrough. Using our “consensus” model virus, we were able to show that some viral proteins that people suspected would make good drug targets were indeed essential for HCV to replicate and spread. It was about this time that I moved to The Rockefeller University to establish the Center for the Study of Hepatitis C.¹¹⁾

Early in her career, Margaret Hamburg conducted neuroscience research at Rockefeller University.¹²⁾ In addition to becoming a member of the board of trustees for the university,¹³⁾ she would also go on to hold prominent positions with the National Institute of Allergy and Infectious Diseases under Dr. Anthony Fauci, the U.S. Food and Drug Administration, United States Department of Health and Human Services, Rockefeller Foundation, Harvard University, Coalition for Epidemic Preparedness Innovations, Gavi, the Vaccine Alliance, the Bill & Melinda Gates Foundation, Wellcome Trust, the University of Washington, Council on Foreign Relations, and the Nuclear Threat Initiative, among others.

In her various positions, Hamburg has participated in several pandemic war games including Operation Dark Winter, Clade X, and the 2021 Monkeypox Tabletop Exercise.