Dr. Koprowski was the first to show it was possible to vaccinate against polio.
Associated Press /file 1961
Dr. Koprowski was the first to show it was possible to vaccinate against polio.
PHILADELPHIA — Dr. Hilary Koprowski, a pioneering virologist who developed the first oral vaccination for polio, has died. He was 96.
Although not as well known as fellow researchers Jonas Salk and Albert Sabin, Dr. Koprowski in 1950 became the first to show it was possible to vaccinate against polio, the crippling and sometimes fatal disease that is now all but eradicated.
Dr. Koprowski’s son, Christopher, said Saturday that his father liked the scientific recognition his work received without the celebrity of Salk and Sabin.
‘‘He enjoyed not having his scientific work disrupted,’’ said Christopher Koprowski, chief of radiation oncology at Christiana Care Health System in Wilmington, Del. ‘‘Not that he was a modest individual, mind you.’’
Christopher Koprowski said his father had been sick for several months before dying Thursday in the Wynnewood home where he had lived since 1957.
Hilary Koprowski self-administered the live-virus oral vaccine he developed before the 1950 clinical trial — about two years before Salk’s injectable version using a dead form of the virus began testing with the backing of the National Foundation for Infantile Paralysis, now the March of Dimes.
Sabin, who Dr. Koprowski’s son said sometimes collaborated with his father, was the first to get the more effective oral version, which didn’t require boosters, licensed for use in the United States.
Dr. Koprowski went on to be the director of the Wistar Institute in Philadelphia from 1957 to 1991. Under his leadership, the independent research institution developed a rubella vaccine that helped eradicate the disease in much of the world, Wistar officials said. It was during that time the institute also developed a more effective rabies vaccine.
Born in Poland, Dr. Koprowski was also a talented musician. After immigrating to Rio de Janeiro, he made money teaching piano before finding work at a lab there and eventually moving to the United States, his son said.
‘‘He was a great dad. He was colorful, charismatic,’’ Christopher Koprowski said. ‘‘He’s still the most brilliant person I’ve ever met.’’



Christopher D. Koprowski, M.D.

Chair, Department of Radiation Oncology

Christopher D. Koprowski, M.D.
Dr. Koprowski graduated from Princeton University and earned a medical degree with honors from Temple University School of Medicine, Philadelphia, PA in 1977. He completed his internship in internal medicine at the University of Chicago Hospitals and completed a neurology residency at the Hospital of the University of Pennsylvania, where he served as chief resident from 1980 to 1981. Subsequently, Dr. Koprowski performed health services research as a Robert Wood Johnson Foundation Clinical Scholar at the Wharton School of the University of Pennsylvania from which he has earned an MBA degree.
Following two years in the practice of neurology, he trained in radiation oncology at Hahnemann University, where he was chief resident in 1989 and was awarded an American Cancer Society Clinical Fellowship.
After completing training, Dr. Koprowski was an attending radiation oncologist at the Cooper Health System and a Clinical Associate Professor at the Robert Wood Johnson Medical School. From 1998 to 2001, he served as acting chief of the Department of Radiation Oncology for the Cooper Health System and at the Robert Wood Johnson Medical School, Camden, NJ. In 2001, he was one of six radiation oncologists selected as a New Jersey "Top Doctor" in New Jersey Magazine, and in 2002, he was selected by the "Guide to Top Doctors" as one of the most highly recommended specialists in the Delaware Valley.
Dr. Koprowski is a member of the American College of Radiology and the American Society of Therapeutic Radiology and Oncology. Research interests and publications have included hypoxic and porphyrin cell sensitizers, treatment of metastatic disease, brain tumors and prostate cancer. Dr. Koprowski has been a Principal Investigator for the RTOG (Radiation Therapy Oncology Group). Current interests include treatment of breast and lung cancer, as well as, image guided radiation therapy.
Specialties:
  • Radiation Oncology
  • Neurology
Practice: Radiation Oncologists, P.A.
Contact: HFG Cancer Ctr.,Radiation Oncology
4701 Ogletown-Stanton Rd.,S-1110
Newark, DE 19713
302-623-4800
Education:
  • Temple University School of Medicine
Residency:
  • Hospital of University of Pennsylvania
  • Medical College of Pennsylvania- Hahnemann Univers
Fellowship:
  • Hospital of University of Pennsylvan

Display Settings:

Send to:

PLoS One. 2012;7(8):e41756. doi: 10.1371/journal.pone.0041756. Epub 2012 Aug 8.

Proof-of-concept, randomized, controlled clinical trial of Bacillus-Calmette-Guerin for treatment of long-term type 1 diabetes.

Faustman DL, Wang L, Okubo Y, Burger D, Ban L, Man G, Zheng H, Schoenfeld D, Pompei R, Avruch J, Nathan DM.

Source

The Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. faustman@helix.mgh.harvard.edu

Abstract

BACKGROUND:

No targeted immunotherapies reverse type 1 diabetes in humans. However, in a rodent model of type 1 diabetes, Bacillus Calmette-Guerin (BCG) reverses disease by restoring insulin secretion. Specifically, it stimulates innate immunity by inducing the host to produce tumor necrosis factor (TNF), which, in turn, kills disease-causing autoimmune cells and restores pancreatic beta-cell function through regeneration.

METHODOLOGY/PRINCIPAL FINDINGS:

Translating these findings to humans, we administered BCG, a generic vaccine, in a proof-of-principle, double-blind, placebo-controlled trial of adults with long-term type 1 diabetes (mean: 15.3 years) at one clinical center in North America. Six subjects were randomly assigned to BCG or placebo and compared to self, healthy paired controls (n = 6) or reference subjects with (n = 57) or without (n = 16) type 1 diabetes, depending upon the outcome measure. We monitored weekly blood samples for 20 weeks for insulin-autoreactive T cells, regulatory T cells (Tregs), glutamic acid decarboxylase (GAD) and other autoantibodies, and C-peptide, a marker of insulin secretion. BCG-treated patients and one placebo-treated patient who, after enrollment, unexpectedly developed acute Epstein-Barr virus infection, a known TNF inducer, exclusively showed increases in dead insulin-autoreactive T cells and induction of Tregs. C-peptide levels (pmol/L) significantly rose transiently in two BCG-treated subjects (means: 3.49 pmol/L [95% CI 2.95-3.8], 2.57 [95% CI 1.65-3.49]) and the EBV-infected subject (3.16 [95% CI 2.54-3.69]) vs.1.65 [95% CI 1.55-3.2] in reference diabetic subjects. BCG-treated subjects each had more than 50% of their C-peptide values above the 95(th) percentile of the reference subjects. The EBV-infected subject had 18% of C-peptide values above this level.

CONCLUSIONS/SIGNIFICANCE:

We conclude that BCG treatment or EBV infection transiently modified the autoimmunity that underlies type 1 diabetes by stimulating the host innate immune response. This suggests that BCG or other stimulators of host innate immunity may have value in the treatment of long-term diabetes.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT00607230.

Comment in

PMID:
22905105
[PubMed - indexed for MEDLINE]

PMCID:
PMC3414482

Free PMC Article