Board Certification and Academic Information
||Pathology - Professor
Internal Medicine - Adjunct Professor
Pediatrics - Professor
Pediatric Immunology and Rheumatology
||American Board of Pediatrics (Pediatrics)
Academic Office Locations
|Academic Office Phone Number
||Academic Office Address
||School of Medicine
30 N 1900 E
Salt Lake City, UT 84132
||School of Medicine
30 N 1900 E
Salt Lake City, UT 84132
Harry R. Hill, M.D. Professor of Pathology, Pediatrics and Internal Medicine, Head, Division of Clinical Pathology and
Clinical Immunology / Immunodeficiency
TRAINING INSTITUTION AND LOCATION DEGREE
Louisiana State University, Baton Rouge, LA pre-med 06/60-08/62
Baylor School of Medicine Houston, TX - M.D. Medicine 06/1966
Intern - Grady Memorial Hospital, Emory University, Atlanta Georgia, 7-1-66 - 6-30-67
Epidemic Intelligence Services, National Communicable Disease Center, Assigned to the Streptococcal Disease Laboratory, Fort Collins, Colorado 8-15--1966 to 7-30-69
University of Washington, Seattle, WA - Residency: Pediatrics / Fellowship: Immunology 07/69-06/71
University of Minnesota, Minneapolis, MN - Fellowship - Infectious Diseases/Host Resistance/Laboratory Medicine -- 07/71-07/73
University of Minnesota, Minneapolis, MN - Instructor - Infectious Diseases/ Clinical Lan\boratory Medicine - 7/1/1973 - 7-15-1974
Assistant Professor of Pediatrics and Pathology, University of Utah, Salt Lake City, Utah - 8-1-74
Associate Professor, Department of Pediarics, University of Utah, Salt Lake City, Utah, July 1976
Associate Professor, Department of Patholog with Tenurey,University of Utah, Salt Lake City, Utah,+-4July 1977
Professor of Pathology, Pediatrics, University of Utah 7-1-1981 to Present
Adjunct Professor of Medicine, University of Utah, Salt Lake City, Utah, July 1 , 1996 to Present
After serving in the Epidemic Intelligence Service of the National Communicable Disease Center for two years, where Dr. Hill investigated outbreaks of group A (NEJM 280:917-921, 1969) and group G streptococcal infections (Lancet i:371-374, 1969), Dr. Hill did a pediatric residency at the University of Washington where the second year was funded by an NIH grant to work in the laboratory of Dr. Ralph Wedgwood, a noted, early authority in primary immune deficiency disorders. It was there that he became interested in Job syndrome of Hyper IgE and recurrent infections, a classic primary immune deficiency disorder. He then went for a fellowship in infectious disease, host resistance, and laboratory medicine at the University of Minnesota where he worked with Dr. Paul Quie, who first described the bactericidal defect in chronic granulomatous disease and Dr. John Matsen, a Clinical Microbiologist. Dr. Hill continued his work on the inflammatory response in Job syndrome of hyper IgE (Lancet i:183-187, 1974; Lancet ii:617-619, 1974) and along with colleagues described the first familial cases of the syndrome (Annals Intern Med 82:766-771, 1975). He also studied the inflammatory response in normal individuals (J Clin Invest 53:966-1002, 1974) to contrast with those with primary immune deficiency disorders. After his fellowship, Dr. Hill accepted a position in the Department of Pediatrics and Pathology at the University of Utah where he realized that no one was seeing primary immune deficient patients in the adult or pediatric population. He, therefore, started a Clinical Immunology/Immunodeficiency Clinic ( and a Clinical Immunolgy Laboratory) that has continued for the past 38 years, and which draws patients from throughout Utah (approximately 3 million) and the surrounding states of Idaho, Wyoming, Montana, Western Colorado, and Nevada. The Clinical Immunlogy laboratory became a major laboratory in ARUP Laboratories, the esoteric reference laboratory owned by the Univesrity of Utah. While his primary research interests have been in host resistance of the neonate to bacterial infection (J Clin Invest 48:1379-1387, 1976; Lancet I:636-638, 1978, et al.), he became interested in the functional activity against bacteria of intravenous immunoglobulin (which of course, is the primary therapy of common variable immune deficiency; (Amer J Med 76:61-66, 1984) as well as the role of inflammatory mediators and cytokines in the host response to bacteria (J Exp Med 159:1618-1628, 1984; J Exp Med 173:767-770, 1991). Dr. Hill has continued to publish on patients with primary immunodeficiency disorders (Amer J Med 105:162-164, 1998; J Pediat 136:176-180, 2000; Pediat Inf Dis J 28:529-533, 2009; J Allergy Clin Immunol 122:181-187, 2008; J Clin Invest 94:616-622, 1994; Amer J Med Genet 95:17-20, 2000). Most recently, Dr. Hill, in association with two superb molecular biologists at the University of Utah, Dr. Carl Wittwer and Dr. Karl Voelkerding, has begun to explore molecular aspects of primary immune deficiency diseases. In a recent article, his laboratory with Dr. Kumanovics as the senior author (a fellow in clinical immunology at the time) has developed a rapid molecular assay for detecting mutations in the STAT3 gene associated with autosomal dominant Job syndrome of Hyper IgE and recurrent infections (J Molec Diagn 12:213-219, 2010). In addition, he, along with Dr. Carl Wittwer, have published on the rapid molecular diagnosis of the X-linked form of chronic granulomatous disease using high resolution melting scanning to identify affected exons followed by targeted sequencing (J Molec Diagn 12:368-376, 2010). Dr. Hill is continuing to investigate the molecular basis of the most common primary immune deficiency, CVID. It is estimated that there are at least 150 active patients who are being seen in our Clinical Immunology Immunodeficiency Clinic including several pedigrees with multiple members affected by the disorder. Dr. Hill, working with his former fellow, Dr. Attila Kumanovics, and Dr. Karl Voelkerding, as well as, Dr. Witter, plans to commit the final years of his research career to deciphering the molecular etiology of, and developing rapid molecular tests for CVID, as well as, other rare primary immune deficiencies seen in our clinic. He has been funded as a PI or Program Project Director for 32 years by the National Institutes of Health. He has also been the Executive Director of the ARUP Institute for Clinical and Experimental Pathology, the Reserach arm of ARUP laboratories which employs approximately 100 individuals and 50 medical directors from 1996 through 2013.
B. Positions and Honors:
1. Epidemic Intelligence Service Officer, National Communicable Disease Center;
Assigned to the Streptococcal Disease Section, Ft. Collins, Colorado 1967-69
2. Resident in Pediatrics and Fellow in Immunology (Ralph Wedgwood), Dept. of Peds., 1969-71
Univ. of Wash., Seattle, WA, Chief Resident, Harborview Medical Center Spring-71
3. Fellow in Infectious Dis, Dept of Pediatrics and Clinical Lab. Med. and Pathology,
2. Univ. of Minnesota (Lewis W. Wannamaker, Paul G. Quie, and John M. Matsen) 1971-74
4. Assistant Professor, Depts. of Peds. and Path., University of Utah School of Medicine 1974-76
5. Associate Professor, Depts. of Peds. and Path, University of Utah School of Medicine 1976-81
6. Professor of Pathology, Pediatrics and Internal Medicine, Univ. of Utah School of Medicine 1981-2010
7. Senior Vice President and Executive Director, ARUP Institute for Clinical and Experimental
Pathology (the research arm of ARUP Laboratories) 1996-2013.
7. Medical Director, Laboratory of Cellular and Innate Immunology, ARUP 1983-present
Member, Bacteriology-Mycology Study Section, Natl. Institute of Allergy and Infectious Diseases, 1978-82; Ross Award, Outstanding Investigator, Western Society for Pediatric Research, 1980; Investigator, Howard Hughes Medical Institute, 7/1/75-6/30/81; Diplomat American Board of Pediatrics (98 percentile); Honor Roll Texas State Board of Medical Examiners; Alpha Epsilon Delta, Phi Eta Sigma; President, Lancefield Society, 1987-88; President, Western Society for Pediatric Research, 1993-94; Cited in The Best Doctors in America. Naifeh, S. and Smith, G.W., Woodward White, Inc. 1993-2013;
Editorial Boards: Infect Immun., 1994-2002, J. Pediatr., 1988-95, Diag. Micro. Infect. Dis., 1982-1999, Amer. J. Clin. Path., 1984-90, Clin. and Diag. Lab. Immunol., 1994-2000; J. Ped. Infect. Dis., 1982-present (currently editor for the “Immunology for the Pediatrician” section of the Pediatric Infectious Disease Journal
C. Most Relevant Peer-reviewed Publications: (selected from over 252 peer-reviewed)
1. Hill, HR and Quie, PG: Raised serum-IgE levels and defective neutrophil chemotaxis in three children with eczema and recurrent bacterial infections. Lancet. I:183-187, 1974.
2. Hill, HR, Quie, PG, Pabst, HF, Ochs, HD, Clark, RA, Klebanoff, SJ, and Wedgwood, RJ: Defect in neutrophil granulocyte chemotaxis in Job's syndrome of recurrent "cold" staphylococcal abscesses. Lancet. ii:617-619, 1974.
3. Van Scoy, RE, Hill, HR, Ritts, RE, and Quie, P.G.: Familial neutrophil chemotaxis defect, recurrent bacterial infections, mucocutaneous candidiasis and hyperimmunoglobulinemia E. Ann Int Med. 82:766-771, 1975.
4. Bale, JF, Jr, Wilson, JF and Hill, HR: Fatal histiocytic lymphoma of the brain associated with hyperimmunoglobulinemia E and recurrent infections. Cancer. 39:2386-2390, 1977.
5. Santos, JI, Shigeoka, AO, Hill, HR: Protective efficacy of a modified immune serum globulin in experimental group B streptococcal infection. J Pediat. 99:873-879, 1981.
6. Hill, HR, Augustine, NH and Shigeoka, AO: Comparative opsonic activity of intravenous gammaglobulin preparations for common bacterial pathogens. Amer J Med. 76:61-66, 1984.
7. Hill, HR, Shigeoka, AO, Augustine, NH, Pritchard, D, Egan, ML, Lundblad, JL and Schwartz, RS: Fibronectin enhances the opsonic and protective activity of monoclonal and polyclonal antibody against group B streptococci. J Exp Med. 159:1618-1628, 1984.
8. Sacchi, F and Hill, HR: Defective membrane potential changes in neutrophils from human neonates. J Exp Med. 160:1247-1252, 1984.
9. Jeppson, JD, Jaffe, HW, Hill, HR Use of recombinant human interferon gamma to enhance neutrophil chemotactic responses in Job syndrome of hyperimmunoglobulin E and recurrent infections. J Pediat. 118:383-387, 1991.
10. Hill, HR, Augustine, NH, and Jaffe, HS: Human recombinant interferon gamma enhances neonatal PMN activation and movement and increases free intracellular calcium. J Exp Med. 173:767-770, 1991.
11. Hollenbaugh, D, Wu, L, Ochs, HD, Nonoyama, S, Grosmaire, LS, Ledbetter, JA, Noelle, RJ, Hill, HR, and Aruffo, A: The random inactivation of the X chromosome carrying the defective gene responsible for X-linked Hyper IgM syndrome in female carriers of HIGM1. J Clin Invest. 94:616-622, 1994.
12. Kumaki, S, Ochs, HD, Timour, M, Schooley, K, Ahdieh, M, Hill, HR, Sugamura, K, Anderson, D, Zhu, Q, Cosman, D, Giri, JG: Characterization of B cell lines established from two X-linked severe combined immunodeficiency patients: Interleukin 15 binds to the B cells but is not internalized efficiently. Blood. 86:1428-1436, 1995.
13. Nester, TA, Wagnon, AH, Reilly, WF, Spitzer, G, Kjeldsberg, CR, and Hill, HR: “Effects of allogeneic peripheral stem cell transplant on Job’s syndrome of Hyperimmunoglobulin E and recurrent infections.” Amer J Med. 105:162-164, 1998.
14. Borges, WG, Hensley, T, Carey, JC, Petrak, BA and Hill, HR: “The face of Job”. J Pediatr. 133:303-305, 1998.
15. Borges, WG, Augustine, NA, and Hill, HR: Defective IL-12/IFN¿ pathway in patients with the hyperimmunoglobulin E Syndrome. J Pediatr. 136:176-180, 2000.
16. Adderson, EE, Viskochil, DH, Carey, JC, Shigeoka, AO, Christenson, JC, Bohnsack, JF, Hill, HR: Growth failure, intracranial calcifications, acquired pancytopenia, and unusual humoral immunodeficiency: a genetic syndrome? Am J Med Genet. 95:17-20, 2000.
17. Martins, TB, Pasi, BM, Pickering, JW, Jaskowski, TD, Litwin, CM, and Hill, HR: Determination of cytokine responses using a multiplex fluorescent microsphere immunoassay. Amer J Clin Pathol. 118:346-353, 2002.
18. Renner, ED, Rylaarsdam, S, Anover-Sombke, S, Rack, AL, Reichenbach, J, Carey, JC, Zhu, Q, Jansson, AF, Barboza, J, Schimke, LF, Leppert, MF, Getz, MM, Seger, RA, Hill, HR, Belohradsky, BH, Torgerson, TR, Ochs, HD: Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced TH17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome. J. Allergy Clin Immunol. 122:181-187, 2008.
19. Bender, JM, Rand, TH, Ampofo, K, Pavia, AT, Schober, M, Tebo, A, Pasi, B, Augustine, NH, Pryor, RJ, Wittwer, CT, and Hill, HR: Family clusters of variant X-linked chronic granulomatous disease. Pediat Inf Dis 28:529-533, 2009.
20. Powers, AE, Bender, JM, Kumánovics, A, Ampofo, K, Augustine, N, Pavia, AT, Hill, HR: Coccidiodes immitis meningitis in a patient with hyperimmunoglobulin E syndrome due to a novel mutation in signal transducer and activator of transcription. Ped. Infect. Dis. J. 28:664-666, 2009.
21. Kumánovics, A, Wittwer, CT, Pryor, RJ, Augustine NH, Leppert, MF, Carey, JC, Ochs, HD, Wedgwood, RJ, Faville, Jr, RJ, Quie, PG, and Hill, HR: Rapid molecular analysis of the STAT3 gene in Job syndrome of Hyper IgE and recurrent infectious diseases. J. Molec. Diagn. 12:213-219, 2010.
22. Hill, H.R., Augustine, N.H., Pryor, R.J., Reed, G.H., Tebo, A.E., Bender, J.M., Pasi, B.M., Chinen, J.I., Hanson, C., and Wittwer, C.T.: Rapid molecular detection of the mutations in the CYBB gene associated with X-linked chronic granulomatous disease. J. Molec. Diagn. 12:368-376, 2010.
1. Hill, HR, Zimmerman, RA, Reid, GVK, Wilson, E and Kilton, RM: Food-borne epidemic of streptococcal pharyngitis at the United States Air Force Academy. New Engl. J. Med. 280:917-921, 1969.
2. Hill, HR, Caldwell, GG, Wilson, E, Hager, D and Zimmerman, RA: Epidemic of pharyngitis due to streptococci of Lancefield Group G. Lancet I:371-374, 1969.
3. Estensen, RP, Hill, HR, Quie, PG, Hogan, N and Goldberg, ND: Cyclic GMP and cell movement. Nature. 245:458-460, Sept. 1973.
4. Hill, HR, Gerrard, J, Hogan, NA and Quie, PG: Hyperactivity of neutrophil leukotactic responses during active bacterial infection. J Clin Invest. 53:996-1002, 1974.
5. Hemming, VG, Hall, RT, Rhodes, PG, Shigeoka, AO and Hill, HR: Assessment of group B streptococcal opsonins in human and rabbit serum by neutrophil chemiluminescence. J Clin Invest. 48:1379-1387, 1976.
6. Shigeoka, AO, Hall, RT and Hill, HR: Transfusion in group B streptococcal sepsis. Lancet. 1:636-638, 1978.
7. Veasy, LG, Wiedmeier, SE, Orsmond, GS, Ruttenberg, HD, Boucek, MM, Roth, SJ, Tait, VF, Thompson, JA, Daly, JA, Kaplan, EL and Hill, HR: Resurgence of acute rheumatic fever in the intermountain area of the United States. New Engl J Med. 316:421-427, 1987 (lead article).
8. Hill, HR, Bohnsack, JF, Morris, EZ, Augustine, NH, Parker, CJ, Cleary, PP and Wu, JT: Group B streptococci inhibit the chemotactic activity of the fifth component of complement. J Immunol. 141:3551-3556, 1988.
9. Yang, KD, Bathras, JM, Shigeoka, AO, James, J, Pincus, SH and Hill, HR: Mechanisms of bacterial opsonization by immune globulin intravenous: Correlation of complement consumption with opsonic activity and protective efficacy. J Inf Dis. 159:701-707, 1989.
10. Hill, HR, Gonzales, LA, Knappe, WA, Fischer, GW, Kelsey, DK, and Raff,HV: Comparative protective activity of human monoclonal and hyperimmune polyclonal antibody against group B streptococci. J Infect Dis. 163:792-798, 1991.
11. The International Chronic Granulomatous Disease Cooperative Study Group (including Hill, HR and Shigeoka, AO); A controlled trail of interferon gamma to prevent infection in chronic granulomatous disease. New Engl J Med. 324:509-516, 1991.
12. Lei, B, DeLeo, FR, Hoe, NP, Graham, MR, Mackie, SM, Cole, RL, Liu M, Hill, HR, Low, DE, Federle, MJ, Scott, JR, and Musser, JM: Evasion of human innate and acquired immunity by a bacterial homologue of CD11b that inhibits opsonophagocytosis: Nature Med. 7:1298-1305, 2001.
13. Pickering, JW, Martins, TB, Greer, RW, Schroder, MC, Astill, ME, Litwin, CM, Hildreth SW, and Hill, HR: A multiplexed flourescent microsphere immunoassay for antibodies to pneumococcal capsular polysaccharides. Amer J Clin Pathol. 117:589-596, 2002.
14. Martins, TB, Hoffman, JL, Augustine, NH, Phansalkar, AR, Fischetti, VA, Zabriskie, JB, Cleary, PP, Musser, JM, Veasy, LG, Hill, HR: Comprehensive analysis of antibody responses to streptococcal and tissue antigens in patients with acute rheumatic fever. Int Immunol. 20:445-452, 2008.
15. Caron, JE, La Pine, TR, Augustine, NH, Martins, TB, and Hill, HR: Multiplex-analysis of toll-like receptor stimulated neonatal cytokine response. Neonatology. 97:266-273, 2010.
D. Research Support:
Ongoing Research Support:
“Exploratory/Developmental Investigations on Primary Immunodeficiency Diseases”, R21 AI094004-01A1, 08/01/11-07/31/13. MPI with Volkerding, K. and Kumánovics, A., Hill, H.R. Total Direct Funds $275,000
Completed Research Support: in reverse order:
“Group A Streptococcal Study Support” - Principal Investigator: Harry R. Hill, M.D.; NIH, NIAID Type: Contract N01-AO-227 Period: 02/01/02-10/31/04 (was to go to 01/31/09) Total Direct Funds Awarded - $4,270,289
“Mechanisms of Host Resistance to Group B Streptococci” - Principal Investigator: Harry R. Hill, M.D.
NIH, NIAID RO1 AI-13150-20 Period: 01/01/1977-08/31/2001 (20 yrs.) Direct Funds - $2,000,000
“Chemotactic Mechanisms in Neonatal Bacterial Infection”- Principal Investigator: Harry R. Hill, M.D.
NIH, NIAID RO1 AI-13150- 07 Period 09/01/1982 – 05/31/89 (7 years); Direct Funds $370,785
“Mechanisms of Diabetic Phagocyte Control by Insulin” – Principal Investigator: Harry R. Hill, M.D.
NIH, NIAM RO1 AM21140 Period 2/1/78-11/30/81 (3 years) Direct Funds - $167,653
“Human Neutrophil Regulation by Cyclic Nucleotides” – Principal Investigator: Harry R. Hill, M.D.
NIH, NIAM; RO1 AM18354 Period 9/20/74-4/30/77 (3 years) Direct Funds- $67,771
Total NIH Funding for thirty two years: (30 years RO1 + NIAID Contract) 9/1/74-10/30/04, + NIH R21 8-1-11 to 7-31-13 – $275,000) = $7,151,498 Total Awarded
Howard Hughes Investigator - 7/1/75 – 6/30/81; Salary plus $30,000 - $100,000 per year