Janet S. Butel

Last updated
Janet S Butel
EducationB.S. Kansas State University (1963) Ph.D. Baylor College of Medicine (1966)
Known forStudy of SV40 in humans through animal model in golden hamsters.
AwardsAmerican Association for the Advancement of Science Fellow (1988)
Scientific career
FieldsVirology, molecular virology, immunology, microbiology
InstitutionsBaylor College of Medicine

Janet S Butel is the Chairman and Distinguished Service Professor in the molecular virology and microbiology department at Baylor College of Medicine. Her area of expertise is on polyomavirus pathogenesis of infections and disease. She has more than 120 publications on PubMed. She also has 6 publications in Nature, which is considered one of the most prestigious science journals. She is a member of 9 different organizations and has 13 honors and awards. [1]

Contents

Education

Butel received her Bachelor of Science degree from Kansas State University in June 1963. She then went on to get her Ph.D. in virology at Baylor College of Medicine in June 1966. After she received her PhD she did a Post-Doctoral Fellowship in virology at Baylor College of Medicine. [1]

Research contributions

Simian virus 40 Symian virus.png
Simian virus 40

Butel has studied polyomavirus SV40 infection in humans and animals for most of her career. She has published studies on the mechanism of SV40 entry into human cells, the role of SV40 in cancer and SV40 genetics. In addition, Butel published an article in 2014 on the use of microRNA and SV40 in golden hamsters. [2] The golden hamster is the animal model that SV40 has been studied in and has provided evidence of its pathogenesis in tumor forming cancer. [3] The animal model has been used to research the development of this virus in humans, but can not conclude any definitive pathogenesis of SV40 in humans. [4] Thus there is controversy over the exact impact of SV40 on human health. Butel's research indicates that SV40 may play a role in some human cancers, such as brain tumors and non-Hodgkin lymphoma. [5] [6] [7] [8] [9]

In the 1990s Dr. Butel discovered the role of P53 in the pathogenesis of SV40 and oncogenesis. [10] [11] [12] [13] [14] [15] By discovering the role of P53 in SV40 she was able to support the research being conducted on P53 as a tumor-suppressor gene. This was perhaps the most important research of her career. [16] [17] [18]

Dr. Butel has also studied the role of the polio vaccine and in human SV40 infection and integration of SV40 into our DNA. It was found that some vaccines contained pieces of SV40 genes. It is suspected that by incorporating SV40 into the vaccine allowed it to enter into our own DNA. [19] Butel has published studies on topics other than SV40. She has studied the immunology of women going into spaceflight, specifically cytokines and antibodies. [20] Butel also researched hepatitis B and the role it plays in DNA repair. [21] [22] Dr. Butel has also contributed to higher education and is a coauthor of a medical microbiology textbook that has been used for over 50 years and in medical colleges around the world. [23] Dr. Butel has over 120 publications with over 10,000 citations, according to Google scholar.

Honors and awards

[1]

Related Research Articles

<i>Polyomaviridae</i> Family of viruses

Polyomaviridae is a family of viruses whose natural hosts are primarily mammals and birds. As of 2020, there are six recognized genera and 117 species, five of which are unassigned to a genus. 14 species are known to infect humans, while others, such as Simian Virus 40, have been identified in humans to a lesser extent. Most of these viruses are very common and typically asymptomatic in most human populations studied. BK virus is associated with nephropathy in renal transplant and non-renal solid organ transplant patients, JC virus with progressive multifocal leukoencephalopathy, and Merkel cell virus with Merkel cell cancer.

SV40 is an abbreviation for simian vacuolating virus 40 or simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that sometimes causes tumors in animals, but most often persists as a latent infection. SV40 has been widely studied as a model eukaryotic virus, leading to many early discoveries in eukaryotic DNA replication and transcription.

Mouse mammary tumor virus (MMTV) is a milk-transmitted retrovirus like the HTL viruses, HI viruses, and BLV. It belongs to the genus Betaretrovirus. MMTV was formerly known as Bittner virus, and previously the "milk factor", referring to the extra-chromosomal vertical transmission of murine breast cancer by adoptive nursing, demonstrated in 1936, by John Joseph Bittner while working at the Jackson Laboratory in Bar Harbor, Maine. Bittner established the theory that a cancerous agent, or "milk factor", could be transmitted by cancerous mothers to young mice from a virus in their mother's milk. The majority of mammary tumors in mice are caused by mouse mammary tumor virus.

<span class="mw-page-title-main">Oncovirus</span> Viruses that can cause cancer

An oncovirus or oncogenic virus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, when the term "oncornaviruses" was used to denote their RNA virus origin. With the letters "RNA" removed, it now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with "tumor virus" or "cancer virus". The vast majority of human and animal viruses do not cause cancer, probably because of longstanding co-evolution between the virus and its host. Oncoviruses have been important not only in epidemiology, but also in investigations of cell cycle control mechanisms such as the retinoblastoma protein.

<span class="mw-page-title-main">SV40 large T antigen</span> Proto-oncogene derived from polyomavirus SV40

SV40 large T antigen is a hexamer protein that is a dominant-acting oncoprotein derived from the polyomavirus SV40. TAg is capable of inducing malignant transformation of a variety of cell types. The transforming activity of TAg is due in large part to its perturbation of the retinoblastoma (pRb) and p53 tumor suppressor proteins. In addition, TAg binds to several other cellular factors, including the transcriptional co-activators p300 and CBP, which may contribute to its transformation function. Similar proteins from related viruses are known as large tumor antigen in general.

<span class="mw-page-title-main">GLIPR1</span> Protein-coding gene in humans

Glioma pathogenesis-related protein 1 is a protein that in humans is encoded by the GLIPR1 gene.

Merkel cell polyomavirus was first described in January 2008 in Pittsburgh, Pennsylvania. It was the first example of a human viral pathogen discovered using unbiased metagenomic next-generation sequencing with a technique called digital transcriptome subtraction. MCV is one of seven currently known human oncoviruses. It is suspected to cause the majority of cases of Merkel cell carcinoma, a rare but aggressive form of skin cancer. Approximately 80% of Merkel cell carcinoma (MCC) tumors have been found to be infected with MCV. MCV appears to be a common—if not universal—infection of older children and adults. It is found in respiratory secretions, suggesting that it might be transmitted via a respiratory route. However, it has also been found elsewhere, such as in shedded healthy skin and gastrointestinal tract tissues, thus its precise mode of transmission remains unknown. In addition, recent studies suggest that this virus may latently infect the human sera and peripheral blood mononuclear cells.

<span class="mw-page-title-main">Murine polyomavirus</span> Species of virus

Murine polyomavirus is an unenveloped double-stranded DNA virus of the polyomavirus family. The first member of the family discovered, it was originally identified by accident in the 1950s. A component of mouse leukemia extract capable of causing tumors, particularly in the parotid gland, in newborn mice was reported by Ludwik Gross in 1953 and identified as a virus by Sarah Stewart and Bernice Eddy at the National Cancer Institute, after whom it was once called "SE polyoma". Stewart and Eddy would go on to study related polyomaviruses such as SV40 that infect primates, including humans. These discoveries were widely reported at the time and formed the early stages of understanding of oncoviruses.

<span class="mw-page-title-main">Bernice Eddy</span> American epidemiologist

Bernice Eddy was an American virologist and epidemiologist. She and Sarah Elizabeth Stewart are known for their discoveries related to polyomavirus, particularly SV40 polyomavirus.

Joan S. Brugge is the Louise Foote Pfeiffer Professor of Cell Biology and the Director of the Ludwig Center at Harvard Medical School, where she also served as the Chair of the Department of Cell Biology from 2004 to 2014. Her research focuses on cancer biology, and she has been recognized for her explorations into the Rous sarcoma virus, extracellular matrix adhesion, and epithelial tumor progression in breast cancer.

Syrian hamsters are one of several rodents used in animal testing. Syrian hamsters are used to model human medical conditions including various cancers, metabolic diseases, non-cancer respiratory diseases, cardiovascular diseases, infectious diseases, and general health concerns. In 2014, Syrian hamsters accounted for 14.6% of the total animal research participants in the United States covered by the Animal Welfare Act.

Hamster polyomavirus is an unenveloped double-stranded DNA virus of the polyomavirus family whose natural host is the hamster. It was originally described in 1967 by Arnold Graffi as a cause of epithelioma in Syrian hamsters.

KI polyomavirus is a virus of the family Polyomaviridae. It was discovered in 2007 in stored samples of human respiratory secretions collected by the Karolinska Institute, after which the virus is named.

<span class="mw-page-title-main">Agnoprotein</span> Viral protein found in some polyomaviruses

Agnoprotein is a protein expressed by some members of the polyomavirus family from a gene called the agnogene. Polyomaviruses in which it occurs include two human polyomaviruses associated with disease, BK virus and JC virus, as well as the simian polyomavirus SV40.

<span class="mw-page-title-main">Large tumor antigen</span>

The large tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. LTag is expressed early in the infectious cycle and is essential for viral proliferation. Containing four well-conserved protein domains as well as several intrinsically disordered regions, LTag is a fairly large multifunctional protein; in most polyomaviruses, it ranges from around 600-800 amino acids in length. LTag has two primary functions, both related to replication of the viral genome: it unwinds the virus's DNA to prepare it for replication, and it interacts with proteins in the host cell to dysregulate the cell cycle so that the host's DNA replication machinery can be used to replicate the virus's genome. Some polyomavirus LTag proteins - most notably the well-studied SV40 large tumor antigen from the SV40 virus - are oncoproteins that can induce neoplastic transformation in the host cell.

<span class="mw-page-title-main">Small tumor antigen</span>

The small tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. STag is expressed early in the infectious cycle and is usually not essential for viral proliferation, though in most polyomaviruses it does improve replication efficiency. The STag protein is expressed from a gene that overlaps the large tumor antigen (LTag) such that the two proteins share an N-terminal DnaJ-like domain but have distinct C-terminal regions. STag is known to interact with host cell proteins, most notably protein phosphatase 2A (PP2A), and may activate the expression of cellular proteins associated with the cell cycle transition to S phase. In some polyomaviruses - such as the well-studied SV40, which natively infects monkeys - STag is unable to induce neoplastic transformation in the host cell on its own, but its presence may increase the transforming efficiency of LTag. In other polyomaviruses, such as Merkel cell polyomavirus, which causes Merkel cell carcinoma in humans, STag appears to be important for replication and to be an oncoprotein in its own right.

The middle tumor antigen is a protein encoded in the genomes of some polyomaviruses, which are small double-stranded DNA viruses. MTag is expressed early in the infectious cycle along with two other related proteins, the small tumor antigen and large tumor antigen. MTag occurs only in a few known polyomaviruses, while STag and LTag are universal - it was first identified in mouse polyomavirus (MPyV), the first polyomavirus discovered, and also occurs in hamster polyomavirus. In MPyV, MTag is an efficient oncoprotein that can be sufficient to induce neoplastic transformation in some cells.

Minor capsid protein VP2 and minor capsid protein VP3 are viral proteins that are components of the polyomavirus capsid. Polyomavirus capsids are composed of three proteins; the major component is major capsid protein VP1, which self-assembles into pentamers that in turn self-assemble into enclosed icosahedral structures. The minor components are VP2 and VP3, which bind in the interior of the capsid.

Vaccine contamination with Simian vacuolating virus 40, known as SV40 occurred in the United States and other countries between 1955 and 1961.

Xiaojiang S. Chen is a Chinese-American virologist, immunologist, and structural biologist. He is a professor of Biological Sciences and Chemistry and Director of the Center of Excellence in Nano Biophysics/Structural Biology at the University of Southern California.

References

  1. 1 2 3 "Janet S Butel Ph.D". Baylor College of Medicine. Baylor College. Retrieved 14 April 2015.
  2. ↑ Zhang, S; Sroller, V; Zanwar, P; Chen, CJ; Halvorson, SJ; Ajami, NJ; Hecksel, CW; Swain, JL; Wong, C; Sullivan, CS; Butel, JS (February 2014). "Viral microRNA effects on pathogenesis of polyomavirus SV40 infections in syrian golden hamsters". PLOS Pathogens. 10 (2): e1003912. doi: 10.1371/journal.ppat.1003912 . PMC   3916418 . PMID   24516384.
  3. ↑ Patel, NC; Halvorson, SJ; Sroller, V; Arrington, AS; Wong, C; Smith, EO; Vilchez, RA; Butel, JS (30 March 2009). "Viral regulatory region effects on vertical transmission of polyomavirus SV40 in hamsters". Virology. 386 (1): 94–101. doi:10.1016/j.virol.2008.12.040. PMC   2668977 . PMID   19181358.
  4. ↑ Sroller, V; Vilchez, RA; Stewart, AR; Wong, C; Butel, JS (January 2008). "Influence of the viral regulatory region on tumor induction by simian virus 40 in hamsters". Journal of Virology. 82 (2): 871–9. doi:10.1128/jvi.01626-07. PMC   2224577 . PMID   17977966.
  5. ↑ Vilchez, RA; Butel, JS (11 August 2003). "SV40 in human brain cancers and non-Hodgkin's lymphoma". Oncogene. 22 (33): 5164–72. doi:10.1038/sj.onc.1206547. PMID   12910253.
  6. ↑ Vilchez, RA; Butel, JS (September 2003). "Simian virus 40 and its association with human lymphomas". Current Oncology Reports. 5 (5): 372–9. doi:10.1007/s11912-003-0021-y. PMID   12895387. S2CID   22078338.
  7. ↑ Vilchez, RA; Kozinetz, CA; Arrington, AS; Madden, CR; Butel, JS (1 June 2003). "Simian virus 40 in human cancers". The American Journal of Medicine. 114 (8): 675–84. doi:10.1016/s0002-9343(03)00087-1. PMID   12798456.
  8. ↑ Butel, JS; Jafar, S; Stewart, AR; Lednicky, JA (1998). "Detection of authentic SV40 DNA sequences in human brain and bone tumours". Developments in Biological Standardization. 94: 23–32. PMID   9776222.
  9. ↑ McNees, AL; Vilchez, RA; Heard, TC; Sroller, V; Wong, C; Herron, AJ; Hamilton, MJ; Davis, WC; Butel, JS (5 February 2009). "SV40 lymphomagenesis in Syrian golden hamsters". Virology. 384 (1): 114–24. doi:10.1016/j.virol.2008.10.035. PMC   3648995 . PMID   19038412.
  10. ↑ Maxwell, SA; Ames, SK; Sawai, ET; Decker, GL; Cook, RG; Butel, JS (February 1991). "Simian virus 40 large T antigen and p53 are microtubule-associated proteins in transformed cells". Cell Growth & Differentiation. 2 (2): 115–27. PMID   1648952.
  11. ↑ Scorsone, KA; Zhou, YZ; Butel, JS; Slagle, BL (15 March 1992). "p53 mutations cluster at codon 249 in hepatitis B virus-positive hepatocellular carcinomas from China". Cancer Research. 52 (6): 1635–8. PMID   1311638.
  12. ↑ Donehower, LA; Harvey, M; Slagle, BL; McArthur, MJ; Montgomery CA, Jr; Butel, JS; Bradley, A (19 March 1992). "Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours". Nature. 356 (6366): 215–21. doi:10.1038/356215a0. PMID   1552940. S2CID   4348340.
  13. ↑ Ozbun, MA; Jerry, DJ; Kittrell, FS; Medina, D; Butel, JS (1 April 1993). "p53 mutations selected in vivo when mouse mammary epithelial cells form hyperplastic outgrowths are not necessary for establishment of mammary cell lines in vitro". Cancer Research. 53 (7): 1646–52. PMID   8453637.
  14. ↑ Jerry, DJ; Ozbun, MA; Kittrell, FS; Lane, DP; Medina, D; Butel, JS (15 July 1993). "Mutations in p53 are frequent in the preneoplastic stage of mouse mammary tumor development". Cancer Research. 53 (14): 3374–81. PMID   8324748.
  15. ↑ Ozbun, MA; Medina, D; Butel, JS (October 1993). "p53 mutations in mouse mammary epithelial cells: instability in culture and discordant selection of mutations in vitro versus in vivo". Cell Growth & Differentiation. 4 (10): 811–9. PMID   8274450.
  16. ↑ Harvey, M; McArthur, MJ; Montgomery CA, Jr; Butel, JS; Bradley, A; Donehower, LA (November 1993). "Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice". Nature Genetics. 5 (3): 225–9. doi:10.1038/ng1193-225. PMID   8275085. S2CID   26741712.
  17. ↑ Ozbun, MA; Butel, JS (1995). "Tumor suppressor p53 mutations and breast cancer: a critical analysis". Advances in Cancer Research. 66: 71–141. doi:10.1016/s0065-230x(08)60252-3. ISBN   9780120066667. PMID   7793321.
  18. ↑ Medina, D; Stephens, LC; Bonilla, PJ; Hollmann, CA; Schwahn, D; Kuperwasser, C; Jerry, DJ; Butel, JS; Meyn, RE (July 1998). "Radiation-induced tumorigenesis in preneoplastic mouse mammary glands in vivo: significance of p53 status and apoptosis". Molecular Carcinogenesis. 22 (3): 199–207. doi:10.1002/(sici)1098-2744(199807)22:3<199::aid-mc8>3.0.co;2-g. PMID   9688146. S2CID   25526449.
  19. ↑ Shah, Keerti V. (15 January 2007). "SV40 and human cancer: A review of recent data". International Journal of Cancer. 120 (2): 215–223. doi: 10.1002/ijc.22425 . PMID   17131333. S2CID   20679358.
  20. ↑ Shearer, WT; Ochs, HD; Lee, BN; Cohen, EN; Reuben, JM; Cheng, I; Thompson, B; Butel, JS; Blancher, A; Abbal, M; Aviles, H; Sonnenfeld, G (April 2009). "Immune responses in adult female volunteers during the bed-rest model of spaceflight: antibodies and cytokines". The Journal of Allergy and Clinical Immunology. 123 (4): 900–5. doi: 10.1016/j.jaci.2008.12.016 . PMID   19232702.
  21. ↑ Becker, SA; Lee, TH; Butel, JS; Slagle, BL (January 1998). "Hepatitis B virus X protein interferes with cellular DNA repair". Journal of Virology. 72 (1): 266–72. doi:10.1128/JVI.72.1.266-272.1998. PMC   109372 . PMID   9420223.
  22. ↑ Butel, JS; Lee, TH; Slagle, BL (March 1996). "Is the DNA repair system involved in hepatitis-B-virus-mediated hepatocellular carcinogenesis?". Trends in Microbiology. 4 (3): 119–24. doi:10.1016/0966-842x(96)81529-0. PMID   8868091.
  23. ↑ Brooks, George; Butel, Janet; Morse, Stephen (June 1, 2004). Jawtz, melnick and adelbergs medical microbiology (3 ed.). McGraw-Hill Medical. ISBN   978-0071239837.
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