Paul Sumby Ph.D.: Biography/Education

Associate Professor

Department of Microbiology and Immunology


  • Ph.D. - Molecular Microbiology - University of Nottingham, England, U.K.
  • B.S. - Genetics - University of Leicester, England, U.K.


Paul Sumby, Ph.D. is an associate professor in the department of microbiology and immunology at the University of Nevada, Reno School of Medicine. Sumby received a B.S. from the University of Leicester followed by a Ph.D. in molecular microbiology from the University of Nottingham. In addition, Sumby completed postdoctoral fellowships at the New England Medical Center (Boston, MA), Rocky Mountain Laboratories (Hamilton, MT), Baylor College of Medicine (Houston, TX), and The Houston Methodist Research Institute (Houston, TX). Sumby joined the University of Nevada, Reno School of Medicine in July 2013.

Courses Taught

MICR350 - Microbial Genomics & Genetics


Sumby has spent nearly 15 years studying how the human bacterial pathogen Streptococcus pyogenes (also known as the group A Streptococcus, GAS) regulates gene expression in a disease-specific manner. GAS causes a broad spectrum of diseases including pharyngitis (a.k.a. strep throat), streptococcal toxic shock syndrome, necrotizing fasciitis (a.k.a. the flesh-eating disease), and the post-infection sequel acute rheumatic fever. The ability of this pathogen to cause such a wide diversity of human diseases is in part due to the coordinate expression of specific subsets of virulence factors in response to microenvironment-dependent stimuli. Through understanding of how GAS regulates virulence factor expression the Sumby laboratory aims to develop novel therapeutic and/or preventative regimes, via translational research approaches, that are based upon the manipulation of these regulatory pathways. Ongoing research projects in Dr. Sumby's laboratory include:

  1. Determination of the molecular mechanisms behind small regulatory RNA (sRNA) - mediated regulation of GAS virulence factor expression. We have characterized the molecular basis behind the ability of the 205 nt sRNA FasX to regulate GAS virulence. Through post-transcriptional regulatory mechanisms FasX enhances the expression of the thrombolytic agent streptokinase, and reduces the expression of multiple cell-surface adhesins. These activities enhance GAS virulence in a mouse model of bacteremia infection and reduce the ability to GAS to adhere to human epithelial cells. Studies aimed at finding additional regulatory targets of FasX, and of identifying how the expression of FasX itself is regulated, are on-going.
  2. Role of the RocA/CovR/CovS proteins in regulating GAS virulence during invasive and non-invasive infections. The CovR/S proteins form a two-component regulatory system that negatively regulates ~10% of the GAS transcriptome, including multiple virulence factor-encoding mRNAs. We and others have identified that covR/S mutant strains are positively selected for during invasive infections, with the resultant mutants being hyper-virulent. While covR/S mutant strains are hyper-virulent during invasive infections they are attenuated for growth in models of non-invasive infections, relative to parental strains. Thus, CovR/S control the ability of GAS to cycle between invasive and non-invasive infections. Recently, it was identified that the putative orphan sensor kinase RocA has a major positive regulatory role on the CovR/S system. The molecular basis of this is currently under investigation.
  3. Contribution of differential gene regulation and horizontal gene transfer in promoting GAS-serotype disease-phenotype associations. Decades of epidemiological studies have indicated that certain GAS serotypes are non-randomly associated with particular disease manifestations. For example, serotype M3 isolates are associated with particularly severe and lethal invasive infections, while serotype M28 isolates are associated with cases of puerperal sepsis. We have identified that serotype M3 isolates uniquely harbor mutations in multiple regulator-encoding genes, resulting in M3 isolates producing a distinct virulence factor expression profile. The importance of the regulator gene mutations with regard to the association of M3 isolates with severe invasive infections is currently under study. In addition, we are also studying whether the presence of a 35 kb pathogenicity island in serotype M28 isolates, of apparent group B Streptococcus origin, is behind the association of M28 isolates with cases of puerperal sepsis.

Sumby lectures on medical microbiology to School of Medicine medical students.

• Bacterial Classification, Structure, Nutrition, and Growth

• Sterilization, Disinfection, and Containment

• Laboratory Diagnosis of Bacterial Diseases

• Bacterial Genetics and Pathogenesis

• Survey of Medical Bacteriology

• Skin and Soft Tissue Infections

Current Lab Members

• Ira Jain, Ph.D. graduate student

• Roshika Roshika, Ph.D. graduate student

• Josette Medicielo, M.Sc. graduate student

Past Lab Members

• Jess Danger Ph.D.

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