Boris Striepen, PhD

Scholar

  •  Mark Whittier and Lila Griswold Allam Professor of Microbiology and Immunology | University of Pennsylvania School of Veterinary Medicine
  •  United States
  •   Diarrheal disease | Malnutrition | OneHealth | Tropical diseases

Languages: English (fluent), German (native), French (basic), Spanish (basic)

Bio statement

Boris grew up in Ruhrort where the German rivers Rhine and Ruhr meet, an industrial area then dominated by coal and steel. He studied biology at the universities of Bonn and Marburg and conducted undergrad research on liver flukes in Bonn and Nagana in Bobo Dioulasso, Burkina Faso. Boris earned a PhD summa cum laude for work on parasite biochemistry with Ralph Schwarz, was a postdoc with David Roos studying parasite cell biology, prior to starting his laboratory at the Center for Tropical & Emerging Global Diseases at the University of Georgia in 2000, where he last was a Distinguished Research Professor. In 2017 he joined the faculty of the University of Pennsylvania. Boris studies the cell and molecular biology of apicomplexan parasites. His current research focus is the parasite Cryptosporidium, a leading global cause of diarrhea and mortality in young children. His lab pioneered molecular genetics for this important infection and leads a range of interdisciplinary efforts to understand fundamental parasite biology and to advance translation towards drugs and vaccines. Boris is also engaged in education and training. He taught undergraduate and graduate classes, directed NIH training grant programs in parasitology, and served as faculty and director of the Biology of Parasitism summer research course at the Marine Biology Laboratories in Woods Hole, MA. Boris is married to a social worker with remarkable patience for scientists and has three children, two are scientists – all are awesome.

Recent global health projects

  1. Cryptosporiosis — A new genetic handle on an important diseases​10.5% of global child mortality is due to diarrheal disease. Comprehensive epidemiology at the global scale recently revealed Cryptosporidium to be the most important diarrheal pathogen in small children after Rotavirus. Recently, we have developed robust molecular genetics for this important pathogen. Currently we lack effective treatment. We collaborate with several groups in academia and industry to change that. Cryptosporidium has a highly stripped down metabolism and steals most of the metabolites it needs from the host. It also interacts with the bacterial flora of the intestine and has acquired the genes for numerous bacterial enzymes by horizontal gene transfer. We use rigorous genetics to unravel this complex metabolism and to evaluate targets for treatment.
  2. Host parasite interaction. Infants are highly susceptible to cryptosporidiosis. However, under constant exposure, children older that two rarely show infection and disease. Most likely they are protected by immunity. The mechanisms that govern host immunity and parasite immune evasion remain largely to be discovered. We have isolate a 'wild' mouse Crytposporidium and have developed a natural mouse model that results in self-limiting infection and protection in immunocompetent mice. We are using this new model to understand the immunology of Cryptosporidium infection and the important role that the microbiome and nutritional state of the host play. We are currently exploring ways to broaden our studies to involve clinical colleagues to contrast findings in the laboratory with those from patients in relevant settings.


Selected publications

Guérin, A., Roy, N.H., Kugler, E.M., Berry, L., Burkhardt, J.K., Shin, J.-B., and Striepen, B. (2021) A screen for
Cryptosporidium rhoptry proteins identifies ROP1 as an effector targeting the host cytoskeletal modulator LMO7. Cell
Host & Microbe 29: 1-14.
Sateriale, A., Gullicksrud, J.A., Engiles, J.B., McLeod, B., Kugler, E.M., Henao-Mejia, J., Zhou, T., Ring, A.M., Brodsky, I.E.,
J.C. Hunter, C.A., and Striepen, B. (2021) The intestinal parasite Cryptosporidium is controlled by an enterocyte
intrinsic inflammasome that depends on NLRP6. Proc. Natl. Acad. Sci. U.S.A. 118: e2007807118.
Guérin, A., and Striepen, B. (2020) The Biology of the intestinal intracellular parasite Cryptosporidium. Cell Host &
Microbe 28: 509-515.


Pawlowic, M., Somepalli, M., Sateriale, A., Herbert, G.T. Gibson, A.R., Cuny, G., Hedstrom, L., and Striepen, B. (2019)
Genetic ablation of purine salvage in Cryptosporidium parvum reveals nucleotide uptake from the host cell. Proc. Natl.
Acad. Sci. U.S.A. 116: 21160-21165.


Sateriale, A., Slapeta, J., Baptista, R., Engiles, J.B., Gullicksrud, J.A., Herbert, G.T., Brooks, C.F., Kugler, E.M., Kissinger,
J.C. Hunter, C.A., and Striepen, B. (2019) A genetically tractable, natural mouse model of cryptosporidiosis offers
insights into host protective immunity. Cell Host & Microbe 26, 135–146


Tandel, J., English, E., Sateriale, A., Gullicksrud, J., Beiting, D.P., Sullivan, M.C., Pinkston, B., and Striepen, B. (2019)
Lifecycle progression and sexual development of the apicomplexan parasite Cryptosporidium parvum. Nature
Microbiology 4: 2226-2236

Manjunatha UH†, Vinayak S†, Zambriski JA*†, Chao AT, Sy T, Noble SJ, Bonamy G, Kondreddi RR, Zou B, Gedeck P, Brooks CF, Herbert GT, Sateriale A, Tandel J, Noh S, Lakshminarayana SB, Lim SH, Goodman LB, Yeung BKS, Bodenreider C, Feng G, Zhang L, Blasco F, Wagner J, Leong FJ, Striepen B*, and Diagana T* (2017) An inhibitor of the Cryptosporidium PI(4)K is a candidate drug for cryptosporidiosis († and * equal first and last author contributions, respectively). Nature 546: 376–380. doi: 0.1038/nature22337.

Vinayak S*, Pawlowic MC*, Sateriale A*, Brooks CF, Studstill JC, Bar-Peled Y, Cirpriano MJ, and Striepen B (2015). Genetic modification of the diarrheal pathogen Cryptosporidium parvum. Nature 253:477-480 (*equal contribution). doi: 10.1038/nature14651.  

Striepen B (2013). Time to tackle cryptosporidiosis, Nature. 2013 Nov 14;503(7475):189-91. doi: 10.1038/503189a.