Colleagues: Recently Tenured


Senior Investigator and Chief, Complement and Inflammation Research Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute

Claudia Kemper

Education: University of Hamburg, Hamburg, Germany (B.Sc. in biology); Bernhard Nocht Institute for Tropical Medicine, Hamburg (Ph.D. in immunology)

Training: Postdoctoral fellowship, Department of Internal Medicine, Washington University School of Medicine (St. Louis)

Before coming to NIH: Professor of innate immunology, Division of Transplant Immunology and Mucosal Biology, King’s College London (London)

Came to NIH: In 2014–2015 as a visiting scientist in NHLBI’s Laboratory of Molecular Immunology; returned to NHLBI in February 2017

Selected professional activities: Member, Grant Review Board, Wellcome Trust; senior editor, Molecular Immunology; visiting professor of innate immunology at King's College London; adjunct professor of translational complement research, University of Lübeck (Lübeck, Germany)

Outside interests: Reading; running; visiting museums


Research interests: The complement system is a critical part of the innate immune system and consists of about 50 serum and cell-expressed proteins (in the blood, lymph, and interstitial fluids) that provide protection against pathogens through direct cell lysis and the mobilization of innate immunity.

Before coming to NIH, I helped discover that the complement system plays other physiological roles such as instructing adaptive T-cell responses. At NIH, my lab is trying to understand the unexpected additional roles of the complement system in regulating key basic processes of the cell.

The complement system affects human T-helper type 1 (Th1) immunity by controlling both the induction and contraction of Th1 CD4+ T cells. Further, we discovered that the activation of the key complement components—glycoproteins C3 and C5—is not, as always thought, confined to the extracellular space but also occurs in intracellular areas. We named this intracellular complement system “the complosome.”

Intracellular C3 and C5 are critical for the homeostatic survival of T cells and for metabolic reprogramming. If there is too little activation of intracellular C3 and C5, there’s a deficient Th1 response, leading to recurrent infections. Too much intracellular C3 and/or C5 activation contributes to hyperactive Th1 responses such as those observed in rheumatoid arthritis and other autoimmune diseases. The hyperactive response can be normalized pharmacologically by inhibiting the intracellular complement activity.

Importantly, although initially discovered in T cells, these complosome-regulated pathways seem to operate in a broad range of cells. We are defining the functional roles and regulative mechanisms and assessing the biological relevance of the intracellular and autocrine complement. We hope to develop druggable targets in these pathways to treat autoimmune diseases. To achieve this goal, we are focusing on the complosome composition in different cells, the functions of the complosome, and how it is regulated.

In our research, we use immune and tissue cells—from healthy donors, patients with complement deficiencies, patients with T-cell-driven autoimmune disease, and patients with deviations in novel complosome-regulated pathways—to do gene and microRNA arrays, epigenetic-landscape evaluation, and proteomic and metabolomic assessments. This approach will be combined with appropriate mouse models to define the biological significance of proteins and pathways and to develop preclinical animal models for future pharmacological targeting.

Understanding all the functions of the complement system will deliver critical new knowledge about cell biology in health and disease.


Senior Investigator and Chief of Structural Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases

Joseph Marcotrigiano

Education: Rutgers, The State University of New Jersey, New Brunswick, N.J. (B.A. in chemistry); The Rockefeller University, New York (Ph.D. in molecular biophysics)

Training: Postdoctoral fellow and research associate, Center for the Study of Hepatitis C, The Rockefeller University

Before coming to NIH: Associate professor with tenure, Department of Chemistry and Chemical Biology, Center for Advanced Biotechnology and Medicine, Rutgers University

Came to NIH: In January 2017

Selected professional activities: Faculty Scholar, Howard Hughes Medical Institute

Outside interests: CrossFit; cooking


Research interests: My laboratory is investigating how positive-sense RNA viruses enter human host cells, replicate, and evade the immune response. In particular, we are interested in how the hepatitis C virus (HCV) enters cells and evades the immune response; exploring the mechanisms of viral polyprotein processing; and examining how the innate immune system distinguishes self from viral RNAs. Our long-term goal is to develop an effective HCV vaccine, novel antiviral drugs, and immunomodulators of retinoic-acid-inducible gene I for use as broad-based antiviral agents.

About two percent of the world’s population is infected with HCV (approximately 150 million people), and an estimated 3 to 4 million more individuals become newly infected each year. Without treatment, hepatitis C may lead to cirrhosis, liver failure, and liver cancer. There are several FDA-approved direct-acting antivirals for HCV, some of which are prohibitively expensive, but there is no vaccine against the virus.

HCV is an enveloped virus with an outer shell composed of many copies of two glycoproteins, E1 and E2. My laboratory developed a cost-, labor-, and time-efficient method for the large-scale production of recombinant glycoproteins in mammalian cell lines. Using this production system, we found that HCV E2 does not share any similarity with other viral glycoproteins, including those from closely related viruses, suggesting that HCV may use a novel entry mechanism.

Numerous viruses, many of which severely impact human health around the globe (such as human immunodeficiency virus, Zika virus, dengue virus, West Nile virus, chikungunya virus, and severe acute respiratory syndrome coronavirus), use a gene-expression mechanism wherein one gene encodes a single polyprotein that is post-translationally cleaved into individual proteins.

To fully understand polyprotein processing in each step of the viral lifecycle, we examined changes in viral-protein properties before and after polyprotein processing. We have determined the structure of the precleavage form of a portion of the alphavirus replication machinery. Our findings, which have provided new insights into viral polyprotein processing and pathogenesis, may be applicable to other important human viruses that undergo polyprotein processing.

In our research that examines the innate immune system, we are trying to understand the mechanism of self versus non-self recognition and immune-signaling actions of certain receptors that detect the presence of viral RNA in infected cells. So far, we have determined the structure of the RNA-binding domains of one of the cytoplasmic proteins.


Senior Investigator and Chief of Pediatric Anesthesia and Critical Care, Department of Perioperative Medicine, Clinical Center

Zena Quezada

Education: Universidade Federal do Ceará, Fortaleza, Ceará, Brazil (M.D.)

Training: Residency, Department of Medicine, Albert Einstein Medical Center, Temple University (Philadelphia); Fogarty Clinical Fellow, Critical Care Medicine Department, NIH Clinical Center; residency and cardiac anesthesia fellowship, Department of Anesthesia and Critical Care, Harvard’s Massachusetts General Hospital (Boston); clinical fellow, Shriners Burn Hospital (Boston)

Before coming to NIH: Anesthesiologist, Children’s National Health System (Washington, D.C.); professor of anesthesiology, Critical Care Medicine and Pediatrics, George Washington University (Washington, D.C.); director, Pain Neurobiology Laboratory and Animal Neurobehavioral Core, Center for Neuroscience Research, Children’s Research Institute (Washington, D.C.)

Came to NIH: In 1990 for training (1990–1994); in 2000 as anesthesiologist at NIH Clinical Center; later became chief of Department of Anesthesia and tenure-track investigator (2005–2010); returned in January 2017 as a senior investigator

Selected professional activities: Associate senior examiner, American Board of Anesthesiology; elected member, Association of University Anesthesiologists, Society for Pediatric Research

Outside interests: Collecting art; traveling around the world to learn about other cultures


Research interests: As a pediatric anesthesiologist, I take care of children before, during, and after surgery. During this perioperative period, one of my major concerns is treating pain. Inspired by my clinical work, I also do basic research—using mouse models—to understand the neurobiology of pain and nociception, develop and evaluate therapeutic agents for treating pain, and develop methods for objectively measuring it.

In my lab, we use mouse models of sickle-cell disease (SCD) and models of autism-like behavior. People with SCD suffer acute and chronic pain that is often inadequately treated. The SCD mice also have high susceptibility to pain. Conversely, some children with autism-spectrum disorders seem to have either a low tolerance for or a low response to pain, as do mice with autism-like behaviors.

In our search for therapeutic agents to treat pain, we have found that the FDA-approved sedative dexmedetomidine, when used in the perioperative period, can significantly decrease the need for opioids. In children undergoing tonsillectomies, my team found that those who were given dexmedetomidine before surgery had a longer opioid-free interval post-surgery than children who were not given the sedative beforehand. These findings were reproduced by others and have changed the way we treat children’s pain during the perioperative period.

A major challenge in my work is the lack of ways to objectively measure pain. Clinicians can ask adults to rank their pain on a scale of 1 to 10, with 10 being the worst. But babies, very young children, or children with developmental disabilities may not be able to verbally express how much they hurt. Thus, it’s difficult to gauge how much pain a child is in and figure out how to treat it. And it’s unclear whether children with autism feel less or more pain compared with other people or whether they are just unable to communicate how they feel.

In an effort to develop objective measures for pain, we collaborated with NIH’s Center for Information Technology to adapt a peripheral neuropathy-diagnostic technique for use as a noninjurious, neurospecific nociceptive behavior assay that elicits and detects pain-avoiding behavior in mice. With this paradigm, we can study the effects of age, sex, and neurologic diseases on pain and monitor the efficacy of pain treatment. We are also developing mobile applications to continue to monitor pain intensity and medication compliance while patients are at home.

This fall, I will be heading up a new pediatric observation unit, which will provide additional support for patient safety in pediatric research. The unit will include four beds where children who require closer observation will have cardiovascular and respiratory monitoring.


Senior Investigator, Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute

Joshua Sampson

Education: Pomona College, Claremont, Calif. (B.A. in chemistry and mathematics); Stanford University, Stanford, Calif. (M.S. in biophysical chemistry); University of Washington, Seattle (M.S. and Ph.D. in biostatistics)

Training: Postdoctoral fellow, Department of Biostatistics, Yale University (New Haven, Conn.)

Came to NIH: In 2009 as a principal investigator in NCI-DCEG’s Biostatistics Branch

Selected professional activities: Associate editor, Annals of Applied Statistics; statistical editor, Journal of the National Cancer Institute

Outside interests: Running; kayaking; reading


Research interests: I am fascinated by the genetic causes of cancer. At NCI-DCEG, I have been fortunate to have collaborated on several complex and exciting genome-wide association studies (GWAS). As a statistician, I have been developing more-efficient designs for studies and more-powerful methods for analyzing data. I have developed a new framework for identifying groups of rare variants associated with cancer, a new analysis for identifying causal variants in GWAS in related individuals, and an approach for identifying associations within only a subset of individuals. The latter approach was recently applied to a GWAS in an attempt to identify genes associated with the risk of secondary neoplasms among childhood-cancer survivors. I have also tried to describe and quantify the heritability of a range of cancers and show that for any given cancer, the majority of heritability is likely explained by a unique set of underlying genetic loci.

In addition, I am curious about understanding how known risk factors increase the risk of cancer. Towards this aim, I am working with a talented postdoctoral fellow, Andriy Derkach, to identify metabolites that may be mediators between risk factors, such as body mass index and diet, and cancer risk.

Over the past two years, I have been part of a team of NCI researchers that is evaluating the efficacy of a single dose of the human papillomavirus vaccine (typically the vaccine is given in three doses over a six-month period). Mitchell Gail and I are developing an innovative statistical approach—that accounts for such complexities as a low infection rate, a lack of a placebo arm, and missing data—for analyzing the study results.

Finally, I have had the opportunity to work on a variety of other epidemiologic studies. I have explored many factors—such as the microbiome, epigenetics, and physical activity—that are associated with health. To better understand how physical activity and its complement, sedentary time, are associated with risk of disease, I have developed methods to assess the measurement error of accelerometers, described novel patterns of activity, and evaluated techniques for handling compositional data.


Senior Investigator, Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute

Zhengping Zhuang

Education: Shanghai Second Medical University, Shanghai, China (M.D.); Molecular Biology and Pharmacology, Department of Pharmacology, Wayne State University, Detroit (Ph.D. in Molecular Biology and Pharmacology)

Training: Residency in general surgery, Rui Jin Hospital, Shanghai Second Medical University; postdoctoral fellow, Harvard Medical School (Boston); residency in transitional medicine, Henry Ford Hospital (Detroit); research associate, University of Michigan (Ann Arbor, Mich.); residency in anatomic pathology, Laboratory of Pathology, NCI

Came to NIH: In 1993 for training; in 1996 became attending staff pathologist and co-director of the Developmental Molecular Diagnostic Unit, Laboratory of Pathology, NCI; in 1999 became head of Molecular Pathogenesis Unit, NINDS; in December 2016, became senior investigator

Selected professional activities: Adjunct professor, Department of Neurology, Uniformed Services University of the Health Sciences School of Medicine (Bethesda, Md.)


Research interests: My laboratory is gaining insights into the pathophysiology of central nervous system (CNS) and other tumors. We focus on inherited and somatic mutations in the cancer genome to demonstrate their critical roles in tumor formation and progression; we develop and apply cutting-edge techniques to identify novel genetic and functional changes in cancer cells; and through collaborations with clinicians and scientists, we translate our laboratory findings into experimental drug development and human clinical trials.

Using functional genomics studies, we identified and characterized cancer-causing gene mutations. For example, we were the first to discover Pacak-Zhuang syndrome, a multiorgan human disorder characterized by the development of multiple paragangliomas (neuroendocrine neoplasms that may develop at different body sites), somatostatinomas (rare neuroendocrine tumors that arise from the pancreas or gastrointestinal tract), and congenital polycythemia (a slow-growing blood cancer in which the bone marrow makes too many red blood cells). We worked closely with NIH intramural physicians and scientists to explore the genetic make-up of a group of patients with similar tumor manifestations and polycythemia.

In our biotechnological advancements and applications work, we addressed the problem of isolating tumor cells from the morphologic heterogeneous solid-tumor specimens. My group developed a tissue-microdissection technique and co-invented laser-capture microscopy (LCM) to facilitate the procurement of highly purified specific cell types from histological tissue samples. The technique, together with the invention of the LCM, substantially improved and facilitated tissue-based cancer research.

We were also the first to identify and clarify the nature of the neoplastic cell in CNS hemangioblastomas and several other tumors found in von Hippel–Lindau (VHL) disease, an inherited disorder characterized by the formation of tumors and fluid-filled sacs in many parts of the body. In separate CNS-tumor studies, we identified several new genes involved in tumorigenesis in primary glial neoplasm (especially gliomas), discovered novel stem-cell-like populations in brain tumors, and elucidated a potential role for dysfunctional beta-catenin signaling in the activation of astrocytes that facilitates the genesis of astrocytomas.

In our drug-development and clinical-translation work, we identified small-molecule compounds that can be used to treat some cancers. We collaborated with a biotechnology firm to develop the drug LB100, an inhibitor of protein phosphatase 2A, which holds promise as a novel means of overcoming treatment-resistant cancer and was recently approved by the FDA for clinical trials. In phase 1 trials, LB100 was associated with the stabilization of several cancer types without dose-limiting toxicity.