Our Students - Louisiana State University Health Shreveport

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Our Graduate Students and Post Doctoral Scientists

Graduate Students
Post Doctoral Scientists

Graduate Students

Temitayo T. Bamgbose

B.S., Microbiology, Federal University of Agriculture Abeokuta, Nigeria, 2014

Research: Inflammasomes are cytoplasmic multiprotein complexes that enhance the inflammatory response of the innate immune system. We have previously demonstrated that the phosphatidic acid phosphatase activity of lipin 1 promotes proinflammatory responses in macrophages. My project seeks to understand how macrophage associated lipin 1 regulates the activation of the inflammasome and the effects of this regulation on disease pathogenesis.

Cassidy M. Blackburn

B.A., Biology, DePauw University, 2016

Research: Atherosclerosis is a hypercholesterolemia-induced inflammatory condition of arteries mediated by macrophages. Why macrophages become inflammatory in response to hypercholesterolemia is enigmatic. We have demonstrated that the glycerolipid synthetic enzyme lipin-1 in macrophages is atherogenic. My project is to elucidate the molecular mechanisms by which macrophage-associated lipin-1 promotes atherogenesis.

Kellie N. Brown

B.S., Biology, University of Memphis, 2015

Research: Rotavirus causes gastroenteritis that can be life-threatening in children. The rotavirus nonstructural protein NSP1 inhibits the host immune response by promoting the degradation of proteins required for interferon production. NSP1 has been shown to interact with cullin RING ligases (CRLs), which are host ubiquitin ligase complexes. My research is investigating the NSP1-CRL interaction to determine if NSP1 is using this complex to induce degradation of host proteins or if the interaction has other roles in viral replication.

Anthony J. Domma

B.S., Louisiana State University, 2017

Research: This lab has found that HCMV protein UL148 induces quality control structures, and formation of these structures are PERK dependent. My project is to identify the protein-protein interactions that are crucial for the formation of these quality control structures. I will use tandem affinity purification and other methods in attempts to elucidate the molecular mechanism of how 148 induces stress and to answer if its effects on Endoplasmic Reticulum Associated Degradation (ERAD) are specific.

Joseph I. Eniafe

B.S., Microbiology, Obafemi Awolowo University, Nigeria, 2016

Research: Triple-negative breast cancer (TNBC) is a recalcitrant form of breast cancer with poor prognosis. Accumulating evidence supports extra-metabolic roles for metabolites of the tri-carboxylic acid (TCA) cycle. Screening membrane-permeable versions of the TCA cycle intermediates identified citrate and fumarate as inhibitors of human TNBC proliferation and migration. My project seeks to identify how treatments with these metabolites affect TNBC cells by modulating the expression of miRNAs and oncogenes that are associated with TNBC tumor progression.

Nicholas First - LSU Health Shreveport — Nicholas First

B.S., Microbiology, Mississippi State University, 2020

Research: New Student

Lauren Henderson — Lauren Henderson

B.S., Biological Sciences, Louisiana State University - Shreveport, 2020

Research: New Student

Rebecca B. Lopez

B.S., Biology, Centenary College, 2019

Research: Human papillomavirus (HPV)-induced cancers are prevalent worldwide. HPV’s viral life cycle depends on keratinocyte differentiation. The stromal microenvironment provided by fibroblasts contribute to proper epithelial differentiation, maintenance, and immune responses. My project seeks to determine how stromal interferon regulatory factor 3 (IRF3) inhibits the late phase of the HPV16 life cycle.

Bailey S. Mosher

B.S., Microbial, Cellular, and Molecular Biology, Auburn University, 2016

Research: HCMV utilizes a unique intracellular trafficking pattern in peripheral blood monocytes. This trafficking pattern is critical for successful nuclear translocation and ultimately a productive viral infection. My project is to determine the mechanics behind this viral trafficking pattern in monocytes. Currently, I am focusing on trafficking through the TGN as a critical trafficking event prior to nuclear translocation.

Julia E. Myers

B.S., Biology, University of Central Arkansas, 2016

Research: Epstein-Barr virus (EBV) and human papillomavirus (HPV) are two viral infections commonly found worldwide. It has been previously shown by our lab that coinfection of HPV and EBV is present in oral squamous cell carcinomas (OSCC). Using an organotypic raft model system, we have found that the expression of HPV E7 inhibits EBV replication. The goal of my project is to investigate the mechanisms behind E7 inhibition of EBV replication.

Danielle L. Schaal

B.S., Biology, Ouachita Baptist University, 2019

Research: Epstein-Barr virus (EBV) is a potential co-factor in human papilloma (HPV)-positive oropharyngeal squamous cell carcinoma. EBV replication is inhibited in HPV-positive keratinocytes generated by stable transfection of the HPV genome. I hypothesize that the process of HPV immortalization driven by E7 inhibits EBV replication. I will use the HPV infection model to establish a timeframe of cellular changes that negatively impact EBV replication.

Robert. M. Schilke

B.S. (2014), M.S. (2017), University of North Carolina Wilmington

Research: Atherosclerosis is a hypercholesterolemia-induced inflammatory condition of arteries mediated by macrophages. We have demonstrated that lipin-1, a key enzyme in the glycerolipid synthesis pathway, regulates oxidized low-density lipoprotein-induced macrophage inflammatory response. Lipin-1 also has transcriptional co-regulatory activity and its contribution to atherosclerosis has yet to be elucidated. My project will seek to identify protein-protein interactions between lipin-1 in macrophages in response to oxLDL to provide insight into the regulation of lipin-1 activity that may contribute to atherogenesis.

Sarah Soorya

B.S., Microbiology, Nicholls State University, 2017

Research: Human papillomavirus (HPV) is the most prevalent sexually transmitted infection globally. After infectious entry, the HPV genome associates with promyelocytic leukemia protein nuclear bodies (PML NB) for efficient transcription. PML protein is recruited to the incoming HPV genome prior to egress from the transport vesicle. My research is to investigate the role of PML NBs and its PML protein during early transcriptional regulation of the incoming HPV genome and its response to innate immune pathways during infection.

Jessica Trammel - LSU Health Shreveport — Jessica Trammel

B.S., Nutrition and Food Sciences, Louisiana State University, 2020

Research: New Student

Geetika Sruti Vutukuri Amaranth

M.S., Biomedical Engineering, Louisiana Tech University, 2016

Research: Epstein-Barr virus (EBV) is a tumor virus shown to induce epigenetic reprogramming B cells and epithelial cells following infection. EBV-infected normal oral keratinocytes (NOK) showed increased DNA hypermethylation, increased invasiveness, and delayed differentiation, features of basal, wounding keratinocytes. The timing of the epigenetic reprogramming and the cellular and viral factors involved are not known. The goal of my project is to use RNA-seq to identify early effectors in EBV-infected NOK which contribute to EBV-induced epigenetic changes.

Billy H. Ward, Jr.

B.S. (2007), M.S. (2016), Mississippi State University

Research: Neisseria gonorrhoeae (Ng) is a human-adapted bacterial pathogen responsible for an estimated 80 million cases of sexually transmitted disease each year. Unable to survive outside the human host, Ng has evolved multiple strategies to promote persistence and growth by modulating host immune system functions. Macrophages are critical mediators of the immune response and tissue homeostasis. The role of macrophages in Ng pathogenesis is poorly understood. Our laboratory has found that Ng exploits macrophages for survival and growth. We have shown Ng displays niche plasticity during macrophage infection, by colonizing and replicating on the cell surface or intracellularly. We also discovered that gonococci invade macrophages by a novel actin-dependent mechanism to establish a unique membrane-bound organelle. The goal of my research is to elucidate the mechanisms by which Ng colonizes the macrophage and to understand the role of this interaction in gonococcal pathogenesis.

Ashley Wilkins

M.S., Microbiology and Immunology, Tulane University, 2019

Research: Legionella are Gram-negative intracellular bacteria that parasitize unicellular amoeba that can also infect humans when contaminated aerosolized water droplets are accidentally inhaled and deposited in the lungs. In these accidental pulmonary infections, alveolar macrophages support bacterial replication and promote the development of a severe pneumonia-like illness known as Legionnaire’s disease. To survive within a eukaryotic cell, Legionella creates a unique, membrane-bound organelle known as the Legionella-containing vacuole (LCV). My project focuses on understanding the mechanism(s) which control the expansion of the LCV lipid bilayer during intracellular bacterial replication.

Post Doctoral Scientists

Dr. Malgorzata Bienkowska-Haba

Research Specialist

Email: mbienk@lsuhsc.edu
Sapp Laboratory

Dr. Bienkowska-Haba is investigating the intracellular trafficking of human papillomavirus during infection. Her focus is the identification of cellular compartments which are targeted by the minor capsid protein L2 and investigation of L2's role in intracytoplasmic trafficking and nuclear translocation of the viral genome.

Dr. Liudmila S. Chesnokova

Email: lchesn@lsuhsc.edu
Yurochko Laboratory

Dr. Chesnokova investigates how human cytomegalovirus (HCMV) glycoprotein complexes contribute to productive cell infection, persistence, and disease.

Dr. Edna Ondari

Email: eondar@lsuhsc.edu
Ivanov Laboratory

Dr. Ondari studies the mechanisms by which Legionellae establish their intracellular niches, particularly cellular trafficking and metabolic pathways exploited by different species.

Dr. Byeong-Jae Lee

Email: blee19@lsuhsc.edu
Yurochko Laboratory

Dr. Lee focuses on how HCMV regulation of host signaling influences cellular differentiation to promote dissemination and monocytes and macrophages to promote life-long viral persistence.

Dr. Chan-ki Min

Email: cmin@lsuhsc.edu
Yurochko Laboratory

Dr. Min investigates HCMV infection in monocytes and the influence on macrophage phenotype.

Dr. Akhalesh K. Shakya

Email: ashaky@lsuhsc.edu
Yurochko Laboratory

Dr. Shakya investigates HCMV regulation of host cell signaling and cytokines in myelosuppression.

Dr. Abida Siddiqa

Email: asidd2@lsuhsc.edu
Sapp Laboratory

Dr. Siddiqa is investigating the underlying biological mechanisms that are involved in establishment of human papillomavirus 16 infection and events of intracellular trafficking during infection.

Dr. Mohammed N. Siddiquey

Email: msidd2@lsuhsc.edu
Kamil Laboratory

Dr. Siddiquey is working to identify the roles UL148 in HCMV cell tropism. He will also be involved in projects concerning mechanisms of viral gene regulation in HCMV.

Dr. Hongbo Zhang

Email: hzhan1@lsuhsc.edu
Kamil Laboratory

Dr. Zhang investigates the role of UL148 in HCMV cell tropism.

Dr. Katarzyna Zwolinska

Email: kzwoli@lsuhsc.edu
Sapp Laboratory

Dr. Zwolinska is investigating immediate early events of the HPV-16 lifecycle.

Graduate Program

Microbiology & Immunology

Graduate Program

Microbiology & Immunology

Graduate Program

Microbiology & Immunology