Ebola virus disease (EVD) is a deadly infectious disease that is caused by ebolaviruses. The 2013-2016 West African outbreak, caused by Zaire ebolavirus, was the deadliest outbreak recorded with 28,616 cases and 11,325 deaths. The virus can be transmitted via direct contact with infected fluids from other people or animal reservoirs. The gold standard to diagnose EVD is reverse transcription-polymerase chain reaction (RT-PCR), however, it can take several days to get a result and it requires specialized equipment and trained personnel. While there is a vaccine available, outbreaks are still occurring. Treatment consists of therapeutic antibodies, but a diagnosis is still beneficial to ensure the appropriate treatment is administered as well as to isolate the patient and prevent further spread. A rapid diagnostic tool would be beneficial to the global burden of EVD. Lateral flow immunoassays (LFI) are rapid point-of-care diagnostic tools that use antibodies to detect a specific biomarker of a disease. Soluble glycoprotein, sGP, is the most abundant protein synthesized from the GP gene and is present during EVD. The goal of this study was to isolate monoclonal antibodies (mAbs) reactive to sGP and develop a LFI prototype to detect sGP in samples. A monoclonal library of seventeen antibodies was established and tested in the LFI format to determine the best pair for detecting recombinant sGP.

Breast milk is a crucial regulator of host-microbiome interactions in early life. In addition to nutrients, breastmilk contains immunoregulatory elements which likely support homeostatic immune responses to newly acquired gut bacteria. Dr. Koch discovered that maternal antibodies, delivered via breast milk, limit the activation of CD4 T follicular helper (Tfh) cells and germinal center (GC) B cell responses in the gut-associated tissues of neonates. These aberrant, T-dependent immune responses depend on microbial colonization and correlate with the transient accumulation of commensal gut bacteria in the mesenteric lymph nodes of neonates at weaning. Together, these findings indicate that neonates lacking breastmilk antibodies generate dysregulated adaptive immune responses to beneficial gut bacteria. Tfh cells interact with B cells within immune structures called germinal centers, which leads to the formation of high affinity, T cell-dependent (TD) antibodies. Tfh cells and TD antibodies are instrumental to maintaining host-microbe homeostasis. Abnormal increases in microbiota-directed TD immune responses can result in profound changes in the composition of the microbiota and even colitis. Considering that antigen-specific adaptive immune cells and their clonal progeny can persist indefinitely, I propose that the inappropriate activation of neonatal adaptive immune cells by gut bacteria results in durable impairments in intestinal homeostasis. I hypothesize that the elevated mucosal Tfh and GC B cell responses generated in the absence of breastmilk antibodies result in long-lived plasma and memory B cells and fundamentally alter the intestinal microbiota.

The Human Cytomegalovirus (HCMV) is an indiscriminate, human beta-herpesvirus that detrimentally affects the immunocompromised and can lead to harmful congenital effects. Alike other viruses, HCMV hijacks and utilizes the host lipid metabolism through its mechanism of replication. To further understand the role and significance of the host lipid metabolism is to understand the specific enzymes responsible for producing necessary metabolites for virion production. One such family of enzymes would be the fatty acid elongases, and one specific enzyme to be more extensively researched is fatty acid elongase 5. Ultimately, what is being determined is whether or not fatty acid elongase 5 is necessary for HCMV replication. Ideally, HCMV may be dependent on the presence or absence of such an enzyme. However, it is possible that the upregulation or downregulation of fatty acid elongase 5 could be dependent on a variety of other metabolic, or general, cellular conditions. Regardless, the implications from this research will improve, and in some cases redefine, what is already known about HCMV and its relation to the host environment for replication.

The timing of human birth is difficult to predict compared to other species due to evolutionary differences. While the causes of these specific differences have been identified, the data collected on gene expression in the mother and fetus hasn't been synthesized enough to be directly applied to predicting the timing of birth. This is detrimental because “preterm birth is the leading cause of infant and under 5 year old child mortality worldwide" and without a precise understanding of how gene expression changes throughout pregnancy, we cannot adequately prevent it. We examined the location and expression of the genes involved in serotonin signaling pathways using the Single Cell Gene Expression Atlas to figure out which cells express serotonin receptors, how this expression changes throughout pregnancy, and how it differs in humans compared to other mammals with placentas. Understanding where these genes are expressed, in the mother’s cells or placental cells, and what their role is during normal pregnancies and those with complications will make it possible to decrease the rates of preterm births and develop ways to treat conditions that lead to increased risk of preterm births.