The microbiome and virome are known to interact within the human body which in turn modulates the health and disease of an individual. While these interactions have been largely studied in bodily sites such as the gastrointestinal tract, the microbiome and virome of the female genital tract (FGT) remains largely understudied. Within the virome exists DNA and RNA viruses which are known to infect both eukaryotes and prokaryotes. While existing virome research within the FGT has focused largely on eukaryote infecting viruses, a large proportion of the virome consists of uncharacterized bacteriophages known as “dark matter”. Due to the lack of a specific gene marker for viruses, which is essential in qPCR quantification of other populations such as bacteria, determination of viral abundance and virome characterization has been limited. However, the staining of viral DNA has been found effective in visualizing and enumerating virus-like particles within various specimens. In this study, we seek to determine viral abundance within the FGT utilizing SYBR Gold nucleic acid stain to visualize VLP present within a cohort of cervicovaginal lavage (CVL) samples. Given these results we intend to draw conclusions regarding the interactions between the FGT virome and viral abundance as well as sexual-reproductive health. Understanding the complex relationship of the virome within the female reproductive tract is likely to have remarkable clinical implications and has the potential to progress both the diagnostic and treatment aspects of female sexual and reproductive health.

On March 11th, COVID-19 was declared a pandemic by the World Health Organization. The ensuing months saw an extensive allocation of resources toward combating the virus and the development of a vaccine. Despite extensive research on SARS-CoV-2, there remains little information regarding the implications of SARS-CoV-2 gastrointestinal shedding on COVID-19 disease. It is hypothesized that SARS-CoV-2 RNA is shed in the stool for up to several weeks and that viral protein persists in the GI tract. This study also explored calprotectin and zonulin levels, markers of inflammation, and intestinal permeability, respectively, to assess if increased viral shedding is associated with elevated levels of either. This study utilized RT-qPCR assays to confirm the presence of viral RNA. Subsequently, RT-qPCR positive samples were heat-inactivated and SARS-CoV-2 spike detection enzyme-linked immunosorbent assay (ELISA) was used to ascertain viral protein shedding. Additional ELISA was performed to assess zonulin and calprotectin levels. Results indicated that 30 of the 758 unique samples were confirmed SARS-CoV-2 positive by RT-qPCR. Spike protein was ultimately not detected by ELISA. Additionally, no significant increase in zonulin was observed in patient samples when comparing RT-qPCR positive and negative Samples. A notable upwards trend approaching significance in calprotectin levels existed for patients who tested positive for SARS-CoV-2 by RT-qPCR, though, it was found that no correlation existed between SARS-CoV-2 copy number and calprotectin levels. Understanding the interaction between SARS-CoV-2 and the GI tract may therefore have significant clinical implications and this study demonstrates the need for additional studies to garner a more comprehensive understanding.

The microbiome and the immune system are known to work in conjunction to modulate the clearance of pathogens and tolerance of beneficial microbes. A growing area of research seeks to study the potential extent of the involvement of the microbiome in modulating and supporting the immune system during acute allograft rejection. It has been hypothesized that the localized microbiota in each organ produce metabolites that instigate inflammatory immune responses, but whether microbiota interactions precipitate acute allograft rejection is unknown. Therefore, this study focuses on microbiome shifts in the gut and kidney after inducing acute renal transplant rejection in order to implicate gut dysbiosis as a precursor or supporter of allograft rejection. This study also subsequently explores the use of an immune-modulating protein in order to determine differences in the outcome of transplant rejection and potential differences in intestinal microbial load. This experiment sought to induce rejection in BALB/c mice through the use of C57BL/6 mouse renal slivers. Microbiome abundance was analyzed in all experimental groups. Understanding the role of the microbiome in transplant rejection has vast clinical implications and has the potential to enhance pre- and post-operative treatment, and immune management and quality of life following organ transplant.

Urologic diseases interstitial cystitis (IC), overactive bladder (OAB), and urinary tract infection (UTI) affect tens of millions of people per year in the US alone. The human microbiome consists of a diverse community of bacteria (bacteriome) and viruses (virome) harbored in each individual that contributes to health and disease. Little is known about how the microbiome impacts urinary disorders. Using next-generation metagenomic sequencing, we characterized the urinary bacteriome and virome of patients with urinary disorders (IC, OAB, and UTI) and healthy controls. We show that the bacteriome was distinctly altered in patients by their respective urinary disorder. IC was characterized by a distinct prevalence of the genus Lactobacillus, while OAB was characterized by the genus Bacteroides, and UTI was characterized by Comamonas. IC, OAB, and UTI all also had significantly differed virome profiles from healthy individuals. In particular, we found that Lactobacillus phages were significantly associated with IC and Corynebacterium virus was associated with UTI samples, meanwhile no particular virus was correlated with OAB samples. Overall, we show that changes in the urinary microbiome are associated with incidence and spectrum of urinary diseases. These findings could lead to new microbiome modalities of treatment.