Alumni
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Please email Microbiology.Immunology@utoledo.edu. We hope to hear from you!

John Presloid, Ph.D.
John Presloid, a scientist with a Ph.D., studies how germs interact with the human body. His highly cited work on RNA virus quasispecies, genetic robustness, and interferon‑mediated restriction in natural reservoir hosts provides conceptual foundations for his current focus on immune‑driven pathogen control. He’s been studying the bacteria that causes Lyme, called Borrelia burgdorferi, and how it affects the body. This research has shown how bacteria can change the way certain immune cells work, which helps the bacteria survive and cause long-term or recurring symptoms. This is important because it helps us understand why Lyme disease can be so hard to get rid of and why some people keep getting sick.
Presloid conducted his research in the lab of Dr. R. Mark Wooten. After testing the theory on mice, he made a pretty significant discovery. What he found was that by slowing down the bacteria's movement through the body, it becomes a lot easier for the immune system to attack and get rid of it. This could be a game-changer for people with this debilitating disease.
Presloid has also made a significant contribution to the field by co-authoring a patent for the University of Toledo, which focuses on detecting exposure to toxic cyanobacteria. This patent, granted in 2021, involves methods, assays, and kits that utilize antibody-based approaches to identify prior cyanotoxin exposure in biological samples. The potential applications of these diagnostic tools range from public health surveillance to clinical toxicology and environmental exposure assessment. By developing these tools, Presloid's research program can help us better monitor and respond to environmental health risks, ultimately contributing to improved public health and safety.

Hugo Sigona Gonzalez
Hugo Sigona Gonzalez studied at the University of Toledo in the Biomedical Science Program. He worked in Dr. R. Mark Wooten's lab looking into Burkholderia pseudomallei, which is a bacterium that causes melioidosis, a pretty severe and often deadly infection.
The U.S. Centers for Disease Control and Prevention even rank Burkholderia pseudomallei as a Tier 1 select agent because it can be lethal and doesn’t respond to many antibiotics.
During his time at , Gonzalez focused on how this bacterium manipulates some key proteins that our immune system uses to fight off infections, weakening our body’s first line of defense. Based on what he discovered, Gonzalez investigated fresh immunotherapeutic methods, like those engineered fusion proteins that are meant to boost our immune response and help kill off the bad bacteria. His findings showed that a few of these next-gen designs could kick up complement activation on the bacteria's surface, which could be useful for treating tough infections where antibiotics alone are ineffective.
Hugo shared his work at the University of Toledo Graduate Research Annual Forum. In addition, he teamed up to write a peer-reviewed article about how these immune-based strategies could really change the game. This effort shows how stands out in translating infectious disease research into something meaningful for public health and biodefense. Through his training at the University of Toledo, Hugo Gonzalez is ready to take on any major infectious disease challenges that we face today.

Ryan Harris, Ph.D.
Ryan Harris, Ph.D., completed his doctoral research in Medical Microbiology and Immunology at the University of Toledo. He investigated how hosts interact with viruses, checked out reservoir host immunity, and explored how tick-borne flaviviruses resist infections, especially focusing on Powassan virus and some related pathogens.
His research focused on cell culture infection models, RT-qPCR, western blotting, and viral genome sequencing. He looked into how viral proteins affect the host's antioxidant systems and set up infectious clone and site-directed mutagenesis systems to pinpoint viral mutations that help flaviviruses sneak past host defenses in reservoir cells. This was crucial for understanding what genetic changes are needed for these viruses to jump between species.
At the same time, he was trying to find new antiviral strategies for tick-borne flaviviruses. His results suggest that if we target the host's antioxidant responses instead of just the virus, we could actually develop a solid broad-spectrum antiviral therapy. Harris wrote an article for The Toledo Blade, breaking down how immune systems of reservoir hosts are different from humans when it comes to dealing with tick-borne viruses, and why understanding those differences is pretty crucial for public health.
His dissertation focused on figuring out why some natural reservoir hosts, like the white-footed mouse (Peromyscus leucopus), can handle or even limit these nasty infections from tick-borne flaviviruses without getting sick. His research showed that these hosts have boosted antioxidant responses that help keep the virus at bay. He also highlighted that when these Nrf2-regulated antioxidant pathways kick in, viral replication gets limited, which explains why these reservoir hosts can bounce back so well.
Once he obtained his Ph.D. at in Medical Microbiology & Immunology, he moved into a postdoctoral role, diving deeper into viral infections, host metabolism, and molecular virology.

Mir Himayet Kabir, Ph.D.
Mir Himayet Kabir, Ph.D., graduated from the University of Toledo’s Biomedical Science Program. He did his doctoral work in the Medical Microbiology and Immunology (MMI) Track from 2020 to 2024. He worked on his dissertation with Dr. Travis Taylor, diving into tick-borne viral infections and how they affect our immune system.
In his role as a molecular virologist, Dr. Kabir used cell-based infection models and molecular tests to break down how viruses interact with their hosts and how the immune system responds. His efforts are in line with what the University of Toledo stands for, connecting the dots between basic science and public health issues.
While pursuing his Ph.D., Dr. Kabir really focused on tick-borne flaviviruses. He looked at how the innate immune system could help kick back against viruses, looking at how to target the body's defenses. By investigating immune pathways that kick in early during infections, his research helped us understand how these viral infections could be “neutralized” before they turn into serious neurological issues, informing new antiviral treatments. Dr. Kabir wrote an article that was featured in The Toledo Blade.
After wrapping up his Ph.D., Dr. Kabir became a virology scientist with the Ohio Department of Agriculture. There, he is putting his knowledge about flavivirus biology, innate immunity, and molecular diagnostics to work, supporting efforts in animal and public health.

Brooke Ring, Ph.D.
Brooke Ring, Ph.D. finished her training in the Medical Microbiology and Immunology Track. Her research was about understanding how bad bacteria cause disease with the goal of finding new ways to fight infections without just using antibiotics. Dr. Ring’s work exemplifies the University of Toledo’s commitment, to doing important biomedical research effecting real world health problems.
During Brooke Ring’s Ph.D. program, she studied Klebsiella pneumoniae, a global health problem and a main cause of infections like pneumonia and bloodstream infections. More specifically, Dr. Ring studied “mucoidy" which is a protective covering that allows Klebsiella to avoid the immune system, causing disease to worsen. Dr. Ring’s research showed certain nutrients in the environment, like a common amino acid, can make the bacteria more harmful by producing more of this protective coating. She identified genes and pathways that control the thickness of this covering which helps explain how Klebsiella adapts quickly inside the human body. You can read more about this at news.utoledo.edu and toledoblade.com. This research has opened up possibilities for therapies that can stop the bacteria from being harmful without killing them which could help reduce the problem of antibiotic resistance.