USF Health preclinical study finds that inhibiting lipoxygenase with a drug alters
innate inflammatory response, delaying heart tissue repair after cardiac injury

TAMPA, Fla. (May 10, 2021) — Blocking the fat-busting enzyme lipoxygenase with a synthetic inhibitor throws the immune system’s innate inflammatory response out of whack, compromising cardiac repair during acute heart failure, USF Health researchers found.

Their new preclinical study was published April 13 in Biomedicine & Pharmacotherapy.

In search of individualized heart failure therapies, Ganesh Halade, PhD, leads a USF Health Heart Institute team studying unresolved inflammation after heart attack. | Photo by Allison Long, USF Health Communications

Acute heart failure – triggered by a heart attack, severely irregular heartbeats, or other causes — occurs suddenly when the heart cannot pump enough blood to meet the body’s demands.

Following a heart attack or any cardiac injury, signals to immune cells called leukocytes carefully control physiological inflammation. Normally, there are two distinct but overlapping processes: an acute inflammatory response (“get in” signal), where leukocytes travel from the spleen to the injured heart to start removing dead or diseased cardiac tissue, and a resolving phase (“get out” signal), where inflammation is cleared with the help of macrophages that arrive to further repair the damage and form a stable scar.

A delay in either the initiation of inflammation or its timely clearance (resolution) can lead to impaired cardiac healing and progression to heart failure, said study principal investigator Ganesh Halade, PhD, an associate professor of cardiovascular sciences at the USF Health Morsani College of Medicine and a member of the USF Health Heart Institute.

The USF Health researchers applied three investigational approaches (in vitro, ex vivo, and in vivo) to assess whether a potent lipoxygenase (12/15 LOX) inhibitor ML351 could selectively alter inflammatory responses in adult mice following cardiac injury similar to a heart attack. Previous studies by Dr. Halade’s laboratory reported that lipoxygenase-deficient mice showed improved cardiac repair and heart failure survival after cardiac injury.

“We wondered if blocking a lipoxygenase with an external pharmacological compound (drug) would have the same beneficial effect — but the answer was no,” Dr. Halade said. “Instead, the collective results of our study indicate that ML351 dysregulated control of the normal physiological pathway of inflammation in cardiac repair, causing collateral damage.”

In the mice treated mice with ML351, leukocyte recruitment to the site of cardiac injury was delayed, which subsequently amplified inflammation at the site. At the same time, instead of leaving once the repair job was done, the immune cells remained at the site beyond the typical acute (and beneficial) inflammatory response phase. Basically, the late arrival (get-in signal) and delayed clearance (get-out signal) of immune cells impaired cardiac repair, Dr. Halade said.

A delay in either the initiation of inflammation or its timely clearance (resolution) can lead to impaired cardiac healing and progression to heart failure.

The latest study helps explain one more piece of the puzzle about the important role of immune-mediated acute inflammation and its clearance – both in promoting cardiac health and stopping the progression of heart failure, Dr. Halade said. Lipoxygenases, fatty-acid modifying enzymes that control metabolic and immune signaling, can promote either resolving (beneficial) or nonresolving (harmful) inflammation, he added.

“The take-home message is do not mess with (block) the lipoxygenase. Preserve it, because it’s a key enzyme for our defensive, innate immune response,” he said. “Knowing how drugs interact with the body’s precisely-balanced immune responses will be critical for understanding mechanisms to prevent, delay or treat the unresolved inflammation influencing heart failure.”

The USF Health study was supported by grants from the NIH’s National Heart, Lung and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases.

USF Health virologist Michael Teng, PhD

The race for a COVID-19 vaccine began when Chinese scientists published the genetic sequence for the SARS-COV-2 virus on Jan. 11, 2020 – a full two months before the World Health Organization declared the novel coronavirus outbreak a global pandemic. Less than a year later, the U.S. Food and Drug Administration approved two vaccines for emergency use within a week of each other (Dec. 11, 2020 and Dec. 18, 2020). Shortly thereafter, the initial COVID-19 vaccine distributions began in the United States. Both these frontrunner vaccines – the first made by Pfizer and its partner BioNtech, and the second by Moderna – are based on new messenger RNA (mRNA) technology.

“As someone who has worked on vaccines for decades and studied RSV (respiratory syncytial virus), which still has no vaccine 60 years after its discovery, I’m excited about the tremendous achievement of this new mRNA technology,” said USF Health virologist Michael Teng, PhD. “It’s been an incredible story to watch unfold – just 11 months from identifying a new pandemic virus to actually getting a safe and effective frontline vaccine.”

We caught up with Dr. Teng recently to find out more about the science behind the mRNA vaccines, each requiring two doses several weeks apart.  He comments on some other vaccine issues as well. The following Q&A has been condensed and edited for clarity.

How do these mRNA vaccines work?

The Pfizer/BioNTech and Moderna mRNA vaccines are based on the same principle as other COVID-19 vaccines in advanced stages of development. These vaccines deliver genetic material that provides the instruction code for your body’s cells to produce a viral protein (antigen). Your immune system recognizes that viral protein as foreign to your body and mounts an immune response to protect against it.  For SARS CoV-2, the antigen is the viral spike (S) protein, which is located on the outside of the virus and allows the virus to enter a human cell in order to replicate.

The Pfizer/BioNTech and Moderna vaccines use messenger RNA (mRNA) as the genetic material and encase it in a protective lipid nanoparticle (small bubble of fat) for delivery.  Once inside your cells, the mRNA can be translated directly by your cells to make the crown-shaped SARS CoV-2 S. The first (priming) dose of the mRNA vaccine trains your immune system to recognize the viral protein and the second dose boosts your immunity. So, after vaccination, if you are exposed to the actual virus your immune system is ready to neutralize the virus quickly.

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In contrast, adenoviral vector vaccines, such as those developed by Oxford/AstraZeneca and Johnson & Johnson (Janssen), employ a DNA gene that encodes the SARS CoV-2 S protein as the genetic material and uses common cold virus particles (rendered harmless) as the delivery system. For these vaccines, the DNA first has to get into the cell nucleus where your cells can make the mRNA coding instructions, which must then be translated into production of the spike protein.

If the mRNA vaccine uses brand new technology, how could it be turned around so quickly?

While mRNA technology is relatively new and was never approved before COVID-19, the research on vaccines using a genetic approach is not.

Both companies (BioNTech and Moderna) have been testing the application of this platform against other infectious diseases and cancers for several years (i.e., Moderna has worked on mRNA vaccines for Zika and the flu). But, until now, none of the mRNA vaccines or therapeutics have made it through advanced clinical trials.

The challenge has been delivering the mRNA, which is very unstable, to its target human cells without the vaccine being degraded too quickly by the body’s naturally-occuring enzymes. You want to make sure the mRNA stays around long enough to make sufficient protein to stimulate an immune response, but not so long that it overstimulates the immune response… Both Pfizer and Moderna found a way to chemically hide the mRNA from the immune system so once it gets into your cells it has enough time to make the viral protein needed to trigger antibodies and activate T-cell production. The mRNA never enters the cell nucleus or alters a person’s genetic makeup.

What are the advantages of mRNA vaccines?

Well, we know they are relatively safe — and 90-plus percent efficacy for a vaccine (94-95%) is really very high. That level of protection rivals what we see with the measles and human papillomavirus (HPV) vaccines. Seasonal flu vaccines are only about 50 to 60 percent effective in a good year.

Another big advantage of this mRNA platform is that it’s easy to change (mRNA coding instructions) based on the disease you are targeting. You just need to swap in the gene sequence of the protein you want encoded to produce an immune response. So, theoretically, you can easily adapt the vaccine to respond to new viruses – or even mutations of the existing virus.

What are the drawbacks?

The major drawback of the mRNA vaccines is that we have not had yet fully marketed this particular type of vaccine. So, we still do not know the long-term effects of the vaccine, or how long immunity lasts.

The mRNA vaccines are significantly more expensive than the adenovirus vaccine and others in the pipeline for COVID-19.  And the cold-storage requirements (-94º F for the Pfizer vaccine and -4º F for the Moderna vaccine) may limit distribution.

SARS-CoV-2 variants recently emerged that may make the virus more contagious. Will current COVID-19 vaccines protect against the mutated virus, or will we need new ones?

It will take some time to get answers.  But, it’s important to know that RNA viruses like coronaviruses mutate, or change, quite frequently. Not every mutation makes the COVID-19 virus more dangerous or contagious; most have no effect, and others may even weaken the virus. Also, there are several sites (epitopes) on the SARS CoV-2 S protein that are recognized by antibodies. It is likely that multiple sites would have to mutate for the virus to escape the immune response from the vaccines. The current vaccines should cover the newly emerging 20B/501Y.V1 variant originally identified in the UK that has recently been found in Florida.

The bigger question is if we can vaccinate everyone within the next year, or year and a half. How much pressure will that put on SARS-CoV-2 to develop variants that escape immunity? It could happen; I don’t think this virus is going to magically disappear.

The most recent study I saw indicated that natural immunity to other coronaviruses seems to last about three years. The COVID-19 virus may become endemic like these other human coronaviruses that cause the common cold. That means you might need to return for a booster providing better immunity against new viral protein mutations — kind of like we do with the seasonal flu vaccine, which changes a little each year.

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Would you get one of these first COVID-19 vaccines?

Absolutely, I’ll get vaccinated as soon as I can.

Most short-term side effects are in line with other established vaccines we’re familiar with – including injection site soreness, muscle stiffness, fever, headache, maybe some chills. These symptoms may occur more commonly with the second dose when your immune system is ramping up.  It’s not the vaccine itself causing the side effects, but rather the routine response of your immune system to a vaccine that’s working.

The risk-benefit calculation is simple for me. I’d rather take my chances of getting a headache than being on a ventilator with COVID-19.

Can people who get the vaccine return their pre-COVID lifestyle (meeting in groups, no masks, etc.)?

The Phase 3 clinical trials data showed that the mRNA vaccines are 90-plus percent effective at preventing you from getting symptomatic COVID-19. However, we do not know whether the vaccine blocks asymptomatic transmission of the virus – so, there is still a possibility vaccinated people can be reinfected or reinfect others without having apparent symptoms.

We really cannot lower our guard until we achieve herd immunity – that is, until 75 to 80% of the population obtains immunity to COVID-19 through vaccination, or immunity developed from from prior infection… Herd immunity by natural infection is a terrible experiment to do, because this virus can cause severe disease and death in up to 2% of the population, some people suffer long-term health consequences, and treating that many COVID-19 patients would overwhelm the health care system… So, until enough of us are vaccinated, we all need to continue following the public health measures that help prevent the spread of COVID-19 – wear masks, physically distance, avoid large gatherings and wash our hands.

I don’t think we’ll ever get completely back to our pre-COVID lifestyles, though.

USF Health-UAB study indicates that lipid mediators may offer new targets for more personalized heart failure diagnosis and treatment

The new study profiled bioactive lipids in blood samples collected from hospitalized black and white patients soon after a severe heart attack.

TAMPA, Fla (May 4, 2020) — Black men and women have higher incidences than whites of developing advanced heart failure following a heart attack. Despite racial disparities in heart attacks (a leading contributor to heart failure), and rehospitalizations and deaths caused by heart disease, the underlying physiology accounting for worse cardiovascular outcomes among blacks is poorly understood.

A new study published May 4 in ESC Heart Failure profiles bioactive lipids in blood samples from hospitalized black and white patients soon after a severe heart attack. The preliminary research was conducted by a team at the University of South Florida Health (USF Health) Morsani College of Medicine and the University of Alabama at Birmingham. The researchers wanted to delineate potential differences in the immune-responsive processes needed to safely clear (resolve) acute inflammation after heart attack-induced tissue injury, with the aim of finding more individualized therapies for heart failure.

“Metabolic and leukocyte-responsive signaling control the acute inflammation needed for timely cardiac repair after a heart attack. But inflammation that is not cleared and remains long-term plays a key role in the pathology leading to heart failure,” said lead author Ganesh Halade, PhD, associate professor of cardiovascular sciences at the Morsani College of Medicine and a member of the USF Health Heart Institute.

“Understanding race and sex-based differences in inflammation and its resolution will help us develop more personalized diagnoses and treatments to delay or prevent heart failure.”

A mouse model study published by Dr. Halade last month discovered that heart repair occurs faster in female mice than males after a heart attack, which improves survival and delays cardiac failure.

In this human study, the researchers collected blood plasma from 53 patients, grouped by race and sex, within 24 to 48 hours after a heart attack. Baseline acute injury caused by the heart attack was similar in all the patients, and so were their ages and body mass indexes. No significant sex-or race-specific differences were detected in total cholesterol, HDL, LDL or triglyceride levels – all indicators (biomarkers) currently used by clinicians to help predict risk and manage cardiovascular disease. Measures of various subtypes of leukocytes (cells that regulate immune fitness) were similar across all patients.

Lead author Ganesh Halade, PhD, associate professor of cardiovascular sciences, USF Health Morsani College of Medicine

Looking for distinct bioactive lipid “signatures,” or inflammatory biomarkers, that might predict poorer cardiovascular outcomes after heart attack, the researchers measured three major polyunsaturated fatty acids: arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA). These omega fatty acids circulate in blood and depend upon what people eat. Also analyzed were dozens of specific proresolving mediator (SPM) indicators and a few other signaling molecules that form when these fatty acids metabolize in response to immune activation.

Overall, black patients showed higher concentrations of the three activated fatty acids after a heart attack than white patients, the researchers found. The comparative analyses of SPMs showed that resolvin E1, a potent proresolving mediator of inflammation derived from the fatty acid EPA, was significantly lower in black men and women than in whites. An earlier major clinical trial linked EPA with reduced ischemic events such as heart attack and stroke in patients with high risk for, or existing, cardiac disease, and another showed that high levels of EPA significantly decreased the risk of heart failure.

The researchers conclude that bioactive lipids are key for diagnosis and treatment of cardiac repair after heart attack to delay heart failure.

Randomized controlled clinical trials will be needed to definitively determine whether distinct SPM signatures can be used to predict, diagnose, treat or prevent heart failure following a heart attack, Dr. Halade said. “If we can stratify risk among larger patient groups to determine who is deficient in SPMs critical for cardiac repair, we may be able to restore those targeted SPMs to improve outcomes.”

The study was supported by grants from the National Institutes of Health.

Heart failure affects about 6.5 million adults nationwide and leads to one in 8 deaths each year, according to the Centers for Disease Control and Prevention. The condition usually develops as the heart gradually loses its ability to pump enough blood through the body.

USF Health’s Dr. Kami Kim probes the epigenetics of two global parasitic infections, malaria and toxoplasmosis

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While an undergraduate at Harvard University, Kami Kim, MD, participated in a research thesis project exploring leukemia’s resistance to chemotherapy and the effectiveness of combination drugs in combatting it.  While she was excited to help figure out (and publish) a mechanism, she recalls that she signed on for this laboratory research primarily “to help in get into medical school.”

Her interest in research intensified in medical school in early 1980s at the beginning of the domestic AIDS era, about the same time tuberculosis cases were exploding and malaria, once considered virtually eliminated as a major public health threat, began to re-emerge globally.

“It was clear that there was much to be done in infectious diseases research — a lot of interesting problems that needed to be solved,” said Dr. Kim, who joined the USF Health Morsani College of Medicine last year as a professor in the Department of Internal Medicine’s Division of Infectious Disease and International Medicine.

Kami Kim, MD, a USF Health professor of infectious disease, with her multidisciplinary laboratory research team, which includes expertise from the medicine, public health, mathematics and statistics

 Undergraduate laboratory work that sparked a lifelong passion for research

Basic science and clinical infectious diseases expertise

After clinical training as an infectious diseases fellow at the University of California San Francisco (UCSF) – and witnessing firsthand the devastating consequences of acquired immunodeficiency syndrome – Dr. Kim returned to laboratory research, with an emphasis on parasitic infectious diseases.  Meanwhile, she continued to see patients as an attending academic physician at some of the nation’s best hospitals in San Francisco and New York City.

That blend of rigorous clinical and basic science expertise makes Dr. Kim one of the first of several high-profile, energetic recruits who will help take USF Health’s global infectious disease research to the next level.

Dr. Kim came to USF Health in November 2017 from Albert Einstein College of Medicine in New York City, where she was a professor of medicine, microbiology and immunology, and pathology.  In addition to her laboratory research at USF, she consults monthly on infectious diseases cases at Tampa General Hospital. At Einstein, she directed the infectious diseases section of the Center for Epigenomics and helped launch and led the National Institutes of Health-funded Geographic Medicine and Emerging Infections Training Program, which supports interdisciplinary training in translational research for pre-doctoral students, post-doctoral research fellows and clinical fellows.

A plaque formation of the intracellular parasite Toxoplasma gondii

Seeking solutions to life-threatening global parasitic diseases

Dr. Kim’s USF Health research team, working out of a laboratory in the university’s research park, focuses on two major areas — malaria and toxoplasmosis.  The world’s most dangerous parasitic disease, malaria claims more than 2 million victims and 445,000 deaths yearly, primarily in sub-Saharan Africa. Toxoplasmosis, often asymptomatic, can be life-threatening to babies born to women infected during pregnancy and people with weakened immune systems.

• Toxoplasmosis project: Combining advanced techniques from genetics, cell biology and proteomics, the researchers investigate the ways that epigenetics – the interface of genetics and environmental factors – regulate development of chronic infection by the cat-borne gondii parasite. They seek to understand how this pervasive parasite switches back and forth between a rapidly dividing acute stage destructive to healthy tissue (tachyzoite) and a chronic, or dormant, stage, where bradyzoite forms within pseudocysts remain invisible to the immune system. Dr. Kim collaborates with other leading Toxoplasma experts: Distinguished USF Health Professor Michael White, PhD, a long-time colleague, as well as investigators at Indiana University, Pennsylvania State University and Albert Einstein College of Medicine.
• Malaria project: In the hot, wet regions of Africa, mosquitoes are ubiquitous and children exposed to malaria from birth may contract the infection several time a year. The overwhelming majority of clinical cases are uncomplicated, with flu-like symptoms of fever and malaise that typically resolve. Researchers are trying to determine why a small percentage of individuals, in particular certain children, are more likely to develop severe malaria with coma and death (cerebral malaria) or long-term neurological complications such as seizures and cognitive and behavioral problems. In particular, the USF team is assessing specific biomarkers, or genetic predispositions, and parasite or host factors that may help predict disease development or its outcomes.

 Dr. Kim discusses research correlating HIV co-infection with cerebral malaria.

Research instructor Iset Vera

Both research initiatives harness the latest genomic technology to better understand how immunity works within the framework of host-parasite interactions – all with the aim of devising better or first-time treatments.

Valuable insights into cerebral malaria, future therapies

With collaborators from the Blantyre Malaria Project, based in Malawi, Africa, Dr. Kim published a high-profile paper in mBIO in 2015 reporting for the first time that children co-infected with HIV were much more likely than those who were not to die from severe malaria. Autopsies of the children who died from cerebral malaria indicated that those with HIV had brain blood vessels more clogged with white blood cells and platelets than those of children with malaria alone.  HIV appeared to rev up brain inflammation that could lead to death.

In another study, published in Cell Host & Microbe in 2017, Dr. Kim and colleagues used neuroimaging, parasite transcript profiling and laboratory blood profiles to develop machine-learning models of malarial retinopathy and brain swelling. The researchers found that the interaction of high parasite biomass, low platelet levels and certain parasite protein variants that bind to the endothelial protein C receptor (EPCR) play a pivotal role in fatal cases of malaria. Their findings added strength to the rationale that anti-inflammatory and anticoagulant treatments counteracting the breakdown of endothelium may benefit those with severe malaria.

“We still don’t entirely know why some of these kids get super sick and have complications requiring hospitalization,” Dr. Kim said. “If we could figure that out we could save lives, reduce complications and use limited healthcare dollars more effectively in these under-resourced countries.”

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 The “Goldilocks” theory of immunity

When it comes to infectious diseases, too much of a good thing may make you sick.  Dr. Kim calls it the “Goldilocks” theory of immunity – not too much (overactive immune system) and not too little (under-responsive immune system).

For instance, “for someone with malaria the right amount of immunity might not be just the right amount if they already also have tuberculosis,” Dr. Kim said. “What we’re realizing now with the human immune response to parasites or other foreign invaders (pathogens) is that you have to get the balance just right, so you get rid of the pathogen without damaging the human host.”

Otherwise, she added, even after the pathogen is eliminated, long-term complications like a damaging autoimmune inflammatory condition may linger.

Rigorously studying the dynamics of host-parasite interaction – including how parasites hijack the epigenome, which adjusts specific genes in response to signals from the outside world such as diet and stress — is critical to bridging the gap between discovery and effective treatments for different subgroups of infected patients.

“Both the pathogen and the infected host are duking it out to see which one wins, so figuring out what’s happening on both sides is really important to understanding immunity – how our body fights off disease,” Dr. Kim said. “Using genomic information to tell us who’s most susceptible to certain conditions will likely help us to tailor therapies to the individual, or perhaps to know who needs to be vaccinated.”

Dr. Kim with Li-Min Ting, PhD, an assistant professor in the Department of Internal Medicine’s Division of Infectious Disease

 Striking the right balance of immunity

Potential applications for other diseases

Within their complex life cycles, both malaria and toxoplasma parasites have dormant forms that the human immune system can’t identify and kill, and antimicrobial drugs can’t touch.  For malaria, this silent form lurks in the liver. For Toxoplasma, cysts can settle quietly into the infected person’s brain and muscle tissue without replicating, sometimes for years, until weakened immunity reactivates the disease.

Dr. Kim and other researchers continue to look for new ways to combat chronic infection by parasites.

“Normally when treating a disease you think of killing the form that makes a person clinically symptomatic,” she said, “but with both malaria and Toxoplasma if you can kill the biologically silent form, which is absolutely essential for the disease to continue, you’re accomplishing the same thing.”

Although Dr. Kim’s group targets specific problems underlying malaria and toxoplasmosis, such immune research may have broad applications for understanding and treating other conditions.  For instance, atherosclerosis has been linked to the release of molecules from the immune system that can cause inflammation, blood vessel injury and plaque instability leading to heart attacks and stroke.

A T. gondii plaque assay

“Even though drug companies, because of financial return on investment, aren’t necessarily willing to invest in research on malaria host factors,” Dr. Kim said, “they are really interested in stroke and cardiovascular disease.  And the big players in the kind of inflammation seen in these two major diseases are platelets and monocytes” – the same inflammatory culprits implicated in cerebral malaria.

While more research is needed, perhaps statin and antiplatelet drugs already approved for another indication could be effective in helping combat malaria,” she said. “It’s entirely possible by better understanding what’s a good immune response to malaria in one situation and bad in another will lead to insights that can be used to develop treatments for other diseases, or insight into what’s protective in another disease.”

Pursuing new approaches to outsmart elusive pathogens

Dr. Kim received her MD degree from the Columbia College of Physicians and Surgeons in New York City. She completed her residency in medicine at Columbia-Presbyterian Medical Center, a clinical fellowship in infectious diseases at UC San Francisco, and two postdoctoral research fellowships – one in parasitology at San Francisco General Hospital and a second in microbiology and immunology at Stanford University.

Dr. Kim is a fellow of the Infectious Diseases Society of America and the American Academy of Microbiology. She is also an elected member of American Society for Clinical Investigation and the Association of American Physicians, national honor societies for physician-scientists. A recipient of the Burroughs Wellcome Fund (BWF) New Investigator Award in Molecular Parasitology early in her career, she has served on the BWF Postdoctoral Research Enrichment Program’s scientific advisory board since 2014.  She is a member of the NIH Pathogenic Eukaryotes Study Section.

The cutting-edge tools of computational genomics contribute to Dr. Kim’s work.

Throughout much of her career, Dr. Kim’s research has been funded by the National Institute of Allergy and Infectious Diseases.  She holds several patents, and was one of the first investigators to develop techniques to genetically manipulate T. gondii. She is the co-editor and currently preparing the third edition of Toxoplasma gondii, the Model Apicomplexan: Perspectives and Methods, a textbook widely considered the seminal source for scientists and physicians working with this parasite.

Dr. Kim said she was attracted to USF because of the university’s upward national trajectory and USF Health leadership’s commitment to building translational research and pursuing innovative approaches and excellence in all its academic missions. She is a member of the USF-wide Genomics Program.

“I enjoy being part of a USF clinical community that excels in the treatment of infectious diseases and working with physicians and scientists who do parasitology research,” she said.  “You constantly have to think outside the box and come up with clever strategies – because we’re dealing with pathogens that do not behave like they are supposed to.”

 Toxplasma parasite strategy for survival

Dr. Kim, one of the first investigators to develop techniques to genetically manipulate Toxoplasma gondii, co-edits a textbook widely considered the seminal source for scientists and physicians working with this parasite.

Some things you might not know about Dr. Kim

• Korean was her first language, and she also speaks Spanish.
• She enjoys food, arts and crafts, and travel. Countries she has visited include Korea, Malawi, South Africa, France, Japan, and Brazil.
• Kim is married to Thomas McDonald, MD, USF Health professor of cardiovascular sciences and director of the new Cardiogenetics Clinic. They have two sons who are both mathematicians, one in a mathematics PhD program and the other in college. They met in the cardiac intensive care unit at Columbia Presbyterian Medical Center when Dr. McDonald was a resident and Dr. Kim was rounding as a medical student.

Dr. Kim’s career as an infectious disease physician-scientist bridges basic research and clinical practice.

-Video and photos by Torie M. Doll, USF Health Communications and Marketing