Researchers at the University of Illinois Chicago (UIC) have achieved a significant breakthrough by repurposing a cancer medication, doxorubicin, which has already received FDA approval, to combat strains of the herpes virus that have become resistant to conventional treatments. The findings of their investigation have been published in the esteemed journal, Drug Resistance Updates.
“This discovery presents an unforeseen and potentially rapid avenue for addressing herpes infections exhibiting drug resistance,” stated study lead Deepak Shukla, a virologist affiliated with the College of Medicine. “Infections caused by HSV-1 can have severe, occasionally life-threatening repercussions, and this therapeutic agent holds the promise of averting mortality.”
Individuals with compromised immune systems, such as those undergoing cancer therapy, are particularly susceptible to HSV-1 infections. Left unchecked, these infections can precipitate cerebral inflammation and lead to the failure of vital organs. The eradication of drug-resistant forms of the virus poses a considerable challenge.
In the year 2024, Dr. Shukla’s research cohort developed an advanced digital instrument named HerpDock. This sophisticated tool is designed to meticulously analyze vast databases of chemical compounds, identifying those with the potential efficacy against herpes infections. Doxorubicin, a well-established chemotherapy agent, was highlighted by this program.
The realization that doxorubicin is already sanctioned by the FDA was met with considerable enthusiasm. This is a crucial factor, as its safety profile and appropriate dosages are thoroughly documented. Consequently, this medication could be introduced to medical practitioners and patients considerably sooner than a novel therapeutic agent.
Deepak Shukla, virologist, College of Medicine, UIC
Dr. Shukla reported that during experimental evaluations, the drug demonstrated consistent effectiveness in inhibiting HSV-1 infections across various strains. This efficacy was observed in human cellular cultures, tissue models, and animal studies involving mice. Furthermore, it proved capable of neutralizing strains that had developed resistance to acyclovir, the standard antiviral medication for herpes.
An additional benefit observed is doxorubicin’s synergistic action with acyclovir. Acyclovir, when administered in high doses, can induce renal complications. The concurrent use of doxorubicin alongside a reduced dosage of acyclovir may lead to a more agreeable and less taxing treatment regimen for patients.
Rather than directly attacking the herpes virus itself, doxorubicin functions by obstructing a critical cellular pathway, specifically the PI3K–AKT–mTOR signaling cascade, which the virus exploits to infiltrate and seize control of host cells.
“The mechanism by which doxorubicin arrests the virus at its origin was a particularly exciting discovery,” commented postdoctoral researcher and lead author Pankaj Sharma.
Divya Kapoor, a contributing author and graduate student researcher at UIC, expressed that her involvement in this endeavor significantly contributed to her academic thesis and provided opportunities to acquire novel research methodologies.
“I found great satisfaction in participating in a project that possesses the potential to profoundly benefit humanity,” she remarked. “This breakthrough could serve to prevent mortality associated with herpes and enhance patient outcomes globally, including for individuals undergoing cancer treatment who are already receiving doxorubicin.”
Other contributors from UIC to this research include Sudhanshu Kumar Singh, Xiang Shen, and Chandrashekhar D. Patil, all from the College of Medicine.
