Archana Joon is a postdoctoral researcher at Albert Einstein College of Medicine. She studies how herpes simplex virus (HSV) reshapes local immune environments to drive human immunodeficiency virus (HIV) persistence and acquisition. In this Postdoc Portrait interview, she discusses her fascination with biology and how it led her to her current research focus.
Biological Interconnections and Host Immune Reshaping
Q | What scientific problem are you trying to solve?
The scientific problem I am trying to solve is understanding the HSV/HIV syndemic, which refers to the interaction between HSV and HIV and how these infections worsen each other's impact on health. HSV-2 infection is highly prevalent among people living with or at risk for HIV and has been shown to increase both susceptibility to HIV acquisition and HIV transmission. Biological mechanisms such as genital ulcers, inflammation, and immune cell recruitment may facilitate HIV entry and replication. At the same time, HIV-induced immune suppression can increase the frequency and severity of HSV outbreaks. Understanding this syndemic is important because it highlights how co-occurring infections can amplify disease burden beyond the effects of either infection alone. My goal is to examine the biological factors that contribute to the HSV/HIV syndemic and identify opportunities for prevention, treatment, and improved health outcomes among affected populations.
Q | What drew you to immunology?
I was drawn to this research because I am fascinated by the ways biology, lived experience, and health inequities intersect. Working in immunology with samples from women has given me a unique window into questions that are both scientifically complex and deeply human. As I learned more about the relationship between HSV and HIV, I became increasingly interested in understanding them not as separate infections, but as a syndemic condition that interact and reinforce one another, often disproportionately affecting vulnerable populations.
What motivates me most is the opportunity to uncover mechanisms that could ultimately improve women's health. Handling patient samples has made the research feel tangible; behind every dataset is a person whose life may be affected by these infections. This perspective has strengthened my commitment to studying the immune responses that link HSV and HIV and to generating knowledge that can inform better prevention and care. For me, research is most meaningful when it bridges fundamental science with real-world impact, and this field allows me to do both.
Q | What’s one thing you learned from your research that you didn’t expect?
One of the most unexpected lessons from this research has been how dynamic and interconnected the immune system is. When I first began studying the relationship between HSV and HIV, I viewed them as two separate viral infections. What surprised me was the extent to which one pathogen can reshape the immune environment in ways that influence another.
Through studying the HSV/HIV syndemic, I learned that HSV is not simply a co-occurring infection: it can create persistent immune activation and alter the populations of immune cells that HIV targets. I was struck by how subtle changes in the local immune environment can have significant consequences for susceptibility, viral persistence, and disease progression. This shifted my perspective from thinking about individual pathogens to thinking about the immune system as a complex ecosystem where interactions matter just as much as the pathogens themselves.
This insight deepened my interest in immunology because it highlighted how much remains to be discovered about host-pathogen interactions and how understanding these mechanisms can lead to more effective prevention and treatment strategies.
Future Directions in Latency and Viral Reservoirs
Q | If your research succeeds, what could it change for science or society?
This work could deepen our understanding of how HSV shapes immune responses that influence HIV acquisition and persistence. By identifying the mechanisms that link these infections, we may uncover new targets for prevention and therapeutic interventions. More broadly, this work could help inform strategies that address both infections together rather than separately, ultimately improving outcomes for patients who are disproportionately affected by the HSV/HIV syndemic.
Q | What question are you most excited to answer next?
The question I am most excited to answer next is whether HSV-driven immune signaling can be leveraged to reverse HIV latency and expose hidden viral reservoirs. If we can better understand how these pathways influence HIV persistence, we may uncover new strategies to target the reservoir—the greatest barrier to achieving a cure.
Responses have been edited for length and clarity.
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