blog

‘Know your status’ was this year’s theme for World AIDs Day. There are an estimated 36.7 million people living with the HIV virus. 1st December 2018 marked the 30th anniversary of this day dedicated to raising awareness and improving education about the virus, and to end the stigma associated with it.

Nicholas Funderburg is December’s Faculty Member of the Month. An Associate Professor with tenure at Ohio State University, US, he is investigating the link between HIV and the risk for cardiovascular disease. In this Q&A, he shares the research taking place at his Funderburg Lab, and explains the need for resilience when pursuing a career in research.

Please tell us a little about your work and research interests.

An estimated 1.1 million Americans are living with HIV, and while no cure exists currently, antiretroviral therapy (ART) has increased the lifespan of People living with HIV (PLWH). Yet, PLWH have nearly twice the risk for cardiovascular disease (CVD) as uninfected individuals. The causes of the increased risk are unknown.

My lab focuses on exploring the drivers of increased CVD risk in PLWH, including the complex interactions among monocytes, macrophages, and T cells that may promote atherosclerotic plaque growth and rupture. Results from our studies may provide insights into CVD risk in PLWH and the ageing population in general.

What triggered your interest in research and studying HIV?

I started doing research as an undergrad in the plant pathology lab of Dr. John McDowell. When I went to grad school, I wanted to apply the basic science lab techniques I’d learned in the McDowell lab to investigating human disease progression.

At Case Western Reserve University, I joined the lab of Dr Michael Lederman and was given an opportunity to explore HIV/AIDS pathogenesis in a lab that focused on translational research. In the Lederman lab I got the chance to learn about the immune system, join the AIDS Clinical Trials Group (ACTG), and I gained a great appreciation for the team work required to run large mechanistic clinical trials.

What research takes place at the Funderburg lab?

Overall, the goals of my lab are to understand the mechanisms behind chronic immune activation in HIV infection, how immune activation promotes increased CVD risk, and to design intervention strategies that reduce immune activation and CVD risk.

I’ve been at Ohio State for five years and have built a group of talented, hardworking young investigators in my lab. We’ve been involved in several studies, through the ACTG and independently, that have explored various strategies to reduce immune activation, including: testing the effectiveness and benefits of various ART regimens, reduction of immune activation through statin or aspirin treatment, and more recently, we’re exploring lifestyle interventions (i.e. diet and exercise) that may reduce pro-inflammatory lipid profiles in PLWH.

I’ve also been involved in the SATURN HIV trial, led by Dr. Grace McComsey, that demonstrated significant reductions in monocyte activation and inflammation in PLWH receiving rosuvastatin. This study, along with several others, helped justify the large clinical endpoint REPREIVE study that is actually measuring the clinical benefit of statin treatment in PLWH.

Briefly describe an article you recently recommended on F1000Prime and explain why you recommended the study?

Understanding the mechanisms related to differentiation of monocytes into tissue resident macrophages is likely to be important to the development of many inflammatory diseases, including CVD.

I recently reviewed an article, “Transcriptome-based network analysis reveals a spectrum model of human macrophage activation,” by Xue and colleagues that described experiments where monocytes were exposed to multiple cytokines and microbial products, and how these exposures influenced the phenotype and transcriptional profiles of the monocyte derived macrophages.

This work  describes the importance of the microenvironment and the signals it may provide to differentiating cells, and how these signals influence cellular function. Work like this will guide future clinical studies by providing information on targets for intervention.

What career advice would you like to pass on to early career researchers?

I would encourage early career researchers to be resilient and to surround themselves with the smartest people they can find, people from diverse thought backgrounds and expertise.

Working with talented people who challenge me to think in different ways makes my science better, and stokes the enthusiasm I need to overcome inevitable paper and grant rejections.