Prestigious Pew Award Goes to the UA’s Felicia Goodrum

[Source: University Communications, University of Arizona] - Felicia Goodrum, a virologist in the department of immunobiology at The University of Arizona College of Medicine and a member of the BIO5 Institute, has won a 2008 Pew Scholars Program award for her work on latency in virus infections.

The award is worth $60,000 a year for four years. It is the UA’s second Pew award, following an award in 2007 to BIO5 member Joanna Masel, an assistant professor in the UA’s department of ecology and evolutionary biology.

The Pew Scholars Program in the Biomedical Sciences supports young investigators of outstanding promise in the basic and clinical sciences relative to the advancement of human health. The funding of the awards is provided by the Pew Charitable Trusts. The award provides assured support, during their earlier years, for junior members of the faculty as they establish their laboratories.

Goodrum, who has a joint appointment in the department of molecular and cellular biology and conducts research in collaboration with experts around the world, works at the forefront of research on how a virus persists within the human body.

In particular, her team is studying a member of the herpesvirus family called cytomegalovirus, or CMV, and how it infects humans and then lays low, or as virologists put it, shifts into latency, without causing disease.

CMV is a virus that inhabits most people from childhood, and that brings little harm, if any, for many years until the host reaches a vulnerable stage. It made headlines in 1981 when it slowed Pope John Paul II’s recovery from a bullet wound suffered in an assassination attempt.

The people most vulnerable to CMV are people who need any kind of transplant – including a liver, a kidney or bone marrow – or have HIV or are being treated with drugs for cancer. In each case, the immune system is weakened and the latent CMV will come to life – reactivating itself, starting to replicate and spread.

How it establishes latency or knows just when to reactivate is something virologists don’t yet understand, Goodrum said.

Virologists have been asking those questions for decades without a breakthrough, but Goodrum says her lab is making fresh inroads employing the new tools in genetics and biochemical, cell biological and molecular techniques. Her lab has recently identified the first molecular factor – a gene – that functions to control CMV latency.

“We’re pushing the envelope,” Goodrum said. “We will use genetic and cellular models and techniques for manipulating the virus that weren’t available in the past.”

Her lab also is taking a novel approach with human cells, called hematopoietic cells, or ones that create blood.

For transplant patients who have been treated with antiviral therapies only to have CMV reactivate later, the fatality rate from CMV can reach 50 percent, Goodrum said. Such treatments must be limited in time because the drugs are toxic, and once they are stopped, if the immune system is still weak the virus becomes free to replicate.

CMV offers a sharp contrast with Ebola, the virus known as a notorious bad guy that kills every one of its hosts, a kind of Sweeney Todd of the virus underworld. Instead, CMV has evolved to coexist in infected humans without causing disease as long as the host has a health immune system.

“CMV is stealthy,” Goodrum said. “It usurps our immune defenses in order to hide. The latent infection was once considered benign in healthy people, but it is becoming more apparent that there is a price that we pay for carrying this virus.

“The coexistence of this virus with us appears to gradually erode our immune system, leaving us more susceptible to other pathogens as we age. Understanding latency is critical to preventing even the less overt CMV pathologies.”