OHSU Researchers Discover Host Site, Activation Mechanism For Virus That Causes Birth Defects And Deaths Following Transplant

October 02, 1997

Researchers in Oregon Health Sciences University's Department of Microbiology and Immunology have zeroed in on the host cells and the activation mechanism for a virus that is the leading viral cause of deaths in bone marrow transplant and AIDS patients as well as the major viral cause of birth defects.

In an article being published in the October 3rd issue of Cell magazine, researchers Cecilia Soderberg-Naucler, M.D., Ph.D., and Jay Nelson, Ph.D., focus on human cytomegalovirus (HCMV), one of eight herpes viruses found in roughly 60 percent of the population in first-world countries. Most individuals become infected early in life and the incidence of infection has increased with the proliferation of day-care centers. The virus remains latent (or inactive) in most of those infected, but can cause severe and sometimes fatal flu-like symptoms in people whose immune systems are compromised (such as AIDS patients or transplant recipients). HCMV acquired during pregnancy can lead to mental retardation, deafness and blood disorders in infants. Studies have shown HCMV can be transmitted through transfer of bodily fluids or tissue, but until now, researchers have not identified the cells that harbor the virus.

Soderberg-Naucler and Nelson were able to reactivate HCMV in specific white blood cells (called monocyte-derived macrophages) found in the blood of healthy donors. "Our study not only identifies the cell type that harbors the virus, but also shows the mechanism of how the virus comes out of those cells," says Nelson.

The basic research technique was simple. "We mixed cells from two different people," says Nelson. "That activated the virus." A number of factors can serve as the "trigger" that reactivates HCMV. Introduction of foreign body fluids or tissue (through a blood transfusion or an organ or bone marrow transplant) can cause the virus to reactivate. So can the presence of other viruses or bacterial infections in those carrying latent HCMV. While viral reactivation in transplant patients has been observed for some time, this study marks the first time researchers have both been able to "wake up" the virus and recover the infectious virus from a specific cell type in a laboratory setting.

This research, funded in part by the National Institutes of Health, could have important clinical applications. In addition to contributing to birth defects and transplant deaths, HCMV has also been implicated in rejection of transplanted organs and acute graft-versus-host disease in bone marrow transplant patients. Identifying the cells where latent HCMV resides and how they're reactivated could help in development of more effective treatments than those currently available. "If we can understand how it's activated, we can come up with techniques to block it," says Nelson.

Oregon Health & Science University

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