Rheumatology Research Laboratory

Basic Science Research
Herpes is a familiar term because of cold sores and genital lesions that are caused by herpes simplex virus. But herpes is more than herpes simplex virus. The term Herpesviridae refers to a large family of viruses, including Epstein-Barr virus, cytomegalovirus, and Kaposis sarcoma-associated herpesvirus that cause diseases ranging from a mild rash to cancer.

All humans are infected with multiple herpesviruses by adulthood. However, unlike most viruses, herpesviruses are never cleared—that is, the immune system never eliminates these viruses from the body. Rather, they persist in certain cells for the life of the host. Most of the time there are no symptoms to reveal the underlying infection. During this period the virus is in a state of relative dormancy called latency. Latency, however, is frequently punctuated later in life by viral reactivation. Reactivation, unfortunately, is frequently associated with severe disease.

For decades, latency has been assumed to be detrimental to the health of the host because it puts the host at risk for reactivation. Interestingly, we recently discovered that herpesvirus latency in mice activates the host innate immune system (macrophages and natural killer cells) and thereby provides a potential benefit to the host by increasing the host's resistance against bacteria and tumors.

Our current research aims to understand how, at a molecular level, herpesviruses interact with the host immune system during latency. This work involves the generation and testing of new viral mutants for their ability to alter the host immune system. These studies are pursued in collaboration with Drs. Erik Barton at Wake Forest University, Laurie Krug at Stony Brook University, and Craig Forrest at the University of Arkansas.

Human Studies
In addition to the basic science studies described above, we participate in human studies through the CORRONA database and an investigator-initiated study measuring the prognostic value of a novel blood test (called the interferon signature) in patients with autoantibodies in their blood (antinuclear antibodies, or ANA). Some patients with a positive ANA go on to develop systemic lupus erythematosis or another autoimmune disease, yet many remain healthy. Our hope is that this new blood test will help clinicians distinguish between these two possibilities. This study, which enrolled its first subjects from Gundersen Lutheran in August of 2010, represents a collaboration with Dr. Erik Peterson at the University of Minnesota.

Please contact Dr. Douglas White (dwwhite@gundersenhealth.org) for an update and more information.

Back to Top