Herpes boosts the immune system and helps fight off other viruses.
Between 50 to 80% of all American 40-year-olds are infected with the herpesvirus CMV. “Yuck!” you may well be thinking: painful sores, ungainly blisters and infectious STDs come to mind. Luckily though, the majority of CMV carriers never show any such symptoms. Surprisingly, having CMV might not be as bad as you think. New research suggests that carrying a CMV virus might even have some surprising benefits.
Age is not just a number
Cytomegalovirus (CMV) is a member of the β herpes virus family that is present in most people around the world. Infections in healthy people usually go unnoticed, but they can be dangerous or life-threatening in immune-compromised patients such as the old, the very young, and the sick. All herpes viruses can persist in the body in latent (or dormant) forms. Latent viruses have integrated the viral genome into host cells, but are not currently producing virus. They can become reactivated later, which may cause other diseases or symptoms.
CMV remains latent in myeloid cells produced by the bone marrow. Many of these cells are vital for normal immune function, and the consequences of latent CMV infection have been debated. Some scientists have suggested that CMV promotes accelerated immunological aging because infection has been linked to immune dysfunction and chronic inflammatory diseases in older patients. However, some experimental studies indicate that CMV infection may improve immune responses to other infectious agents in younger people and mice. It is important to separate the effects of CMV infection from the effects of age, as normal immune function declines as a person gets older.
Immune system benefits
A recent paper attempted to examine the effect of CMV infection on the immune system and its dependence on an individual’s age. The study authors collected blood from old and young CMV positive and CMV negative donors. They measured multiple factors in the blood, including antibody levels, protein levels, and immune cell function. These variables were measured both before and after participants received a seasonal influenza vaccination.
Scientists found that as the age of the donor increased, immune function decreased regardless of CMV status. Surprisingly, CMV positive young adults show increased immune function as compared to CMV negative young adults after influenza vaccination. They had higher flu-specific antibody levels, increased T cell sensitivity, and higher levels of interferon gamma (IFN-γ) in their blood. Interferon gamma is a cytokine that plays a very important role in mediating host anti-viral immune responses.
When scientists repeated the experiments in mice, the results were the same. They determined that the positive effects of CMV infection were mediated by interferon gamma by repeating the experiment in IFN-γ knockout mice. Knockout animals have been genetically engineered to lack a certain gene. In this case, IFN-γ knockout mice can’t produce interferon gamma. Because the animals were not able to produce IFN-γ, they did not exhibit the improved immune responses that normal CMV positive animals displayed.
What about other herpes types?
The herpes virus family has many members. To determine whether the positive effects of CMV infection were unique to CMV, blood from patients with or without Epstein-Barr virus (EBV) infection was also analyzed. EBV is another widespread herpes virus, and is responsible for causing infectious mononucleosis. EBV infection showed no effect on immune cell function after influenza vaccination. The authors speculate that this may be due to the different sites of virus latency, and they conclude that they found no evidence to suggest that CMV infection accelerates immunological aging.
Surprisingly, a herpes infection may be good for something after all.
Furman, D., Jojic, V., Sharma, S., Shen-Orr, S., L. Angel, C., Onengut-Gumuscu, S., Kidd, B., Maecker, H., Concannon, P., Dekker, C., Thomas, P., & Davis, M. (2015). Cytomegalovirus infection enhances the immune response to influenza Science Translational Medicine, 7 (281), 281-281 DOI: 10.1126/scitranslmed.aaa2293