Cytomegalovirus (CMV) is a common virus that can infect almost anyone. Once infected, your body retains the virus for life. Most people don’t know they have CMV because it rarely causes problems in healthy people. But if you’re pregnant or have a weakened immune system, CMV is cause for concern. A woman who develops an active CMV infection during pregnancy can pass the virus to her baby; who might then experience signs and symptoms. For people with compromised immunity, especially due to organ transplantation, CMV infection can be fatal.

Newborns infected with CMV before birth

CMV spreads from person to person through body fluids, such as blood, saliva, urine, semen and breast milk. There’s no cure for the virus. However, medications can help treat newborns and people with weak immune systems. Most people infected with CMV who are otherwise healthy experience few if any signs and symptoms. People at greater risk of signs and symptoms of CMV include, newborns infected with CMV before birth (congenital CMV), infants who become infected during birth or shortly afterward (perinatal CMV). This group includes babies infected through breast milk, people with weakened immune systems, for example due to organ transplant or HIV infection.

Cytomegalovirus (CMV) infection can convert a harmless, inhaled protein antigen into an allergen, according to a study published in the open-access journal PLOS Pathogens by Rafaela Holtappels from the University Medical Center of the Johannes Gutenberg-University Mainz, and colleagues. According to the authors, the findings suggest that CMV airway infection significantly enlarges the spectrum of potential environmental inducers of allergic airway disease.

CMV infection of the airways activates dendritic cells

CMV infection of the fetus causes birth defects, and in immunocompromised patients, CMV infection of the lung can result in life-threatening pneumonia. Holtappels and colleagues add a novel aspect of how CMV can contribute to airway disease. Primary infection with CMV occurs in early childhood and involves the airway mucosa, where CMV and inhaled environmental allergens can meet. This medically relevant situation was studied experimentally by using a mouse model of airway co-exposure to CMV and ovalbumin — a protein antigen with inherently low allergenic potential.
Ovalbumin exposure or CMV infection alone failed to sensitize for allergic airway disease. By contrast, airway infection with CMV at the time of ovalbumin sensitization predisposed for allergic airway disease. This effect was mediated by activation of airway dendritic cells. The results show that even a protein antigen; that has low-to-no allergenic potential on its own can sensitize for allergic airway disease; when CMV activates airway dendritic cells for more efficient antigen uptake.

According to the authors, future research should focus on defining the conditions; under which CMV airway infection could possibly contribute; to the development of full-blown asthma. The authors add, “CMV infection of the airways activates dendritic cells; for a more efficient uptake of inhaled environmental antigens of otherwise; low-to-no intrinsic allergenic potential. This mechanism sensitizes detrimental immune cells; that can cause allergic airway disease after antigen re-exposure.”