Abstract
Cytomegalovirus (CMV) permanently resides in its human-restricted host by toggling between productive and latent states of infection. CMV infection is serologically marked by immunoglobulin (Ig) G antibody against CMV. CMV seroprevalence varies widely by geographic region, ranging from 45% to 100% for women of reproductive age. In the US population, CMV seroprevalence is 50% overall and varies by age, socioeconomic status, sexual activity/practice, and race/ethnicity. Over 90% of all persons are CMV seropositive by age 80, 55% of women are seropositive by age 30, and the annual CMV seroconversion (primary infection) rate is ~2% for women of reproductive age. Congenital CMV infection afflicts ~1% of all babies born in the United States, is the leading infectious cause of birth defects, and the most common non-genetic cause of sensorineural hearing loss. CMV is transmitted through close mucosal contact with body fluids bearing infectious CMV particles, i.e., saliva, urine, breast milk, semen, and cervical secretions. Infants and young children experiencing a primary (acute) CMV infection often continue to shed CMV in urine and, sometimes, saliva for several weeks to months. Immunosuppression or underlying illness may bring about viral shedding in body fluids at any stage of the infection. CMV persists in virtually all tissues and resides latently in monocytes, dendritic cells, and myeloid precursors. Viable tissue or leukocytes of CMV-seropositive donors are a source of CMV infection in seronegative persons. Risk for intrauterine CMV transmission is greatest for maternal primary CMV infection and less for reinfection with another CMV strain or CMV reactivation.