Dr. Grebenciucova of Northwestern University has received honorariums from AlphaSights, Medscape, and Trinity Partners for consulting work.)
Dr. Roos serves on the Scientific Advisory Board of Revalesio Corporation and a Data and Safety Monitoring Board for a clinical trial of a Mallinckrodt Pharmaceuticals product and Drug Monitoring Board for gene therapy study of Sarepta Therapeutics. He has also received consulting fees from Best Doctors and Guidepoint Network, and holds shares in Amgen, Merck, Ionis, and Express Scripts.)
Dr. Greenlee of the University of Utah School of Medicine has no relevant financial relationships to disclose.)
This article includes a discussion of congenital cytomegalovirus, intrauterine cytomegalovirus infection, prenatal cytomegalovirus, and cytomegalic inclusion disease. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Cytomegalovirus (CMV) is a ubiquitous agent responsible for most intrauterine infections. Besides well-known symptoms and findings such as hearing loss and microcephaly, congenital cytomegalovirus infection can also underlie certain cerebral anomalies and static leukodystrophies. In this article, the authors discuss uncommon presentations of asymptomatic congenital cytomegalovirus, predicted outcomes of congenital multi-strain cytomegalovirus infection, and updates on potential cytomegalovirus vaccines.
• Cytomegalovirus is the most common infection of the developing brain.
• Congenital cytomegalovirus infection can cause a host of cerebral abnormalities, including calcifications, ventriculomegaly, white matter lesions, cortical atrophy, and cortical migration abnormalities.
• Affected children can have neurologic impairments that range from sensorineural hearing loss to profound mental and motor deficits.
Historical note and terminology
In 1904, Ribbert described a stillborn infant with congenital syphilis who had large inclusion-bearing cells in the kidney (Ribbert 1904). A similar report followed (Jesionek and Kiolemenoglou 1904). These are probably the first cases of congenital cytomegalovirus described in literature. By 1921, it was postulated that the inclusions were due to an infectious agent, most likely a virus (Goodpasture and Talbot 1921; Lipschutz 1921). The agent was subsequently called "salivary gland virus," and the infection was referred to as "cytomegalic inclusion disease.” Murine cytomegalovirus was successfully grown in tissue culture in 1954 (Smith 1954). Two years later, human cytomegalovirus was isolated from congenitally infected children using similar techniques (Smith 1956; Weller et al 1957). The name "cytomegalovirus" was accepted in 1960 (Weller et al 1960).
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