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Cytomegalovirus (CMV), an enveloped, double stranded DNA betaherpesvirus, is species-specific and has a slow replication cycle. Nearly a century ago, pathologists reported that postmortem examination of infants less than 1 year of age often revealed large cells containing intranuclear and cytoplasmic inclusion bodies in submandibular salivary glands and, less frequently, in livers, lungs, kidneys, pancreas and thyroid. The large cells ("cytomegalia") were found in acini and ducts of the infected salivary glands and the ducts were often dilated. By the 1950s, human CMV was isolated and it became apparent that CMV infection was common (from birth to adulthood). CMV establishes a long-lasting persistence in salivary glands and the virus is shed in saliva for months to years before termination of productive infection and establishment of latency. Human clinical studies and mouse models clearly demonstrate that CMV disrupts organ and tissue development, most frequently that of the central nervous system (microcephaly, mental retardation, deafness and blindness). About 1 in 500 newborns will exhibit major CMV-induced congenital pathology, making CMV one of the most common causes of major birth defects in humans. Recent studies in our laboratory has demonstrated that branchial arch derivatives (submandibular salivary gland, mandible, and teeth) are vulnerable to CMV infection during critical stages of their organogenesis, and that CMV has a particular tropism for neural-crest-derived ectomesenchyme.
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