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45 - HCMV: persistence in the population: potential transplacental transmission
- from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HCMV
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- By Lenore Pereira, Departments of Cell and Tissue Biology, Anatomy, Pharmaceutical Chemistry, and the Biomedical Sciences Graduate Program, and the Oral Biology Graduate Program, University of California San Francisco, CA, USA, Ekaterina Maidji, Departments of Cell and Tissue Biology, Anatomy, Pharmaceutical Chemistry, and the Biomedical Sciences Graduate Program, and the Oral Biology Graduate Program, University of California San Francisco, CA, USA, Susan J. Fisher, Departments of Cell and Tissue Biology, Anatomy, Pharmaceutical Chemistry, and the Biomedical Sciences Graduate Program, and the Oral Biology Graduate Program, University of California San Francisco, CA, USA, Susan McDonagh, Departments of Cell and Tissue Biology, Anatomy, Pharmaceutical Chemistry, and the Biomedical Sciences Graduate Program, and the Oral Biology Graduate Program, University of California San Francisco, CA, USA, Takako Tabata, Departments of Cell and Tissue Biology, Anatomy, Pharmaceutical Chemistry, and the Biomedical Sciences Graduate Program, and the Oral Biology Graduate Program, University of California San Francisco, CA, USA
- Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
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- Book:
- Human Herpesviruses
- Published online:
- 24 December 2009
- Print publication:
- 16 August 2007, pp 814-830
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- Chapter
- Export citation
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Summary
Congenital cytomegalovirus infection and the placenta
Congenital CMV infection
Human cytomegalovirus (CMV) is a ubiquitous virus that causes asymptomatic infections in healthy individuals (for review see Pass, 2001). Because breast feeding (Stagno et al., 1980), exposure to young children (Pass et al., 1987) and sexual contact (Fowler and Pass, 1991) are major risk factors for infection, most adults are seropositive. Diverse organs and specialized cells, including polarized epithelial cells (Tugizov et al., 1996) and endothelial cells (Fish et al., 1998; Maidji et al., 2002), are susceptible to CMV infection. CMV establishes latent infection in granulocyte-macrophage progenitors (Kondo et al., 1996) and reactivates upon cellular differentiation (Hahn et al., 1998; Soderberg-Naucler et al., 1997). Congenital CMV infection is estimated to affect 1 to 3% of infants in the United States annually and remains an important public health problem causing significant morbidity and mortality (for review see Britt, 1999).
It has long been appreciated that maternal neutralizing antibodies reduce the risk of symptomatic congenital disease in the fetus (Ahlfors et al., 1984; Boppana and Britt, 1995; Fowler et al., 2003; Stagno et al., 1982). The importance of adaptive immunity to CMV is apparent in women with primary infection, often with low-avidity neutralizing antibodies (Boppana and Britt, 1995; Lazzarotto et al., 1998; Revello et al., 2002). Approximately 15% of these women spontaneously abort in early gestation (Griffiths and Baboonian, 1984).