Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- 41 HCMV: pathogenesis and disease consequences
- 42 HCMV: molecular basis of persistence and latency
- 43 HCMV: immunobiology and host response
- 44 HCMV: persistence in the population: epidemiology and transmisson
- 45 HCMV: persistence in the population: potential transplacental transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
45 - HCMV: persistence in the population: potential transplacental transmission
from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HCMV
Published online by Cambridge University Press: 24 December 2009
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- 41 HCMV: pathogenesis and disease consequences
- 42 HCMV: molecular basis of persistence and latency
- 43 HCMV: immunobiology and host response
- 44 HCMV: persistence in the population: epidemiology and transmisson
- 45 HCMV: persistence in the population: potential transplacental transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
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).
- Type
- Chapter
- Information
- Human HerpesvirusesBiology, Therapy, and Immunoprophylaxis, pp. 814 - 830Publisher: Cambridge University PressPrint publication year: 2007
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