Human Cytomegalovirus Infection and Disorders of the Nervous System

Human Cytomegalovirus Promotes Survival of Infected Monocytes via a Distinct Temporal Regulation of Cellular Bcl-2 Family Proteins

“…In contrast, HCMV infection leads to significant morbidity and mortality in the immunocompromised. HCMV is an important opportunistic pathogen in AIDS patients (16)(17)(18)(19)(20), is a leading infectious cause of complications in transplant recipients (21-28), and causes severe neurological disease in congenitally infected neonates (29)(30)(31)(32)(33)(34).HCMV pathogenesis and disease result from viral spread to multiple organ sites following primary HCMV infection, a process which appears to be a critical step in the viral persistence strategy, as it allows for the establishment of lifelong persistence within the host, as well as for viral shedding and spread to additional hosts (1,35,36). Monocytes are the primary blood-borne targets for HCMV infection and are thought to be centrally involved in the hematogenous dissemination of the virus to target organ systems (37-41).…”

“…In contrast, HCMV infection leads to significant morbidity and mortality in the immunocompromised. HCMV is an important opportunistic pathogen in AIDS patients (16)(17)(18)(19)(20), is a leading infectious cause of complications in transplant recipients (21)(22)(23)(24)(25)(26)(27)(28), and causes severe neurological disease in congenitally infected neonates (29)(30)(31)(32)(33)(34).…”

Maintenance of Large Numbers of Virus Genomes in Human Cytomegalovirus-Infected T98G Glioblastoma Cells

“…In immune immature fetuses, congenital HCMV infection is the most common viral cause of birth defects, particularly disorders of the central nervous system (CNS). Among congenitally infected newborns, approximately 5% to 10% manifest serious neurological defects at birth, including microcephaly, hydrocephalus, and cerebral calcification (2)(3)(4)(5)(6). In addition, 10% to 15% of infants suffering congenital infections are asymptomatic at birth but subsequently develop late-onset sequelae, including sensorineural hearing loss (SNHL), mental retardation, and learning disabilities.…”

“…Coverslips were blocked with 4ϫ SSC (1ϫ SSC is 0.15 M NaCl plus 0.015 M sodium 8.0], 150 mM NaCl, 0.05% Tween, and 0.5% BSA) for 10 min. After extensive washes in 4ϫ SSC-0.1% Tween (PBD), coverslips were incubated with sheep anti-mouse IgG DIG-conjugated secondary Ab [F(ab) 2 fragments] (Chemicon International, Temecula, CA) diluted in TNB solution for 10 min followed by washes in PBD. Coverslips were incubated with anti-DIG-rhodamine Fab fragments (Roche) diluted in TNB for 10 min followed by repeated washes in PBD.…”

Concordancia entre una función de crecimiento del perímetro cefálico y la discapacidad intelectual en relación con la etiología de la microcefalia

“…Un estudio sobre la rubéola congénita 15 mostró una capacidad intelectual normal en presencia de microcefalia cuando se excluyó a niños con pérdidas de audición y visión. Por el contrario, en un estudio de la infección congénita por citomegalovirus se observó que la microcefalia era el predictor precoz más específico de retraso mental 16 , mientras que la mayoría de los niños con infecciones congénitas no desarrolló trastornos neurológicos 17 . En su estudio de recién nacidos de muy bajo peso, Hack y Breslau 18 observaron que el PC a los 8 meses de edad era el factor relacionado con el crecimiento que mejor predecía el coeficiente intelectual a los 3 años de edad.…”