Abstract
Congenital cytomegalovirus (CMV) infection may cause severe long-term sequelae. Recent studies have demonstrated that early antiviral therapy for infants with symptomatic congenital CMV (cCMV) infection may improve neurological outcomes; thus, accurate identification of newborns at high risk of cCMV infection may contribute to improved outcomes in affected children. However, maternal serological screening for cCMV infection by diagnosing primary infection during pregnancy, which is a popular screening strategy, is inefficient, because the number of cCMV infections with nonprimary causes, including reactivation of or reinfection with CMV, is larger than that of cCMV infections with primary causes. Low levels of neutralizing antibodies against pentameric complex and potent CMV-specific T cell-mediated immune responses are associated with an increased risk of cCMV infection. Conversely, our prospective cohort studies revealed that the presence of maternal fever/flu-like symptoms, threatened miscarriage/premature delivery, or actual premature delivery are risk factors for cCMV infection among both women with normal pregnancies and those with high-risk ones, regardless of whether the infection is primary or nonprimary. This review focused on host immune responses to human CMV and current knowledge of potential biological and clinical factors that are predictive of cCMV infection.
Highlights
Introduction published maps and institutional affilHuman cytomegalovirus (CMV) is the most common congenital viral infection and can lead to severe long-term neurological sequelae and even death in affected children.The prevalence of congenital CMV infection among newborns worldwide is estimated to be 0.7%, and 10–15% of infected fetuses have symptoms of cCMV infection at birth
This review focuses on host immune responses to HCMV and on the current knowledge of potential biological and clinical factors that are predictive of cCMV infection
Univariable and multivariable logistic regression analyses revealed that a maternal age of
Summary
Myeloid cells (i.e., monocytes, macrophages, and dendritic cells) play a key role in sensing HCMV infection and producing cytokines. These cells possess direct antiviral activities and play important roles in inducing adaptive immune responses [10]. HCMV can evade innate immune responses, for example, by impairing the antigen-presenting ability of myeloid cells by downregulation of major histocompatibility complex (MHC). The UL 16 and UL 142 glycoprotein of HCMV downregulate ULBPs, MICA, and MICB by causing intracellular retention of these ligand proteins [13,14,15]. HCMV evades NK cell attack by downregulation of the ligands of activating NK cell receptors. Decidual NK cells are thought to be important in preventing CMV transmission to fetuses in early pregnancy because these cells can exert cytotoxic activity when exposed to HCMV-infected decidual fibroblasts [17]
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