By Prim. Univ.-Prof. Dr. Gabriele Halwachs-Baumann MSc, MBA (eds.)
Congenital cytomegalovirus (CMV) an infection is the commonest intrauterine transmitted viral an infection, with an enormous influence on fetuses and newborns. during this e-book the background of this disorder, its pathophysiological historical past, epidemiology and indicators, in addition to diagnostic and healing techniques, can be mentioned. on the grounds that financial elements are gaining progressively more value in overall healthiness politics, one bankruptcy is devoted to this factor within the context of congenital CMV an infection. The content material relies at the most modern clinical findings and written in an comprehensible demeanour, permitting folks now not operating within the box of congenital CMV to additionally benefit from it. therefore, this publication is of curiosity for doctors, nurses, midwives, economists, but additionally for women and men who are looking to tell themselves approximately this topic.
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Extra info for Congenital Cytomegalovirus Infection: Epidemiology, Diagnosis, Therapy
The eﬀects of CMV on dendritic cells depend on the state of maturation and on the DC subsets. Infection of immature DCs leads to increased cell death and altered chemokine receptor expression (CCR1 and CCR5 downregulation) leading to altered migration properties . Moreover, the ability of DCs to migrate to the lymph nodes and presentation of antigen to T cells is blunted by the inhibition of the expression of T cell costimulatory molecules such as CD80, CD83, CD86 as well as MHC class I and II, and reduction of CCR7 expression, resulting in a lack of antigenspeciﬁc stimulation of T cells and inhibition of Th1 and Th2 response [45, 47].
The CD8+ T lymphocytes enact their eﬀector functions through lysis of infected or antigen-presenting cells and by localized delivery of cytokines to infected cells (particularly IFN-γ and TNF-α). If the host has previously encountered the virus, any freshly infected cell will present its viral antigens in the context of MHC class I to these already primed exterminators, permitting more rapid clearance of virus-infected cells . The predominant CD8+ T lymphocyte response following CMV infection was initially proposed to be directed against a limited set of virus-encoded antigens.
This hypothesis could be one explanation for the phenomenon that the unborn child is aﬀected only in about 50 % of primary CMV infections of the mother. Yet in every second primary maternal CMV infection the virus crosses the placenta. This takes about 3 weeks, as was shown in explants of ﬁrst-trimester human placenta, and the virus is passed from the trophoblasts to the stromal ﬁbroblasts and fetal endothelial capillary cells . In the case of CMV infection of the placenta, the virus alters and modiﬁes trophoblast cell functions.