INTRODUCTIONPerinatal infection was the main cause of neonatal liver damage, especially the fetal infection caused by TORCH syndrome (ie, toxoplasmosis, listerellosis, rubella virus, cytomegalovirus and herpes simplex virus). Human cytomegalovirus (HCMV) was widely located in the nature, and the positive rates of HCMV antibodies were, respectively, around 95% among pregnant women and 83.2% among children in China. Infection of HCMV could induce proportional changes of the subsets of T lymphocyte cells within infants, and determination of the cell subsets was of significance to judging the severity of active HCMV infection and guiding early‐stage treatment. Besides, liver not merely regulated the digestion, metabolism and endocrine systems, but also participated in the immune adjustment. For instance, there existed diverse immunoregulation‐related cells within liver (eg, Kupffer cell, dendritic cell and lymphocyte), and the cells were responsible for antigen presentation, engulf of pathogens, as well as secretion of cytokines and antibodies. To sum up, HCMV was vital for prediction of neonatal liver damage, and the genetic mechanisms underlying HCMV was hypothesized to partly explain the presence of neonatal liver damage.Toll‐like receptors (TLRs), which belonged to the pattern recognition receptor (PRR), were considered to count much in both innate immunity response and acquired immunity
Journal of Clinical Laboratory Analysis – Wiley
Published: Jan 1, 2018
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