4. Discussion
Infants or children infected with HCMV are prone to missed diagnosis
because the vast majority of infants and children are mainly
characterized by occult infection. However, CMV can cause some infants
with corresponding complications such as low cellular immune function,
deafness and mental retardation.
In the process of HCMV infection, the number, distribution and
proportion of WBC in peripheral blood may change. In a retrospective
study, it was found that WBC and L% in pneumonia children with HCMV
infection within 6 years were higher than those respiratory infection
caused by other viruses but no bacterial infection 15.
Moreover, in HCMV-infected children within 3 months,their WBC and LYM
were higher than those in normal group (P <0.01)16. In this study, we found that the LYM and L% of
HCMV-infected children aged 0d-6y were higher than control group, but
not all WBC of HCMV-infected children aged 0d-6y were higher than
control group. We speculate that the reason may be related to the
occurrence of autoimmune neutropenia after HCMV infection or neutropenia
caused by ganciclovir treatment 17, 18. Further
studies have found that HCMV can induce specific changes in lymphocyte
subsets, which mainly show that HCMV-positive people have more
lymphocytes, CD8+T cells and CD28+T cells, and the ratio of CD4+/ CD8+
cells decrease 19. Moreover, some scholars believe
that CD4+ and CD8+T lymphocyte reaction is related to HCMV infection
rate and mortality 20, so lymphocyte response plays an
important role in controlling HCMV infection.
CMV has a wide tropism to cells, and the liver and gallbladder are also
the prone organs of CMV infection. The main manifestations of HCMV liver
injury in children are jaundice, hepatomegaly and cholestasis. A
significant association between HCMV antibodies and liver enzymes (ALT,
AST, and GGT) was found in a HCMV-screening of 455 patients with liver
dysfunction 21. In 49 children with HCMV between 7
days and 32 months of age, Alt and AST were elevated in all patients and
26.5% suffered from cholestasis 22. Goel et al. found
that 52% newborns with cholestasis had HCMV in their liver23, and a report showed that HCMV can also cause acute
cholecystitis in adults with normal immunity 24. These
results suggest that HCMV infection may cause liver and biliary system
damage in children. In our study, HCMV-infected childrens’ GGT, ALT, and
AST were significantly higher than their corresponding control group.
But not all children infected with HCMV showed abnormal liver function.
About 50% of infants who have been exposed to cervical and vaginal
secretions containing HCMV during perinatal period and 50%-60% of
infants who have eaten breast milk containing HCMV after birth will
develop HCMV infection 25. In addition, our data
showed that the damage of HCMV to gallbladder and bile duct in children
aged 0-21d is greater than that to liver, and the damage of HCMV to
liver and gallbladder will be weakened with the growth of infant age. we
speculate the reason may be related to the maturation of the infant
immune system.
HCMV can replicate in the renal tubules of congenital HCMV-infected
children and excrete in urine, which suggests that kidney is the target
organ of HCMV 26. Infants and children are generally
susceptible to CMV, but there are few reports about kidney damage caused
by CMV infection in infants and children 27. It is now
known that HCMV infection is part of major infection complications
following kidney transplantation 28. In addition, it
has been found that HCMV reactivation can lead to an increase in UREA
and CREA in patients with sepsis, and these variables are correlated
with viral load, but infection with the virus may not be associated with
an increased risk of renal malformation 29. Our data
showed that the renal function was no statistical difference between
HCMV-infected childrens’ and their control groups. Therefore, it can be
considered that renal dysfunction caused by HCMV infection is a rare
event. In addition, it can also be considered that the degree of renal
damage caused by HCMV infection is relatively light, and some more
sensitive indicators are needed to monitor.
In addition, the CREA of HCMV-infected children aged 0d-21d was
significantly higher than other age groups, but it was no significant
difference compared with control group. The reason may be that the CREA
of the newborn reflects the state of the mother’s renal function, and
within 1-2 weeks after the baby is born, CREA will gradually decrease
and turn into the real creatinine of the baby 30。