cytomegalovirus infection among children with blood diseases

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CYTOMEGALOVIRUS INFECTION AMONG CHILDREN WITH BLOOD
DISEASES
Abstract
Cytomegalovirus (CMV) is ubiquitous agent that commonly infects people throughout
the world. Although most CMV infections are asymptomatic, symptomatic infections
occasionally result. CMV is a member of herpes virus group. Following primary
infection, it is believed that CMV, like other herpesviruses, remains latent in the host
cells for lifetime. The latent virus may be abruptly reactivated under certain natural
(pregnancy) or iatrogenic conditions (immunosuppression) and results in productive
infection.
In developing countries CMV infection is acquired very early in life. Infants and children
acquire CMV from their mother, either at birth or during the perinatal period, or from
infected contacts.
Repeated blood transfusion is one of the main methods of transmission of CMV.
Aside from being the major control for virulence, the host immune response is apparently
the main controlling factor for maintaining the latent state in sero-positive population.
Depression of cell-mediated immunity (CMI) may result in CMV chronic infection or in
prolonged virus shedding, in spread of the virus and in superinfection with other agents.
In immunosuppressed population depression of CMI causes reactivation of CMV
infection in the majority of CMV l sero-positive individuals.
Blood diseases in infants and children may be associated with depressed CMI. CMV has
been recovered from the blood and urine of children with leukemia and lymphoma.
This study was undertaken to assess the frequency of CMV infections among these
patients at King Abdulaziz University Hospital in Jeddah (KAUH).
The subjects of the study were twenty seven children suffering from different malignant
diseases who were under chemotherapy. Twenty two children were included in the study
as control. Human foreskin fibroblast (HFF) cell culture were employed gor virus
isolation from urine, throat swab and peripheral blood lymphocyte samples from both
patients and controls. Immunofluorescence identification of CMV isolates using
monoclonal antibodies was performed on all infected cultures. Antibodies for CMV in
sera were detected by enzynme-linked immunosorbant assay (ELISA) IgM and IgA and a
latex agglutination for (IgG).
Correlation between the results of CMV isolation by culture and the presence of serum
immunogamma-globulin G (IgG), M (IgM) and A (IgA) specific to CMV was evaluated.
All patients showed seropositivity to anti-CMV IgG. Eighteen patients with CMV sero
positive for anti-CMV IgG showed no evidence of active infection or excretion of CMV.
Two patients of the remaining nine patients showed serpositivity with excretion of
CMVin the urine but with no evidence of active infection and the other seven patients
developed active CMV infection presented by excretion of CMV from one or more body
sites, elevated serum or non-elevated serum anti-CMV IgG and with or without the
presence of the anti-CMV IgM. Out of these nine patients, two had evidence of primary
infection as indicated by the presence of serum anti-CMV IgM and absence or low antiCMV IgG in the first sampling and the remaining seven patients had latent CMV
reactivation episode.
The presence of anti-CMV IgA had no relation neither to the excretion of CMV, nor to
the elevated anti-CMV IgG and to positive anti-CMV IgM.
Among the control subject twenty out of twenty two showed presence of anti-CMV IgG.
Two had no anti-CMV IgG, eight had 1:2, seven had 1:4, one had 1:8, two had 1:16, one
had 1:32 and one had 1:64. None showed evidence to CMV excretion. None had positive
anti-CMV IgM. Thus, there was no CMV active infection in control subjects presented
on the basis of the absence of the excretion of CMV in any sample and the absence of
anti-CMV IgM in the serum, though anti-CMV IgG indicated past exposure to CMV in
early childhood.
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