MBLdeficiency is thought to be a risk factor for the development
of viral infection, such as genital herpes and HSV-2 meningitis.
However, there is limited data on the possible interaction
between MBL and CMV, especially after organ transplantation.
Between 2003 and 2005, we measured MBL levels in 16 kidney
transplant recipients with high-risk CMV serostatus (donor
positive/recipient negative, D+/R−). All patients receivedCMV
prophylaxis of valganciclovir 450 mg/day for 3 months after
transplantation. After stopping valganciclovir, CMV-DNA was
measured in whole blood by real time PCR every 2 weeks for 3
months. CMV infections were diagnosed according to the recommendations
of the AST. MBL levels were measured in stored
pre-transplantation sera by an investigator blinded to the CMV
complications. MBL levels below 500 ng/ml were considered as
being functionally deficient.
After a follow-up of at least 10 months, seven patients out
of 16 developed CMV disease (three CMV syndrome, and
four probable invasive disease, i.e. two colitis and two hepatitis),
four patients developed asymptomatic CMV infection,
and five patients never developed any sign of CMV replication.
Peak CMV-DNA was higher in patients with CMV disease
than in those with asymptomatic infection (4.64 versus 2.72
mean log copy CMV-DNA/106 leukocytes, p < 0.05). Overall,
9/16 patients (56%) had MBL deficiency: 5/7 (71%) of patients
with CMV disease, 4/4 (100%) of patients with asymptomatic
CMVinfection, and 0/5 (0%) of patients withoutCMVinfection
(p < 0.005, between CMV infection/disease versus no infection
or control blood donors). There were no significant differences
in age, gender or immunosuppressive regimens between the
groups. MBL deficiency may be a significant risk factor for the
development of post-prophylaxisCMVinfection in D+/R−kidney
recipients, suggesting a new role of innate immunity in the
control of CMV infection after organ transplantation.