CMV infection has led to the development of diagnostic procedures for the rapid identification of CMV disease
and infants with congenital infection.
Studies of children with symptomatic central nervous system congenital CMV disease
provide evidence of improvement (or lack of progression) in hearing loss in those treated with valganciclovir.
Even if they get the recommended 100 days of prophylaxis immediately following the diagnosis, 50 per cent still have CMV recorded in the blood following that and 36pc go on to suffer from CMV disease
(9) In more severe cases of immunosuppression CMV disease
can present as Guillain-Barre syndrome, myocarditis, thrombocytopenia, or meningoencephalitis.
The above-mentioned 82 patients coinfected with CMV included those with CMV viremia without definitive evidence of CMV gut involvement as well as those with CMV disease
of the gut.
CMV infection is defined as the virus detection in blood without clinical symptoms, but CMV disease
is viremia with clinical symptoms ranging from mononucleosis-like viral syndrome to less common tissue-invasive disease [11, 12].
In AIDS patients, extraocular CMV disease
seems to be a strong predisposing factor for developing CMV retinitis.
Clinically significant CMV disease
is typically seen in profound immunocompromised state such as in AIDS and bone marrow transplant patients.
A healthy immune system typically protects an infected person against CMV disease
, but does not prevent or clear latent infection.
 However, as CMV retinitis is asymptomatic in almost half of affected patients in the early stages of disease,  routine screening fundoscopy for those at high risk of CMV disease
by a trained clinician, not necessarily an ophthalmologist, is necessary.
International guidelines reported that CD4 cell level is less predictive of risk for CMV disease
in young infants with HIV, and CMV infection can occur in HIV-infected children with higher CD4 counts.
The pathogenesis is related to specific drugs, especially aromatic anticonvulsants, altered immune response, sequential reactivation of the human herpesviruses, and association with human leukocyte antigen alleles.[sup] The human herpesviruses reactivation such as human herpesvirus (HHV)-6, HHV-7, EBV, and CMV reactivation may stimulate proliferation of both viral-specific and nonspecific CD4 and CD8 T-cells, triggering massive cytokine release, and causing a hypersensitivity reaction.[sup] CMV disease
is usually seen in immunocompromised patients with HIV infection or postorgan transplantation under immunosuppressant.