Here we report how variability in the human cytomegalovirus genome sequence may seriously affect the outcome of its molecular diagnosis. A real-time quantitative PCR assay targeting the major immediate-early gene failed to detect the viral load in some, but not all, clinical samples from hematooncological patients. By amplification and sequencing the DNA across the regions targeted by this assay we found a number of nucleotide substitutions which accounted for decreased primer/probe binding. This decreased the sensitivity of the assay up to 1,000-fold.

We report an 18-yr-old female patient with repeated CMV reactivations after HSCT treated by several pre-emptive courses of virostatic therapy. Seven months after HSCT, she developed CMV encephalitis/retinitis. Initial therapy with GCV and hyperimmune globulin failed, and later on GCV-resistant strain was detected. Continual increase of CMV DNA in peripheral blood led us to combined therapy with CDV and FCV, which was successful and free of severe renal toxicity. To our best knowledge, this is the first reported case of successful CMV treatment with a combination of CDV and FCV.

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A poor prognosis in chronic lymphocytic leukemia (CLL) is associated particularly with the presence of del(17p) aff ecting tumor suppressor gene TP53 . Th is deletion is in almost all cases of progressive leukemia accompanied by a mutation in the other TP53 allele, and in a smaller proportion of patients the TP53 mutation occurs also independently of del(17p) [1]. Recently, we demonstrated that patients with CLL harboring a missense mutation located in the p53 DNA-binding motifs (DBMs) (structurally well-defi ned parts of the DNA-binding domain) manifested a clearly shorter median survival in comparison with those having a missense mutation outside DBMs or a non-missense alteration [2]. However, a limitation of this study resulted from the unpredictable survival impact of diverse therapy given to patients with p53 mutations. Th e therapeutic approach currently taken for patients with CLL with loss and/or mutation of TP53 relies mostly on the use of agents which do not act through DNA damage followed by apoptosis induction. Th e success of this approach has been documented for the monoclonal antibody alemtuzumab.