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CMV HSCT (Introdução (CMV acquisition in a popula- tion is characterized…

- - - - Eighty-
        seven possible publications related to CMV
        infection in hematopoietic stem cell transplant
        patients were found.
        
        After exclusion of nonrel-
        evant, non-English, and review articles, poten-
        tially relevant articles were selected. Sufficient
        data available for further analysis of the role of
        risk factors were found in nine articles for early
        or late CMV infection and three articles for
        CMV disease. In the analysis of the raw data,
        odds ratios (ORs) and 95% confidence intervals
        (CIs) were determined.
  - - - CMV infection is defined as virus isolation or
        detection of viral proteins (antigens) or
        nucleic acid in any body fluid or tissue
        specimen
      - ‘‘CMV replication’’ indicates evidence of viral
        multiplication and is sometimes used
        instead of ‘‘CMV infection.’’
      - Primary CMV infection is defined as the first
        detection of CMV infection in an individual
        who has no evidence of CMV exposure.
      - Recurrent CMV infection is defined as new
        CMV infection in a patient with previous
        evidence of CMV infection in whom the
        virus has not been detected for at least
        4 weeks during active surveillance. Recurrent
        infection may result from reactivation of
        latent virus (endogenous) or reinfection
        (exogenous).
      - CMV reinfection is defined as detection of a
        CMV strain that is distinct from the strain
        that caused the initial infection.
      - CMV reactivation is likely if the two viral
        strains (prior and current strain) are found to
        be indistinguishable either by sequencing of
        specific regions of the viral genome or by use
        of a variety of molecular techniques that
        examine genes known to be polymorphic.
      - Symptomatic CMV infection is diagnosed in
        patients developing symptoms (fever with or
        without bone marrow suppression) and who
        have CMV virions, antigens, or nucleic acid
        detectable but with no sign of CMV end-
        organ disease [
        3
        ].
      - CMV disease is diagnosed in a patient with
        symptoms and/or signs from the affected
        organ together with detection of CMV by a
        test with appropriate sensitivity and speci-
        ficity from an organ in a biopsy sample or
        samples from other invasive procedures,
        with exception for CMV retinitis, for which
        typical findings from ophthalmologic exam-
        ination are sufficient [
        3
        ]
      - Definitions on treatment of CMV: ‘‘prophy-
        laxis’’ means that antiviral agents are given
        to a patient to prevent a primary, reacti-
        vated, or recurrent CMV infection; ‘‘preemp-
        tive therapy’’ (sometimes called ‘‘preemptive
        prophylaxis’’) means antiviral agents are
        given for an asymptomatic CMV infection
        detected by a screening assay [
        3
        ]
  - - - CMV recurrence after allogeneic HSCT in
        seropositive patients is 30–80% [
        15
        –
        21
        ], with a
        median value of 37% (Fig.
        1
        )
      - The
        rate of CMV recurrence after allogeneic HSCT in
        seronegative patients is 0–12% [
        15
        –
        21
        ], with a
        median value of 7%
- - - - The risk factors for CMV recurrence after allo-
        geneic HSCT depend on the recipient (CMV
        serostatus; age), donor [CMV serostatus match;
        age; sex match; type of family/unrelated donor
        (UD); HLA match; stem cell source], transplant
        (intensity of myeloablative or reduced-intensity
        conditioning; type of conditioning—TBI based
        or chemotherapy based; T-cell depletion),
        immunosuppressive treatment (prophylaxis,
        occurrence and treatment for acute and/or
        chronic GVHD; specific immunosuppressive
        drugs used in prophylaxis and therapy), and
        immune recovery after HSCT (speed of immune
        reconstitution for natural killer cells, B cells, T
        cells; recovery of CMV-specific CTLs)
      - Some reports indicate the role of other fac-
        tors such as the experience of the center and
        improvement in all kinds of antimicrobial pro-
        phylaxis (e.g., regarding blood products, infec-
        tions with other herpesviruses, the use of
        preemptive prophylaxis, or race of the patient)
      - In analysis of studies by multivariate analysis
        for risk factors for CMV recurrence in patients
        after allogeneic HSCT, donor-negative (D
        -
        )/re-
        cipient-positive (R
        ?
        ) pretransplant CMV
        serostatus had a major role as a risk factor
      - ost of these studies
        indicated also other risk factors: UD or mis-
        matched donor (MMD) transplantacute GVHD
        nd older
        age [
        Several other risk factors
        were found in these analyses: bone marrow as a
        stem cell source [
        67
        ], reduced-intensity condi-
        tioning [
        18
        ], TBI-based conditioning [
        68
        ], year
        of transplant before 2004 [
        18
        ], herpes simplex
        virus infection [
        63
        ], non-Caucasian race [
        18
        ], no
        T-cell depletion [
        66
        ], and use of steroids [
        68
        ]. A
        protective effect of sirolimus use in GVHD
        prophylaxis was shown in one study [
        67
        ]. Sir-
        olimus possibly has a protective effect against
        CMV infection because of the inhibition of
        cellular signaling pathways that are triggered
        during CMV infection for the synthesis of viral
        proteins. It has also antiproliferative properties,
        and thus probably inhibits the kinetics of CMV
        replication