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Flow cytometric immunophenotyping (FCI) is recommended in the evaluation of cerebrospinal fluid (CSF) specimens for hematologic neoplasms. This study reviewed FCI of CSF specimens collected for primary diagnosis (n = 77) and follow-up for known malignancy (n = 153). FCI was positive in 11 (4.8%) of 230 specimens: acute myeloid leukemia, 6; precursor B-acute lymphoblastic leukemia, 2; B-cell lymphoma, 2; and T-cell lymphoma, 1. Positive results were obtained in low-cellularity specimens, including 2 with fewer than 100 events in the population of interest. FCI was indeterminate in 19 (8.3%) of 230 specimens, including 3 with only sparse events, 8 with possible artifact (apparent lack of staining, nonspecific or background staining, and aspirated air), and 8 with phenotypic findings considered insufficient for diagnosis. Indeterminate specimens were often limited by low cellularity and lacked normal cell populations to evaluate for appropriate staining. FCI may be of value in low-cellularity CSF specimens, although the results should be interpreted with caution.

A variety of rare clinical syndromes are seen with strikingly increased prevalence in HIV-1-infected individuals, many with underlying viral etiologies. The emergence of these diseases in AIDS reflects a reduction in the ability of the immune system to mount an adequate defense against viruses in general due to the damage inflicted to the immune system by HIV-1 infection. However, in many cases, it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses. This can occur either directly by HIV-1 proteins such as Tat enhancing the activity of heterologous viral promoters, and/or indirectly by HIV-1 inducing the expression of cytokines and activation of their downstream signaling that eventually promotes the multiplication of the other virus. In a reciprocal manner, the effects of other viruses can enhance the pathogenicity of HIV-1 infection in individuals with AIDS through stimulation of the HIV-1 promoter activity and genome expression. The purpose of this review is to examine the cross-interactions between these viruses and HIV-1.

Reactivation of the human polyomavirus BK (BKV) has emerged as an important cause of allograft rejection in renal transplant recipients. Expression of the viral early promoter that leads to production of T-antigen is the first event in viral lytic infection. In an effort to understand the mechanism involved in the activation of BKV early gene (BKV(E)) expression, we analyzed the promoter/enhancer region of the virus and identified binding motifs for the inducible transcription factors NF-kappaB and C/EBPbeta, which are in juxtaposition to each other downstream from the early gene transcription initiation site. Results from transfection studies demonstrate that overexpression of the p65 subunit of NF-kappaB, but not C/EBPbeta stimulates transcription of the BKV(E) promoter in CV-1 cells. Interestingly, low level expression of C/EBPbeta showed a synergistic effect on p65 activation of the BKV(E) promoter, suggesting a functional cooperativity between these two regulators upon viral gene transcription. Results from DNA-binding studies showed the ability of p65 and C/EBPbeta to bind independently with BKV DNA as removal of the binding site for p65 or C/EBPbeta had no significant effect on the interaction of p65 and C/EBPbeta with their motifs, respectively. Functional evaluation of the mutant promoter with no binding sites for either NF-kappaB or C/EBPbeta showed that the observed synergism requires the p65 but not the C/EBPbeta binding site, suggesting cross-talk between C/EBPbeta and p65 in this event. Results from the co-expression of p65 and C/EBPbeta showed no evidence for the formation of a DNA-protein complex containing both p65 and C/EBPbeta, although results from protein-protein interaction studies verified the ability of C/EBPbeta to interact with p65. A dominant-negative isoform of C/EBPbeta which contains the DNA binding but not activation domain of full-length C/EBPbeta cooperated with p65 in activating the BKV(E) promoter, suggesting a functional interaction between the b-ZIP domain of C/EBPbeta and NF-kappaB.