Activating KIR/HLA complexes in classic Kaposi's Sarcoma.

BACKGROUND: Classic Kaposi's Sarcoma (cKS) is a rare vascular tumor associated with Human Herpesvirus 8 (KSHV) infection, nevertheless not all KSHV-infected individuals have cKS. OBJECTIVE: We investigated whether particular KIR/HLA receptor/ligand genotypes would be preferentially present in KSHV-infected and uninfected individuals who have or have not developed cKS. METHODS: KIR/HLA genotypes were analyzed by molecular genotyping in 50 KSHV-infected individuals who did or did not have cKS and in 33 age-and sex-matched KSHV seronegative individuals. RESULTS: There was no association of individual KIR, HLA or receptor ligand combinations with KSHV infection. However, activating KIR and KIR/HLA genotypes were significantly more frequent in cKS cases, specifically KIR3DS1, KIR2DS1, and KIR2DS1 with its HLA-C2 ligand. CONCLUSION: A nonspecific inflammatory response triggered by activation of NK cells upon KIR-HLA interaction could be associated with the pathogenesis of KS.

Presence, quantitation and characterization of JC virus in the urine of Italian immunocompetent subjects.

Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation.

Angiotensin-converting enzyme inhibitors slow recovery from anemia following cardiac surgery.

OBJECTIVES: Angiotensin-converting enzyme (ACE) inhibitors, which are frequently administered in patients with heart disease, have a known inhibitory effect on erythropoiesis. The aim of this study was to detect whether early ACE inhibitor administration slows recovery from anemia following recent cardiac surgery. METHODS AND RESULTS: Forty male patients with anemia (hemoglobin < 12 g/dL) an average of 9 days after cardiac surgery were randomized to receive enalapril (ACE inhibitor group) or not. All of the patients received ferrous sulfate, 525 mg, in addition to standard therapy. Patients with anemia due to other causes were excluded. Blood samples were obtained at baseline, and after 8 days, 16 days, and 60 days. A 6-min walking test and echocardioscan were performed at baseline, and after 16 days and 60 days of treatment, and a chest radiograph was obtained at baseline and after 60 days. The ACE inhibitor group showed a statistically significant lower increase in hemoglobin and RBC values. The peak between-group differences of 1 g/dL of hemoglobin (p = 0.012) and 444 RBCs per milliliter (p = 0.017) were observed on day 16. CONCLUSIONS: Early enalapril maleate administration in anemic patients after heart surgery significantly inhibits erythropoiesis. This unfavorable effect on anemia should be considered when prescribing ACE inhibitors for such patients.