Background Since the introduction of nucleic acid testing (NAT) for routine blood donor screening, hepatitis C virus (HCV) RNA-only detection rates reported from Poland have been higher than in most other European countries. Methods To examine the factors likely contribute to these window-period donations, we conducted a case-control study among 47 recently HCV-infected blood donors, who gave blood between July 2002 and June 2014, with 141 controls matched by age, gender and donation dates. Firth-corrected conditional logistic regression models were fitted to estimate adjusted odds ratios (AORs) and 95% confidence intervals (CIs). Adjusted population attributable fractions (PAF) were calculated, based on the distribution of exposure among the cases. Results In a multivariate analysis, recent exposures in health care environments not routinely ascertained through pre-donation questionnaires, were strongly associated with recently-acquired HCV infection. These exposures included minor medical procedures and dental procedures in the preceding 6 months, AOR = 5.77 (CI = 2.01, 18.53). More important, however, based on PAF were behavioral deferrable risks that went unreported at the time of donation, such as high-risk sexual behaviors in the preceding 6 months (PAF=34%), or lifetime histories of drug use (PAF=28%). Conclusions This study raises questions about the effectiveness of deferral policy in excluding high-risk individuals. In addition, it provides further evidence supporting short, temporal deferrals for small medical procedures and dental treatments in Poland.

The human SUV3 helicase (SUV3, hSUV3, SUPV3L1) is a DNA/RNA unwinding enzyme belonging to the class of DexH-box helicases. It localizes predominantly in the mitochondria, where it forms an RNA-degrading complex called mitochondrial degradosome with exonuclease PNP (polynucleotide phosphorylase). Association of this complex with the polyA polymerase can modulate mitochondrial polyA tails. Silencing of the SUV3 gene was shown to inhibit the cell cycle and to induce apoptosis in human cell lines. However, since small amounts of the SUV3 helicase were found in the cell nuclei, it was not clear whether the observed phenotypes of SUV3 depletion were of mitochondrial or nuclear origin. In order to answer this question we have designed gene constructs able to inhibit the SUV3 activity exclusively in the cell nuclei. The results indicate that the observed growth rate impairment upon SUV3 depletion is due to its nuclear function(s). Unexpectedly, overexpression of the nuclear-targeted wild-type copies of the SUV3 gene resulted in a higher growth rate. In addition, we demonstrate that the SUV3 helicase can be found in the HeLa cell nucleoli, but it is not detectable in the DNA-repair foci. Our results indicate that the nucleolar-associated human SUV3 protein is an important factor in regulation of the cell cycle.

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