Zn(ll) picolinate and aspartate, Zn(pic). and Zn(asp)., have been shown to inhibit key steps of the replication of HSV-I. In the present study we describe the effect of Zn(pic). and Zn(asp). on the replication of VZV and on the infectivity of free virions. The experiments are done using BHK-21 cells, a clinical isolate of VZV and Zn-complexes in concentration of 10/M. When Zn-complexes are present during the whole period of infection, the yield of infectious virus progeny decreases up to 98%. The infectivity of VZV is completely restored after the removal of zinc. The virucidal effect is manifested at the 2nd h of contact, when 90% of the virions are inactivated. The results show that both Zn(pic). and Zn(asp)= specifically inactivate free VZV virions with no effect on viral replication.

We evaluate and analyze the quality of click models with respect to their ability to simulate users' click behavior. To this end, we propose distribution-based metrics for measuring the quality of click simulation in addition to metrics that directly compare simulated and real clicks. We perform a comparison of widely-used click models in terms of the quality of click simulation and analyze this quality for queries with di erent frequencies. We nd that click models fail to accurately simulate user clicks, especially when simulating sessions with no clicks and sessions with a click on the rst position. We also nd that click models with higher click prediction performance simulate clicks be er than other models.

2090 BACKGROUND. Coinfection with hepatitis B virus (HBV) and hepatitis C virus (HCV) in immunocompromised patients (pts) with hematological malignancies is not well-studied problem. Early recognition of HBV and HCV infectioning incidence in such pts is difficult due to influence of cytostatic and immunosuppressive therapy and possible mutual HBV or HCV inhibitions. Independence of HBV and HCV infection events has to be discussed. AIM. To determine the prevalence of HBV and HCV co-infection in pts with hematological malignancies to check the possible correlation between the incidence of the infections. PATIENTS AND METHODS. All 265 patients treated in hematology department during 2004–2006 years were prospectively continuously monitored and examined for markers HBV and HCV (HBsAg, anti-HCV, DNA HBV, RNA HCV, HBeAg, anti-HBs, anti-HBc, anti-HBe) in serum, plazma, blood cells, bone marrow, cerebrospinal fluid) and clinico-biochemical symptoms of liver dysfunction were registered approximately every 3 weeks until 2008 year. Liver biopsy was performed on 64 pts in 2004–2006 yy, 23 pts esch with HBV and HCV immunohistology. Approximately 80% of pts were with acute leukemias (AL) and aplastic anemias (AA). Male; 47% (n=125), female; 53% (n=140). The median age was 38 years (range, 15 to 79). RESULTS. At the beginning of treatment and monitoring 17 of 265 pts (6.4%) had positive markers of HCV and the number of pts with positive markers of HCV increased up to 70 (26%) to the end of monitoring, and for HBV markers increased from 23 pts (8.7%) to 174 pts (65.3%). We found, that many pts were co-infected with HBV and HCV, and their total number increased from 5 pts (1,9%) äî 37 pts (14%). Positive tests of HBV and HCV co-infection was found in 57 pts of 265, that is 32.8% of 174 HBV-positive pts and 81.4% of 70 HCV-positive pts, odds ratio (OR=2.9) (95%CI =1.5–5.7), xi square significance p=0.0012. More complicate longitude analysis did not show that the incidence rate of second infection is significantly higher than the first. That means that the correlation between first and second infections is still questionable. Coinfection with HBV and HCV resulted in clinical presentation of hepatitis B and/or hepatitis C in most cases and cumulative incidence rate rises up to 100% at 630 day after the first appearance of any positive marker. CONCLUSION. The high prevalence of HBV and HCV coinfection of pts with hematological malignancies is attributed to common risk factors for infection transmission after transfusions of blood components and parenteral medical procedures. For pts with hematological malignancies after first detection of positive test for single marker of HBV and/or HCV it is very reasonable to intensify the monitoring of HBV and HCV markers and to follow clinical signs. Disclosures: No relevant conflicts of interest to declare.

INTRODUCTION. Patients (pts) with hematological malignancies are at high risk of infection by Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) due to multiple transfusions and the large number of invasive procedures. The aim of the study was to evaluate the presentation rate of clinical hepatitis, pt survival and how hepatitis infection influenced survival. RESULTS. The study group was comprised of all pts admitted to the hematology department from Feb 2004 to June 2006. The pts were followed until June 2008. All pts were monitored by testing of HBsAg, anti-HCV, DNA-HBV, RNA-HCV, HBeAg, anti-HBs, anti-HBc, anti-HBe approximately every 3 weeks. Liver biopsy was performed on 64 pts, 23 pts each with HBV and HCV immunohistology. A total of 7800 biological samples were collected for HBV and HCV testing; of these, 4000 were tested by PCR methods. Acute leukemias (AL) and aplastic anemias (AA) constituted 77% (205/265) of all pts. The median age was 38 years (range, 15 to 79), Male; 47% (n=125), female; 53% (n=140). Median transfusion load (the number of donors per pt for the study period) was 45 (range, 0 to 418). When patients new to the hematology dept were examined: HBV was detected in 15% (39/265) of new pts and HCV in 7% (19/265) of new pts respectively. We postulated that the rate of infection is extremely high in the hematology clinic. For the entire study period from Feb 2004 to Jun 2006, 51% (135/265) pts had positive markers for HBV infection, 19% (51/265) pts had positive markers for HCV, and 14% (37/265) pts had positive markers for both HBV+HCV. We have shown that up to 95% of HCV-positive pts and up to 60% of HBV-positive pts developed clinical and biochemical symptoms and signs of viral hepatitis with 3 years of initial detection of HBV and HCV markers. 154 (58%) pts survived, 111 (42%) pts died. Of these, 2 pts developed fulminant liver failure due to severe hepatitis B. The analysis of survival risk factors demonstrates that the expected life duration significantly decreases after HBV infection. For AL pts RR=1.8 (p=0,034), for AA pts RR=4.3 (p=0,022). There was no significant association between the expected life duration and HCV infection. Proportional hazard regression model with time dependent covariates (PHREG SAS) was used for the analysis. CONCLUSION. The majority of pts infected by HBV and HCV developed clinically recognizable viral hepatitis within 3 years from the first detection of viral markers. Pts with severe immunosupression often do not manifest obvious features of acute viral hepatitis. Pts with hematological malignances should be monitored regularly (at least once in a month) for HBV and HCV markers during all period of treatment and for 1–2 years after completion of therapy. Viral hepatitis B is a risk factor associated with survival risk factor for AL and AA pts.