Rabies is considered a disease of the highest mortality rate and all humans are vulnerable to infection. Specific anti-rabies immunoprophylaxis is the only efficient method of protection. The analysis of indications for active alone and active and passive immunization among patients reported to the dispensary of rabies prophylaxis in the Department of Infectious Diseases of Medical University of Lublin (eastern Poland) in 2004-2005 is presented. Prophylactic procedures were applied in 120 persons (14.98% of overall number consulted). Passive immunization, i.e. rabies immune globulin, was administered in 1 person (0.12%). In 2004, 64 persons (7.99%) received active vaccination, and 56 patients (6.99%) were vaccinated in 2005. Most of vaccinated patients lived in an urban area where the risk of rabies should be lower; however, in cities like Lublin there is a higher risk of being bitten by homeless animals. The most common species with rabies suspicion were dogs and cats. The decrease in the number of patients bitten by animals with confirmed rabies in Lublin province, and of the number of cases of animal rabies may indicate that oral vaccination of red foxes, representing a main reservoir of rabies virus in Poland, has been shown to be effective.
The aim of the study was to assess the expression of TNFRp55 mRNA and to examine if the antisense inhibition of Epstein-Barr virus (EBV) encoded EBNA1 gene product alters the expression of gene encoding TNFRp55 in lymphoblastoid cell line (LCL). The experiment was performed on LCL derived from EBV infected human peripheral blood B lymphocytes. The lymphocytes were isolated and cultured. RNA was isolated and examined according to the RNase protection assay. The hybridisation was done with HCR-4 probe. RNA was quantified by densitometry and presented in extinction units. The level of expression was calculated with TotalLab software programme. The results of the study suggest that EBV gene, responsible for the synthesis of EBNA1 protein, has an inhibitory effect on human TNFRp55 gene expression in LCL.