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Viral inactivation is one of the possibilities to reduce the residual risk of blood products. It is now applied to all plasma derived products (PDP). Application of such techniques to labile blood products (LBP) is difficult for two main reasons: any method should inactivate cell-associated viruses and should avoid any injury of the cells constituting the active ingredient. Physical techniques may reduce the viral content of cellular BPL (leucodepletion, washing, gamma irradiation), but none of them is active enough to comply with the present requirements for efficacy. An important work has been dedicated to the development of virus photoinactivation techniques. They consist of the addition of a photoreagent followed by illumination at an appropriate wavelength which results in a photochemical reaction responsible for the viral inactivation. Treatment of platelet concentrates by psoralen derivatives and UV-A illumination significantly inactivate in vitro enveloped and naked viruses, free and cell-associated viruses and also sequences integrated in the viral genome. Recent progresses have led to these results without detectable functional alteration of platelets and mutagenicity. Viral inactivation of red blood cells yet did not reach the same level because hemoglobin does not allow the use of the photoreagent compounds applicable to platelet concentrates. Viral decontamination of fresh frozen plasma by solvent and detergent, active on enveloped viruses, has been used in France since 1992. Other techniques of comparable efficacy, have received an agreement in other countries. The research on viral inactivation of LBP could prove to be of great importance in the near future in bringing additional safety to patients not only for the residual viral risk but maybe also for the residual bacterial risk of LBP.

Viral inactivation is one of the possibilities to reduce the residual risk of blood products. It is now applied to all plasma derived products (PDP). Application of such techniques to labile blood products (LBP) is difficult for two main reasons: any method should inactivate cell-associated viruses and should avoid any injury of the cells constituting the active ingredient. Physical techniques may reduce the viral content of cellular BPL (leucodepletion, washing, gamma irradiation), but none of them is active enough to comply with the present requirements for efficacy. An important work has been dedicated to the development of virus photoinactivation techniques. They consist of the addition of a photoreagent followed by illumination at an appropriate wavelength which results in a photochemical reaction responsible for the viral inactivation. Treatment of platelet concentrates by psoralen derivatives and UV-A illumination significantly inactivate in vitro enveloped and naked viruses, free and cell-associated viruses and also sequences integrated in the viral genome. Recent progresses have led to these results without detectable functional alteration of platelets and mutagenicity. Viral inactivation of red blood cells yet did not reach the same level because hemoglobin does not allow the use of the photoreagent compounds applicable to platelet concentrates. Viral decontamination of fresh frozen plasma by solvent and detergent, active on enveloped viruses, has been used in France since 1992. Other techniques of comparable efficacy, have received an agreement in other countries. The research on viral inactivation of LBP could prove to be of great importance in the near future in bringing additional safety to patients not only for the residual viral risk but maybe also for the residual bacterial risk of LBP.

The prevalence of anti-hepatitis C virus (anti-HCV) antibodies and of hepatitis B markers (HBs antigen, anti-hepatitis B core antigen) was assessed in 63 haemodialysis patients from the Tunisian Sahel. As measured by second generation ELISA assays (Ortho and Organon), the frequency of anti-HCV antibodies was 42% (27/63), while 4 patients (6.3%) were HBs Ag positive and 30 (47.6%) anti-HBc positive. Anti-HCV seropositivity was significantly correlated with duration of dialysis (p = 0.007) and number of blood transfusions (10 units, p = 0.0004). Among 12 subjects with a history of abnormal ALAT levels, 10 were anti-HCV positive (p = 0.0016) and the results suggest hepatitis C viral infection to be the main cause of liver disease in haemodialysis patients in Tunisia.

The technical parameters of blood filtration through cotton Imugard IG 500 filters were evaluated. Sixty units of red cell concentrates were filtered. The mean value of the residual leukocytes indicated a leukocyte depletion greater than 98%, disregarding the unit age and the filtration temperature. The number of residual leukocytes was below 1 X 10(8) in 94% of the filtered units and less than 0.3 X 10(8) in 68%. The number of residual platelets was less than 1 X 10(10) in 92% of these units.

An accidental case of delayed haemolytic reaction due to an anti-D allo-immunization in a patient suffering from multiple traumatic injuries allows us to define a procedure of emergency treatment towards non iso-Rhesus transfusions and the problems posed by the detection of acquired allo-antibodies.

Frequent allergic reactions following transfusion are observed. Usually, they are benign but sometimes we observe severe allergic reactions. Adverse reactions may be brought about by least two mechanisms. First, immediate-type hypersensibility reactions due to IgE. Secondly, anaphylactic-type reactions due to interaction between transfused IgA and class specific anti IgA in the recipient's plasma. They are characterized by their severest form (anaphylactic shock). The frequency of severe reactions following the transfusion blood plasma is very low. These transfusion reactions are complement-mediated and kinins-mediated. Prevention of allergic reactions is necessary among blood donors and recipients.