In Washington, DC, at a Metro Station, on a cold January morning in 2007, this man with a violin played six Bach pieces for about 45 minutes. During that time, approximately 2,000 people went through the station, most of them on their way to work. About 3 minutes: The violinist received his first dollar. A woman threw money in the hat and, without stopping, continued to walk. At 6 minutes: A young man leaned against the wall to listen to him, then looked at his watch and started to walk again. At 45 minutes: The musician played continuously. Only 6 people stopped and listened for a short while. About 20 gave money but continued to walk at their normal pace. The man collected a total of $32. After 1 hour: He finished playing and silence took over. No one noticed and no one applauded. There was no recognition at all. No one knew this, but the violinist was Joshua Bell, one of the greatest musicians in the world. He played one of the most intricate pieces eve
Continued from Part - I & II ..........
In transfusion medicine safety of blood products is a major concern. The hepatitis B virus getting transmitted through blood transfusion is far more than the hepatitis C virus it is around 1:60000 vs 1:103000 (Schreiber, Busch, Kleinman, Korelitz. 1996). This is despite of availability of assay for screening quite sensitive to detect hepatitis B virus surface antigen or HBsAg. It is very common incidence of hepatitis B infection in post-transfusion cases (Saraswat, Banerjee, Chaudhury, Mahant,Khandekar, Gupta, et al.1996). Common explanations what offered for incorrect negative findings or results with the common assays are due to circulation of viral protein in low level. This can escape detection and screening of HBsAg mutant`s infection by assays in blood donors. Obviously this cause hazards in post blood transfusion (Jongerius, Wester, Cuypers, van Oostendorp,Lelie, van der Poel, et al.1998). Besides this other reason is cited as the higher infection caused by hepatitis C virus or HCV may offer a clearance of detection of hepatitis B. This is attributed to the dominancy of eliciting immune response by the virus of hepatitis C (Tsai, Liaw, Yeh, Chu, Kuo. 1995). One more explanation is given that the yield sequences of virus variants are not identified by the antibodies available with the assays (Carman.1997). This is because of other variants in the genom; that regulates down production of hepatitis B surface antigen (Carman, Mimms.1997). However, the aitbodies to hepatitis B core or HBC antigen are the marker of chronic, acute or resolved infection of hepatitis B virus and they remain traceable thought out the life. They are present even in absence of both HBs and HBsAg antibodies or during the recovery period after acute hepatitis B infection and even before the resurfacing anti-HBs antibodies or among patients who has been cured of hepatitis B infection and lost trace of anti-HBs antibodies. So, it is always possible to detect antibodies to hepatitis B core or HBc antigen in one who has been infected with hepatitis B virus (Lee.1997).
Discussion
The detection of anti-HBc presence and positivity of hepatitis B virus DNA in the serum of blood donors who are healthy is prevalent though their blood may show negativity for HBsAg and anti- HCV. At present in many countries for the purpose of blood donation HBsAg detection is undertaken as only and major test for diagnostic screening of hepatitis B virus in blood transfusion centers. But in varied degrees; the donated blood despite of being negative for HBsAg ,is found positive for HBc-Ag. The number in terms of percentage varies one country or ethnic group to other. It is also observed in most study reports that hepatitis B virus infection is detected with HBV-DNA traced in peripheral mononuclear cells or liver in comparison with sera or plasma (Torii, Hasegawa, Joh, and Hayashi.2003). The hypothesis offered by Brechotet et al, the blood donor groups can be divided into two certain groups; HBsAg negative and HBsAg positive (Brechot, Thiers, Kremsdorf, Nalpas, Pol,Paterlini-Brechot.2001). The subjects who are seronagative should be divided further into two sub-groups one anti-HBc (+)ve and other anti-HBc (-)ve individuals. Again the anti-HBc (+)ve subgroup may be divided in two groups with and without anti –HBs individuals. It is observed HBV-DNA presence is detected in HBsAg negative, anti-HBs positive and anti-HBc positive donors (Hennig, Puchta, Luhm, Schlenke, Goerg,Kirchner.2002: Roche, Feray, Gigou, Roque-Afonso,Arulnaden, Delvart, et al.2003). Studies found that the rate of HBV-DNA detection is highest among donors found anit-HBc positive but negative for antigen hepatits B surface antibody. Most of these donors might have suffered and subsequently recovered from hepatitis B infection but they still have HBV with a lower level. The persons with anti-HBs titre more than 10 IU/ml have no symptom of hepatitis B since they are immunized. So with some, who take vaccine may develop anti-HBc and that is indicative of infection by hepatitis B virus; but it is so in absence of any infection or disease (Zervou, Dalekos, Boumba, Tsianos.2001).
To be continued..............
In transfusion medicine safety of blood products is a major concern. The hepatitis B virus getting transmitted through blood transfusion is far more than the hepatitis C virus it is around 1:60000 vs 1:103000 (Schreiber, Busch, Kleinman, Korelitz. 1996). This is despite of availability of assay for screening quite sensitive to detect hepatitis B virus surface antigen or HBsAg. It is very common incidence of hepatitis B infection in post-transfusion cases (Saraswat, Banerjee, Chaudhury, Mahant,Khandekar, Gupta, et al.1996). Common explanations what offered for incorrect negative findings or results with the common assays are due to circulation of viral protein in low level. This can escape detection and screening of HBsAg mutant`s infection by assays in blood donors. Obviously this cause hazards in post blood transfusion (Jongerius, Wester, Cuypers, van Oostendorp,Lelie, van der Poel, et al.1998). Besides this other reason is cited as the higher infection caused by hepatitis C virus or HCV may offer a clearance of detection of hepatitis B. This is attributed to the dominancy of eliciting immune response by the virus of hepatitis C (Tsai, Liaw, Yeh, Chu, Kuo. 1995). One more explanation is given that the yield sequences of virus variants are not identified by the antibodies available with the assays (Carman.1997). This is because of other variants in the genom; that regulates down production of hepatitis B surface antigen (Carman, Mimms.1997). However, the aitbodies to hepatitis B core or HBC antigen are the marker of chronic, acute or resolved infection of hepatitis B virus and they remain traceable thought out the life. They are present even in absence of both HBs and HBsAg antibodies or during the recovery period after acute hepatitis B infection and even before the resurfacing anti-HBs antibodies or among patients who has been cured of hepatitis B infection and lost trace of anti-HBs antibodies. So, it is always possible to detect antibodies to hepatitis B core or HBc antigen in one who has been infected with hepatitis B virus (Lee.1997).
Discussion
The detection of anti-HBc presence and positivity of hepatitis B virus DNA in the serum of blood donors who are healthy is prevalent though their blood may show negativity for HBsAg and anti- HCV. At present in many countries for the purpose of blood donation HBsAg detection is undertaken as only and major test for diagnostic screening of hepatitis B virus in blood transfusion centers. But in varied degrees; the donated blood despite of being negative for HBsAg ,is found positive for HBc-Ag. The number in terms of percentage varies one country or ethnic group to other. It is also observed in most study reports that hepatitis B virus infection is detected with HBV-DNA traced in peripheral mononuclear cells or liver in comparison with sera or plasma (Torii, Hasegawa, Joh, and Hayashi.2003). The hypothesis offered by Brechotet et al, the blood donor groups can be divided into two certain groups; HBsAg negative and HBsAg positive (Brechot, Thiers, Kremsdorf, Nalpas, Pol,Paterlini-Brechot.2001). The subjects who are seronagative should be divided further into two sub-groups one anti-HBc (+)ve and other anti-HBc (-)ve individuals. Again the anti-HBc (+)ve subgroup may be divided in two groups with and without anti –HBs individuals. It is observed HBV-DNA presence is detected in HBsAg negative, anti-HBs positive and anti-HBc positive donors (Hennig, Puchta, Luhm, Schlenke, Goerg,Kirchner.2002: Roche, Feray, Gigou, Roque-Afonso,Arulnaden, Delvart, et al.2003). Studies found that the rate of HBV-DNA detection is highest among donors found anit-HBc positive but negative for antigen hepatits B surface antibody. Most of these donors might have suffered and subsequently recovered from hepatitis B infection but they still have HBV with a lower level. The persons with anti-HBs titre more than 10 IU/ml have no symptom of hepatitis B since they are immunized. So with some, who take vaccine may develop anti-HBc and that is indicative of infection by hepatitis B virus; but it is so in absence of any infection or disease (Zervou, Dalekos, Boumba, Tsianos.2001).
To be continued..............
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