Thursday, 25 December 2008

Blood transfusion and Hepatitis B part -II

The studies observed that more than 300 million people all over the world are infected by hepatitis B virus. This virus belongs to Hepadnaviridae family, a non-cytopathic hepatotropic DNA virus. Though there is a prophylactic vaccine deemed to be effective still the high prevalence of this virus is found in continents like Africa and Asia (Lok,. & McMahon, 2001).
Hepatitis B virus induces the liver ailments, the degree of which varies from person to person ((Ganem & Prince, 2004). The effects of infections by hepatitis B virus are controlled efficiently and cleared from the blood without any symptom or clinical evidence of liver disease by some persons. They may have inflammation severely in the liver i.e. acute hepatitis but after being resolved leave no long term squeal. There are others who cannot clear the virus and likely to develop a chronic infection but most of them may remain without any symptom and any acute liver disease, around 10 to 30 per cent of them contract cirrhosis of liver what may finally lead to liver cancer (Alberti et al., 1999 : Lok & McMahon, 2001). The adult infection rate is low , around 5 per cent or even lower but the course of infection and age persuade the effect with revelation in neonatal life progressing to a higher rate of HBV perseverance (Lok & McMahon, 2001 : Ganem & Prince, 2004). The pathogenesis in lever ailments and result of infections are determined by host and virus factors. This could not be fully understood since hepatitis B virus or HBV has the host range limited within men and Chimpanzees. The immunological response to hepatitis B virus is based upon innate immunity and that plays a rapid role after infection to restrict the spread of pathogen and trigger an effective development of adaptive response to the infection. The inborn host response during the initial phase of virus infections are characterized by creation of type 1 interferon or IFN cytokines and this activates the NK or natural killer cells. The cellular mechanism helps virus replication what produces the type 1 IFNs and that detects viral DNA or RNA presence (Alexopoulou et al., 2001: Lund et al., 2003: Heil et al., 2004). Whereas the natural killer cells or NKs are produced when molecules being stress-induced are recognized or/and modulation of the degree or quantum of MHC or major histocompatibility complex class I available on the surface of the cells which are infected (Moretta et al., 2005).

To be continued..........

No comments: