Hepatitis B Infection Is A Global Health Problem Biology Essay

Hepatitis B infection is a planetary wellness job. Harmonizing to World Health Organization, an estimated 600,000 people die every twelvemonth due to the ague or chronic effects of Hepatitis B infection ( WHO fact sheet, 2008 ) .

For the twelvemonth 2000, a mathematical theoretical account to gauge planetary hepatitis B load and inoculation impact estimated that, 620aˆ‰000 individuals died worldwide from HBV-related causes. Therefore, 580aˆ‰000 ( 94 % ) from chronic infection-related cirrhosis and hepatocellular carcinonoma and 40aˆ‰000 ( 6 % ) from ague hepatitis B ( Goldstein et al. , 2005 ) . In the lasting birth cohort for the twelvemonth 2000, the theoretical account estimated that without inoculation, 64.8 million would go HBV-infected and 1.4 million would decease from HBV-related disease ( Goldstein et al. , 2005 ) .

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HBV infection histories yearly for 4000 to 5500 deceases in the United States and 1 million deceases worldwide from cirrhosis, liver failure, and hepatocellular carcinoma ( Lee, 1997, Ganem et Al, 2004 ) .

HBV besides plays an of import function in the development of liver cirrhosis in Ghana. Studies done on 70 patient with liver cirrhosis, 30 ( 42.86 % ) were positive for HbsAg. ( Blankson et al, 2005 ) . It is hence critical to efficaciously test the general populace for Hepatitis B to assist cut down the transmittal of the infection.

There are about 50 million chronic bearers of hepatitis B virus ( HBV ) in Africa, with a 25 % mortality hazard ( Kiire C F, 1996 ) .

Blood transfusion services is a critical portion of modern wellness attention system, with a every unit of blood there is 1 % opportunity of transfusion associated jobs including transfusion transmitted diseases ( Garg S, et al. , 2001 ) . Transfusion infected blood to patients is considered a offense. It is hence compulsory to prove each and every unit of blood for antibodies to HIV-1 and 2, pox, hepatitis C and Hepatitis B surface antigen ( Nanu A, et al. , 1997 )

The surface antigen of HBV ( HBsAg ) may be detected in serum 30-60 yearss following infection and may prevail for widely variable periods of clip. An of import proportion ( 7-40 % ) of persons who are HBsAg-positive may besides transport the hepatitis B ‘e’antigen ( HBeAg ) , which is associated with high infectivity. Unless vaccinated at birth, the bulk of kids born to female parents who are HBeAg-positive will go inveterate septic. ( Beasly et al. , 1983 )

All patients with acute hepatitis B are HBeAg positive and hence extremely infective and contact with their blood or organic structure fluids can take to HBV infection ( Hollinger, 2001 ) .

HBeAg-positive specimens contain high concentrations of infective virions and HBV DNA, in contrast to anti-HBe positive samples, in which the figure of hepatitis B virions is well reduced ( Hollinger FB, 2001 ) .

Chronic hepatitis is characterized by either the presence or absence of HBeAg. ( Fattovich, 2003 ) A survey conducted in Italy on HBsAg positive samples had 86.4 % being HBeAg-negative and the Mediterranean, Asia and in the Far East had a population of 30-80 % besides being HBeAg-negative. The proportion of HBeAg-negative is lifting worldwide, with patients with HBeAg-negative chronic hepatitis developing more active, advanced, and progressive liver disease. ( Laras et al. , 1998 )

The screening trial for hepatitis B infection is sensing of HBsAg which does non govern out the hazard of transmittal of hepatitis B as the giver may be in the ‘window period ‘ . During this period, sensing of the antibody to the hepatitis B nucleus antigen ( anti-HBc ) IgM type serves as a utile serological marker. ( Kumar H et al. , 2009 )

Antibody to hepatitis B nucleus antigen is the first to develop, following ague hepatitis B infection, which appears preponderantly as IgM anti-HBc at approximately 6 hebdomads after infection. The antibody typically persists for life except declaration of ague hepatitis B virus infection occurs ( Hollinger, et al. , 2001 )

Some chronically-infected patients will decide their HBV infection, either of course or on occasion following interferon-based therapy. These patients typically show clearance of HBsAg but are anti-HBc positive and normally develop anti-HBs, along with anti-HBc ( Perrilo RP, 2001 ) A

Sheik et al reported a seroprevalence of 10 % of IgM anti-HBcore in Pakistan ( Sheikh et al. , 2011 ) . A 4 % seroprevalence of IgM anti-HBcore was reported in Italy amongst HBsAg positive givers who were inveterate infected but 85 % of the same patients tested positive to IgM anti-HBcore when they were acutely infected ( Lavarini et al. , 1983 ) .A entire prevalence of anti HBcore ( dwelling of both IgG anti-HBcore and IgM anti-HBcore ) of 16.2 % was reported in Yemen and 13.5 % in Korea amongst blood givers. ( Bawazir et al. , 2011, Seo, et al. , 2011 ) . This present survey besides seeks to find the prevalence of anti-core antibody among blood givers in Ghana.

HBV DNA has been detected in the serum of patients with anti-HBc hepatitis. ( Antar et al.2010 )

Antar et al reported a 6.25 % noticeable serum HBV DNA amongst Egyptian blood givers. ( Antar, et Al, 2010 ) The issue of stray hepatitis brings to forefront the ineffectualness of HBsAg showing ( which is what is used in Ghana ) in protecting blood receivers from hepatitis B infection. It has been suggested that anti-HBc testing should be combined with HBsAg showing of blood givers to cut down the hazard of HBV infection ( Findik et al. , 2007 ) .

The serological markers of Hepatitis B virus are HBsAg, anti-HBs, HBcAg, anti-HBc ( IgM and IgG ) , HBeAg, anti-HBe, and HBV DNA ; these are of import as they can be used in the diagnosing of the infection and to find the badness of the infection ( Gitlin Norman, 1996 ) .

One of the most sensitive and specific methods for naming HBV infections is enzyme-linked immunosorbent check ( ELISA ) and early sensing of HBsAg may be helpful for simplifying the intervention of HBV-associated diseases. ( Fontirrochi et al. , 1993 )

The prevalence of hepatitis B virus ( HBV ) chronic passenger car in sub-Saharan Africa ranges between 3 % and 22 % in blood givers ( Allain et al. , 2003, Nkrumah et al. , 2011, Dongdem et al. , 2012, Sarkodie et al. , 2001 ) .

Surveies from different parts of Ghana have reported variable prevalence rates among blood givers. Surveies conducted in one rural country have reported HBsAg prevalence of 13.8 % . ( Nkrumah et al. , 2011 ) Another research done in the Northern portion of Ghana reported a prevalence rate of 10.79 % for voluntary givers and 11.59 % for replacing givers ( Dongdem et al. , 2012 ) .

A seroprevalence rate of 19.5 % was besides found in blood givers in the Upper West Region of Ghana ( Adu-Sarkodie et al. , 1997 ) .

A survey done in three dumbly populated communities in Kumasi, Ghana had an overall sero-prevalence rate of hepatitis B surface ( HBsAg ) antigen of 8.68 % ( Amidu N et al. , 2012 ) .

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This survey will therefore provide information on extra viral markers which will be used for measuring the province and hazard of blood givers.

The HBeAg will find the infectivity province of the persons while the anti-core IgM and IgG will separate person who are acutely infected from those who have recovered from HBV infection. Therefore this survey will inform us about the Hepatitis B position of Blood Donors and besides estimate the entire prevalence of the infection.

1.1 Justification

Although there are some informations on the seroprevalence of HBsAg in some parts of Ghana, there is no established informations on HBsAg prevalence in Techiman in the Brong Ahafo. This present survey will find the prevalence of Hepatitis B infection in Techiman and besides provide information on extra viral markers which could be used in set uping the hazard factors of the viral hepatitis infection. Knowledge of this will be of import in finding policies and intercession, which will control the spread of viral hepatitis.

This research seeks to turn to the prevalence of HBV septic persons and to place the proportion with high infectivity among the pool of chronic bearers in the Techiman country.

1.2 Aims of the survey

To find the prevalence of Hepatitis B infection among blood givers in the Techiman municipality of Ghana.

To gauge the proportion of HBV septic persons with the undermentioned viral serological markers ; HBeAg, HBsAg and anti-hepatitis B nucleus Antibody.

To find the hazard factors associated with exposure to HBsAg, HBeAg and anti-hepatitis B nucleus Antibody.

Chapter Two

Literature Review

2.0 Hepatitis B virus ( HBV )

Hepatitis B is an infective inflammatory unwellness of the liver and is most normally caused by the hepatitis B virus ( HBV ) . It was originally known as “ serum hepatitis ( Barker et al. , 1996 ) . The liver is the primary site of HBV reproduction ( Krugman et al. , 1994 ) .

Hippocrates described episodes of icterus, which were probably to hold been viral hepatitis caused by assorted viruses. In 1883 hepatitis transmitted through blood or blood merchandises was foremost documented in Germany during a smallpox immunisation run. McCallum proposed the term hepatitis B for ‘serum ‘ hepatitis in 1947. The Australia antigen, now called the hepatitis B surface antigen ( HBsAg ) , was foremost identified in 1967 and the find of this antigen facilitated the isolation and word picture of the viral atoms. It is besides the footing for the current recombinant vaccinums ( Alter, et al 1993, Blumberg et al. , 1965 ) .

There are five chief hepatitis viruses, referred to as types A, B, C, D and E. ( WHO factsheet, 2012 ) Types B and C lead to chronic disease in 100s of 1000000s of people and, together, are the most common cause of liver cirrhosis and malignant neoplastic disease. ( WHO factsheet, 2012 )

2.1 Epidemiology

The prevalence of chronic hepatitis B virus ( HBV ) infection varies greatly in different parts of the universe and this could be categorized as high, intermediate and low endemicity. ( Margolis et al. , 1991 ) ( Figure 1 )

Hepatitis B is extremely endemic in developing parts with big population such as South East Asia, China, sub-Saharan Africa and the Amazon Basin, where at least 8 % of the population are HBV chronic bearer. In these countries, 70-95 % of the population shows past or present serological grounds of HBV infection. Most infections occur during babyhood or childhood. Since most infections in kids are symptomless, there is small grounds of acute disease related to HBV, but the rates of chronic liver disease and liver malignant neoplastic disease in grownups are high ( Alter, 2003 ) .

Hepatitis B is reasonably endemic in portion of Eastern and Southern Europe, the Middle East, Japan, and portion of South America. Between 10-60 % of the population have grounds of infection, and 2-7 % are chronic bearers ( Toukan, 1990 ) . Acute disease related to HBV is common in these countries because many infections occur in striplings and grownups ; nevertheless, the high rates of chronic infection are maintained largely by infections happening in babies and kids ( Toukan, 1990 ) .

The endemicity of HBV is low in most developed countries, such as North America, Northern and Western Europe and Australia. In these parts, HBV infects 5-7 % of the population, and merely 0.5-2 % of the population are chronic bearers ( McQuillan et al. , 1989 ) . In these countries, most HBV infections occur in striplings and immature grownups in comparatively chiseled bad groups, including injection drug user, homosexual males, and wellness attention workers, patients who require regular blood transfusion or haemodialysis ( McQuillan et al. , 1989 ) .

Figure 1: Geographic distribution of hepatitis B infection.

Beginning: CDC ( 2008 ) Traveler ‘s wellness ; xanthous book.

2.2 Hepatitis B construction

The hepatitis B virus, is a 42 nanometer partly double stranded DNA virus, composed of a 27 nm nucleocapsid nucleus ( HBcAg ) , surrounded by an outer lipoprotein coat incorporating the surface antigen ( HBsAg ) ; ( Figure 2 ) ( Gatlin et al. , 1997 ) .

The 42A nanometer, double-shelled atom, originally called the Dane atom, consists of a 7A nm thick outer shell and a 27A nm inner nucleus. The nucleus contains a little, round, partly double-stranded DNA molecule and an endogenous Deoxyribonucleic acid polymerase. This is the paradigm agent for the household Hepadnaviridae ( Hollinger et al. , 2001 ) .

The viruses have enveloped virions incorporating 3 to 3.3 kilobits of relaxed handbill, partly duplex DNA and virion-associated DNA-dependent polymerases and besides have rearward RNA polymerase activities ( Robinson. 1994 ) .

The most abundant are little, spherical, noninfectious atoms, incorporating HBsAg, that step 17 to 25 nanometers in diameter. ( Robinson, 1995 ) .The Hepatitis B surface antigen are complex of antigenic determiners found on the surface of HBV. They are cannular, filiform signifiers of assorted lengths, but with a diameter comparable to that of a little 22nm atom. They besides contain HBsAg polypeptides ( Hollinger et al. , 2001 ) .

The HBV nucleus cistron codifications for two distinguishable protein merchandises: a 21.5-kDa protein that assembles to organize nucleocapsid atoms designated HBcAg, which in mature virions contains the viral DNA every bit good as the viral polymerase and RNase H, and a precore protein, which is directed to the endoplasmic Reticulum ( ER ) , and is N- and C-terminally processed and secreted as non-particulate e-antigen ( HBeAg ) ( Florian et al. , 1993 ) .

The nucleus antigen ( HBcAg ) is present on the surface of nucleus atoms. HBcAg and nucleus atoms are non present in the blood in a free signifier, but are found merely as internal constituents of virus atoms ( Mahoney, 1999 ) .

Hepatitis B envelope antigen is the antigenic determiner that is closely associated with the nucleocapsid of HBV. It besides circulates as a soluble protein in serum ( Hollinger et al. , 2001 ) .

The nucleus antigen portions its sequences with the vitamin E antigen ( HBeAg ) , identified as a soluble antigen, but no cross responsiveness between the two proteins is observed ( Robinson et al. , 1995 ) .

Antibody to HBsAg, HBcAg, and HBeAg are specific antibodies that are produced in response to their several antigenic determiners ( Hollinger et al. , 2001 ) .

The protein coat of HBV contains HBsAg, which is extremely immunogenic and induces anti-HBs ( humoral unsusceptibility ) . Whereas the structural viral proteins bring on specific T-lymphocytes, capable of extinguishing HBV-infected cells through cell mediated unsusceptibility ( Chisari FV et al. , 1997 ) .

Figure 2: The Dane atom.

Beginning: Fenner F. , White D. Medical Virology. New York: Academic Press.

2.3 HBV Genome

The genome of the HBV is a round partly double stranded DNA molecule of about 3.2 kilobits in length that contains four overlapping unfastened reading frames ( ORFs ) named S, P, C and X ( Figure 3 ) The ORF S contains three induction codons and encodes three polypeptides of different sizes called big, in-between, and little that form the outer envelope of the virus pre-S1, 5 pre-S2, and S ( hepatitis B surface antigen or HBsAg ) . The ORF P encodes the viral polymerase. The ORF C has two induction codons that encode the hepatitis nucleus antigen ( HBcAg ) that forms the nucleocapsid and a soluble antigen that is secreted into the blood watercourse, termed hepatitis B ‘e ‘ antigen ( HBeAg ) , The map of the protein coded for by cistron X is non to the full understood ( Juergen, 2007 ) .

Figure ( 3 ) : Organization of Hepatitis B virus genome. ORF stands for Open Reading Source: GrahamColm

2.4 Viral Stability

The stableness of HBV may depend on the concentration of the virus. Excessively high concentration of the virus may consequences in uncomplete inactivation or devastation, if expose to ether, acid of PH of 2.4 for at least 6 hours and heat at 98A°C for 1 min. ( Hollinger et al. , 2001 ) . However, antigenicity and infectivity are destroyed after exposure of HBsAg to sodium hypochlorite for 3 min, autoclaving at 121CA° for 20 min or dry heat intervention at 160A°C for 1 hr ( Hollinger et al. , 2001, Robinson, 1995 ) .

HBV is besides inactivated by exposure to 2 % aqueous glutaraldehyde at room temperature for 5 min, Sporicidin, methanal at 18.5 g/l ( 5 % formol in H2O ) , 70 % isopropylalcohol, 80 % ethyl intoxicant at 11A°C for 2 min, an iodophor germicide and UV irradiation ( WHO. , 1993 ) .

HBV is able to retain its infectivity when stored at 30-32A°C for at least 6 months and when frozen at 215A°C for 15 old ages. HBV present in blood can defy drying on a surface for at least a hebdomad ( Robinson, 1995, Hollinger et Al, 2001 )

2.5 Life Cycle of Hepatitis B Virus

The HBV virion binds to a receptor at the surface of the hepatocyte ( Ganem, 2001 ) . A figure of campaigner receptors have been identified, including the beta globulin receptor, the 35 asialoglycoprotien receptor molecule, and human liver endonexin. The mechanism of HBsAg adhering to a specific receptor to come in cells has non been established yet. Viral nucleocapsids enter the cell and make the karyon, where the viral genome is delivered ( Chisari, et al. , 1997, Guidotti, et al. , 1994, Mahonney, et al. , 1999 ) .

In the karyon, second-strand DNA synthesis is completed and the spreads in both strands are repaired to give a covalently closed handbill ( ccc ) supercoiled DNA molecule that serves as a templet for written text of four viral RNAs that are 3.5, 2.4, 2.1, and 0.7 kilobits long ( Chisari, et al. , 1997, Guidotti, et al. , 1994, Mahonney, et al. , 1999 ) These transcripts are polyadenylated and transported to the cytol, where they are translated into the viral nucleocapsid and precore antigen ( C, pre-C ) , polymerase ( P ) , envelope big ( L ) , medium ( M ) , little ( S ) , and transcriptional transactivating proteins ( X ) long ( Ganem 2001. , Chisari et al. , 1997, Guidotti et al. , 1994, Mahonney et al. , 1999 ) . The envelope proteins insert themselves as built-in membrane proteins into the lipid membrane of the endoplasmic Reticulum ( ER ) .

The 3.5-kb species, crossing the full genome and termed pregenomic RNA ( pgRNA ) , is packaged together with HBV polymerase and a protein kinase into nucleus atoms where it serves as a templet for rearward written text of negative strand DNA. The RNA to DNA transition takes topographic point inside the atoms ( Ganem, 2001, Mahonney et al. , 1999 ) . The new, mature, viral nucleocapsids can so follow two different intracellular tracts, one of which leads to the formation and secernment of new virions, whereas the other leads to elaboration of the viral genome inside the cell karyon ( Ganem, 2001, Mahonney et al. , 1999 ) .

In the virion assembly pathway, the nucleocapsids reach the ER, where they associate with the envelope proteins and bud into the lms of the ER, from which they are secreted via the Golgi apparatus out of the cell ( Ganem, 2001, Mahonney et al. , 1999 ) . In the genome elaboration tract, the nucleocapsids deliver their genome to magnify the intranuclear pool of covalently closed round DNA ( cccDNA ) ( Ganem, 2001, Mahonney et al. , 1999 ) . The precore polypeptide is transported into the ER lms, where its amino- and carboxy-termini are trimmed and the attendant protein is secreted as precore antigen

( eAg ) . The X protein contributes to the efficiency of HBV reproduction by interacting with different written text factors, and is capable of exciting both cell proliferation and cell decease ( Ganem, 2001, Mahonney et al. , 1999 ) . The HBV polymerase is a multifunctional enzyme. The merchandises of the P cistron are involved in multiple maps of the viral life rhythm, including a priming activity to originate minus-strand DNA synthesis, a polymerase activity, which synthesizes Deoxyribonucleic acid by utilizing either RNA or DNA templets, a nuclease activity which degrades the RNA strand of RNA-DNA loanblends, and the packaging of the RNA pregenome into nucleocapsids ( Chisari et al. , 1997, Ganem, 2001, Mahonney et al. , 1999 ) . Nuclear localisation signals on the polymerase intercede the conveyance of covalently linked viral genome through the atomic pore ( Chisari et al. , 1997 ) .

2.6 HBV Transmission

The virus is transmitted by transdermal and permucosal exposure to infected blood and other organic structure fluids. Infectious degrees of the virus are besides found in fecal matters, spit, piss, serous fluids, vaginal secernments, and seeds ( Larsen et al. , 1995 ) .

Another of import manner of HBV transmittal is from kid to child during early life ensuing from blood contact ( Gatlin N, 1997 ) .

Hazard factors associated with Centers for Disease Control and Prevention ( CDC ) reported Hepatitis B instances in the United States include 36 % spread by heterosexual activity, 13 % by endovenous drug usage, 11 % by homosexual activity, 3 % by family contact, 2 % healthcare employment and 33 % by unknown causes ( Duma, 1995 ) .

Most hepatitis B virus ( HBV ) infections in sub-Saharan African babies and kids are acquired through horizontal transmittal. ( Francis E A. Martinson et al. , 1998 ) .

In Ghana, the behaviours most strongly associated with prevalence of HBV were sharing of bath towels, sharing of masticating gum or partly eaten confects, sharing of dental cleansing stuffs and biting of fingernails in concurrence with rubing the dorsums of bearers ( Francis E A. Martinson et Al, 1998 ) .

2.7 Clinical Manifestation of Hepatitis B virus Infection

After exposure to the Hepatitis B virus, the incubation period before symptoms appear scopes from 60 to 180 yearss ( Larsen et al. , 1995 ) .

The disease can attest in three ways acute, fulminant or chronic ( Figure 4 ) . Acute viral hepatitis begins with general ill-health, anorexia, unease, febrility, sickness, diarrhea, abdominal tenderness and comprehensiveness in the right upper abdominal quarter-circle is besides felt ( Drew L W, 1994 ) .

Chronic infection with hepatitis B virus either may be symptomless or may be associated with a chronic redness of the liver, taking to cirrhosis over a period of several old ages ( Gan Si et al. , 2005 ) .

Chronic hepatitis is strongly linked to the development of hepatocellular carcinoma ( HCC ) . Fulminant infections cause monolithic liver mortification, intellectual map alterations, hepatic failure and frequently decease ( Drew L W, 1994 ) .

Acute hepatitis B occurs in about 1 % of perinatal infections, 10 % of early childhood infections ( kids aged 1-5 old ages ) and 30 % of late infections ( people aged & gt ; 5 old ages ) . Fulminant hepatitis develops in 0.1-0.6 % of acute hepatitis instances ; mortality from fulminant hepatitis B is about 70 % . The development of chronic HBV infection is reciprocally related to the age of acquisition, happening in about 80-90 % of people infected perinatally, approximately 30 % of kids infected before the age of 6 old ages, and in & lt ; 5 % of infections happening in otherwise healthy grownups ( Hyams KC, 1995 ) .

Figure 4

Beginning: Murray et Al, Medical Microbiology, 6th Edition

Copyright @ 2009 by Mosby an imprint of Elsevier, Inc. All rights reserved.

2.8 Pathogenesis of Hepatitis B virus infection

Initial exposure to the HBV infection may happen through injection, heterosexual and homosexual sex and birth. The virus so spreads to the liver, replicates, induces a viraemia, and is transmitted in assorted organic structure secernments to get down the rhythm ( Murray et al. , 2009 )

The virus starts to retroflex in the liver within 3 yearss of its acquisition, but as already noted, symptoms may non be observed for 45 yearss or longer, depending on the infective dosage, the path of infection, and the individual. The virus replicates in hepatocytes with minimum cytopathic consequence. Infection returns for a comparatively long clip without doing liver harm ( i.e. , lift of liver enzyme degrees ) or symptoms. During this clip, transcripts of the HBV genome integrate into the hepatocyte chromatin and stay latent. Intracellular buildup of filiform signifiers of HBsAg can bring forth the ground-glass hepatocyte cytopathology feature of HBV infection. ( Murray et al. , 2009 )

Cell- mediated unsusceptibility and redness are responsible for doing the symptoms and impacting declaration of the HBV infection by extinguishing the septic hepatocyte. However, it has been suggested that much of the liver harm is due to secondary antigen non specific inflammatory responses that are set in gesture by the response, such as TNF, free groups and peptidases. Other immune cell populations, notably natural slayer T cells, likely besides contribute to liver hurt ( Ganem et al. , 2004 )

2.9 Hepatocellular Carcinoma

Epidemiologic surveies have demonstrated that there is a consistent and specific causal association between HBV infection and HCC ( Beasly RP et al. , 1981, Chen et al. , 1997, Popper et al. , 1982 ) .

In patients with relentless HBV infection, the hazard of HCC was 100 times higher than in non-infected persons ( Beasley et al. , 1981 )

The planetary distribution of hepatocellular carcinoma correlatives with the geographic prevalence of chronic bearers of HBV, who figure 400 million worldwide. The highest rates are in Southeast Asia and sub-Saharan Africa, with the HCC incidence & gt ; 50/100, 000 population ( Bosch et al. , 1999 )

Virological factors in the pathogenesis of hepatocellular carcinoma have late been defined. Both retrospective and prospective surveies strongly supported the relation between positive HBeAg and the hazard of HCC ( Lin et al. , 1991, Yang et al. , 2002 ) . HBV DNA was identified as the most of import forecaster of the development of hepatocellular carcinoma in HBsAg-positive patients with different clinical conditions ( Ishikawa et al. , 2001, Ohata et al. , 2004 )

Therefore, attempts at eliminating or cut downing the viral burden may cut down the hazard for HCC. Additionally, HBV genotype might play a function in the development of HCC. ( Ikeda et al. , 2003 )

2.10 Occult Hepatitis B infection

A soundless signifier of hepatitis B infection called supernatural hepatitis B infection ( OBI ) has been recognized for about 20 old ages with the betterments in sensitiveness of serological and genomic elaboration check, it is defined as the presence of HBV-DNA without noticeable HBsAg with or without anti-HBc or anti-HBs, outside the pre-seroconversion window period. Serum HBV degree is normally less than 104 copies/ml ( Xu et al. , 1999 ) .

The frequence of supernatural hepatitis B infection depends on the comparative sensitiveness of both HBsAg and DNA checks, and besides depends on the prevalence of HBV infection in the population. Occult hepatitis B infection ( OBI ) may follow recovery from infection, exposing antibody to hepatitis B surface antigen ( anti-HBs ) and relentless low-level viraemia, flight mutations undetected by the HBsAg checks, or healthy passenger car with antibodies to hepatitis B envelope antigen ( anti-HBe ) and to hepatitis B nucleus antigen ( anti-HBc ) ( Allain, 2004 )

Overall, supernatural HBV infection is seen in 7 % -13 % of anti-HBc-positive and/or anti-HBs-positive topics, and in 0 % to 17 % of blood givers. Occult HBV infection represents a possible transmittal beginning of HBV via blood transfusion or organ organ transplant. The clinical significance of supernatural HBV infection remains ill-defined. ( Brechot, et al. , 2001 )

2.11 Host Immune Response to Hepatitis B virus infection

During HBV infection, the hostA immune responseA causes both hepatocellular harm and viral clearance. Although the innate immune response does non play a important function in these procedures, the adaptative immune response, in peculiar virus specific cytotoxic T lymphocytes ( CTLs ) , contributes to most of the liver hurt associated with HBV infection. CTLs eliminate HBV infection by killing septic cells and bring forthing antiviral cytokines, which are so used to take HBV from feasible hepatocytes. ( Innacone et al, 2007 ) A Although liver harm is initiated and mediated by the CTLs, A antigen-nonspecificA inflammatory cellsA can decline CTL-induced immunopathology, andA plateletsA activated at the site of infection may ease the accretion of CTLs in the liver. ( Innacone et al. , 2005 )

Primary infection leads to an IgM and IgG response to HBcAg shortly after the visual aspect of HBsAg in serum, at oncoming of hepatitis. Anti-HBs and anti-HBe appear in serum merely several hebdomads subsequently, when HBsAg and HBeAg are no longer detected, although in many HBsAg-positive patients, HBsAg-anti-HBs composites can be found in serum ( Robinson, 1994, Mahoney, 1991 )

2.12 Diagnosis of Hepatitis B virus infection

The trials called checks used for sensing of hepatitis B virus infection involve serum or blood which detects viral antigens orA antibodies produced by the host. ( Bonino et al, 1987 )

The diagnosing of HBV infection requires the rating of the patient ‘s blood for HBsAg, hepatitis B surface antibody ( HBsAb ) , and hepatitis B nucleus antibody ( HBcAb ) . The presence of HBsAg indicates either ague or chronic infection ; the presence of HBsAb indicates recovery and unsusceptibility from HBV infection or successful immunisation against HBV. HBcAb appears at the oncoming of acute HBV infection, but may besides bespeak chronic HBV infection. Whiles sensing of Hepatitis E surface antigen ( HBeAg ) indicates that person with a chronic infection is more contagious ( Table 1 ) .

Serologic Markers

Interpretation

HBsAg infection

Acute / Chronic infection

Anti-HBc Igm

Acute infection

HBeAg

High infectivity

Anti-HBe

Low infectivity

Anti-HBs

Unsusceptibility

Anti-HBc IgG and HBsAg

Chronic infection

Anti-HBc IgG and anti-HBs

Resolved infection

Table 1: Interpretation of HBV immunologic markers.

Beginning: Sjogren MH. Serologic diagnosing of viral hepatitis

PCRA trials have been developed to observe and mensurate the sum of HBV DNA, called theA viral burden, in clinical specimens. These trials are used to measure a individual ‘s infection position and to supervise intervention. ( Zoulim, 2006 )

The enzyme-linked immunosorbent check ( ELISA ) is one of the most sensitive and specific methods for naming HBV infections. It is utile for early sensing of HBsAg. ( Fontirrochi et al. , 1993 )

2.13 Prevention of Hepatitis B infection

i»? Hepatitis B virus infection is a preventable disease. Transmission of HBV via transfusion of blood and plasma-derived merchandises has been eliminated in most states through giver showing for HBsAg and viral inactivation processs. However, transmittal besides occurs with inadequately sterilized acerate leafs and medical instruments, reuse of disposable acerate leafs and panpipes, and taint of multiple-dose medicine phials ( Alter, 2003 ) . The usage of rubber is recommended to avoid infection through sexual contacts. Immune-prophylaxis with Hepatis B immune-globulin ( HBIG ) has shown important protection against infection in HBV open persons ( Szmuness et al. , 1974 ) . Hepatitis B immune-Globulin ( HBIG ) is besides powerful to cut down HBV intrauterine infection when administered to pregnant adult females during late gestation ( Li et al. , 2004 ) . However, inoculation is the most of import tool in forestalling the transmittal of HBV. In 1992, the World Health Organization recommended that childhood hepatitis B inoculation should be included in immunisation plans of all states ( World Health Assembly, 1992 ) . High efficaciousness and safety have been proved for the vaccinums used with protective degrees of antibodies elicited in more than 90 % of the receivers ( Hammond et al. , 1991 ) . The execution of inoculation has dramatically changed the epidemiology of HBV in states where the transmittal has been largely perpendicular ( Chang et al. , 1997 ) .

Education sing infection bar and transmittal particularly of the groups at hazard of hepatitis exposure is supposed to be one of the cost- effectual ways of infection control ( Alavian et al. , 2007 ) . However, despite the execution of public wellness intercessions, such as cosmopolitan immunisation and injury decrease plans for HBV, HBV transmittal still persists among new coevalss of shooting drug users ( Lum et al. , 2008 ) .

2.14 Treatment of Hepatitis B virus infection

TheA hepatitis BA infection does non normally require intervention because most grownups clear the infection from their organic structure ( Hollinger et al. , 2006 ) . Treatment with antiviral drugs may be required in less than 1 % of people, whose infection takes on really aggressive class and in those who are in immunocompromised. Treatment stopping points from six months to a twelvemonth, depending on medicine and genotype ( Lai et al. , 2007, Alberti, et al. , 2011 ) .

Available drugs for intervention of Hepatitis B infection do non necessary clear the virus, but they can halt the virus from retroflexing, therefore minimising liver harm. As of 2008, seven medicines have been licenced for the intervention of Hepatitis B infection in the United States. These antiviral drugs are lamivudine, tenofovir, adefovir, telbivudine, entecavir and two immune system modulators interferon, alpha-2a and PEGylated interferon alpha-2a ( Pegasys ) ( Dienstag JL, 2008 ) . The intervention reduces viral reproduction in the liver, thereby cut downing the sum of virus atoms in the blood ( viral burden ) ( Pramoolsinsup, 2002 )