THE PRESENCE OF HEPATITIS B ENVELOPE ANTIBODY IN PATIENTS WHO HAVE BEEN PREVIOUSLY SCREENED FOR THE SURFACE ANTIGEN

THE PRESENCE OF HEPATITIS B ENVELOPE ANTIBODY IN PATIENTS WHO HAVE BEEN PREVIOUSLY SCREENED FOR THE SURFACE ANTIGEN

Chapter one

INTRODUCTION

A virus is a tiny infectious agent with a simple acellular structure and a nucleic acid/protein coat. It lacks independent metabolism and can only replicate in living hosts. A virus enters living cells and uses its chemical machinery to remain alive and proliferate in the host.

It can reproduce with fidelity or with faults (mutations); this ability to mutate is what causes some viruses to differ significantly in each infected individual, making therapy difficult. Viruses cause a wide range of human infections as well as a number of unusual disorders.

The human disorders they produce can impact many organs or sections of the body. Hepatitis is a broad word used to describe liver inflammation caused by a range of viruses such as hepatitis A, B, C, D, and E. Hepatitis B is one of the most important viral causes of hepatitis worldwide.

The hepatitis B virus (HBV) is part of the Hepadnaviridae family, which includes hepatotropic DNA viruses. The Hepadnavirus family includes members recovered from animal species such as the woodluck hepatitis virus (WHV), ground squirrel hepatitis virus (GSHV), and duck hepatitis virus (HBV). All of these viruses are enclosed, contain 3 to 3.3 kb of relaxed circular partly duplex DNA, and have reverse transcriptase activity.

Hepadnaviruses have narrow host ranges, growing only in species that are near to their natural host, such as gibbons, African green monkeys, rhesus monkeys, and woolly monkeys (Gitlin, 1997). Hepatitis virus belongs to the Hepadnavirus genus.

It is a 42nm partially double-stranded DNA virus made up of a 27nm nucleic acid core (HBcAg), a DNA polymerase reverse transcriptase, and an outer lipoprotein coat (called envelope) containing the surface antigen (HBsAg), which plays an important role in the diagnosis of HBV infection (Ganem et al; 2001; Gitlin, 1997).

The genome is made up of a partly double-stranded circular DNA molecule that is around 3200 base pairs long and has a defined sequence and genetic organisation.

Virion particles are identical to virion ‘tails’; they vary in length and have an average diameter of about 22nm. They occasionally exhibit regular, non-helical transverse striations.

The polymerase gene [P] encodes the viral DNA polymerase-reverse transcriptase, which is critical for virus replication. Unlike all known mammalian DNA viruses, hepadnaviruses replicate by reverse transcription of an RNA intermediate, the pregenomic RNA (Summerset et al.,1982), which is a key strategy in the life cycle of RNA retroviruses.

Nassal (1999) defined the similarities and differences between retroviral and hepadnaviral replication. Based on HBV’s unique replication cycle, antiviral therapeutic strategies aimed at reverse transcription of HBV RNA or HBV reverse transcriptase have been used successfully to treat HBV infection (Feld, 2002).

The prevalence of HBV infection varies by country, region, and ethnic group. HBV endemicity is classified into three categories: high (>8%), intermediate (2-8%), and low (<2%), based on the prevalence of HBsAg seropositivity.

East and Southeast Asia, the Pacific, sub-Saharan Africa (including Nigeria), and southern Europe are among the world’s most endemic regions.

HBV infection is uncommon in North America, as well as western and northern Europe, with a prevalence of less than 0.1%. Hepatitis B virus (HBV) infection is a major global health concern, with 2 billion people infected worldwide and 350 million suffering from chronic HBV infection. HBV is the world’s 10th leading cause of death, accounting for 600,000 deaths each year (Ott et al 2012).

Chronic hepatitis, cirrhosis, and hepatocellular carcinoma all cause 1.2 million deaths per year, with the latter accounting for 320 000 deaths (WHO, 2000).

In Western countries, the disease is relatively uncommon and acquired primarily in adulthood, whereas chronic HBV infection is common in Asia and most of Africa and is usually acquired perinatally or during childhood.

The whole of Africa is regarded as highly endemic, coming only behind Asia. Although overall Africa is considered a high endemic area with 7–26% prevalence of HBsAg, Tunisia, Morocco, and Zambia have intermediate endemicity (Andre, 2000).

In West Africa, countries like Senegal and Gambia have over 90% of their populations exposed to and becoming infected with HBV during their lives (Edmund WJ. et al., 1996).

In Nigeria, not less than 23 million people are estimated to be infected with HBV (Bukola, 2015), making Nigeria one of the countries with the highest incidence of HBV infection in the world.

Hepatitis B is caused by hepatitis B virus. The virus interferes with the functions of the liver while replicating in hepatocytes. The immune system is then activated to produce a specific reaction to combat and possibly eradicate the infectious agent. As a consequence of pathological damage, the liver becomes inflamed.

HBV may cause up to 80 per cent of all cases of hepatocellular carcinoma (HCC) worldwide, second only to tobacco among known human carcinogens (WHO, 2001). Most people do not experience any symptoms during the acute infection phase.

However, some people have acute illness with symptoms that last several weeks, including yellowing of the skin and eyes (jaundice), dark urine, extreme fatigue, nausea, vomiting and abdominal pain. In some people, the hepatitis B virus can also cause a chronic liver infection that can later develop into cirrhosis of the liver or liver cancer (WHO, 2014).

Susceptibility to HBV infection is general. Only people who have been vaccinated successfully or have developed anti-HBs antibodies after HBV infection are immune to HBV infection.

Persons with congenital or acquired immunodeficiency including HIV infection, those with immunosuppression including those with lymphoproliferative disease, patients treated with immunosuppressive drugs including steroids and by maintenance haemodyalisis are more likely to develop persistent infection with HBV.

Hepatitis B can be spread by;

• unprotected sex

• sharing IV drug needles

• living in a family with an infected individual

• an infected mother to her newborn kid during birth

• exchanging earrings, razors, or toothbrushes with an infected individual

• unsterilized needles, including tattoo or piercing needles

• human bites.

People are most at risk for hepatitis B if they

Children are born to moms who are infected with HBV

• live in close household contact with a chronically diseased individual

• adopt a child from a nation where HBV is widespread

• have unprotected sex or have more than one sexual partner in a six month period

• Have you ever had a sexually transmitted illness (STD)?

• are males having sex with men.

• Share needles and syringes.

• are a health care worker or emergency responder who may come into contact with bodily fluids.

You are undergoing renal dialysis.

• reside or work in an institutional setting, such as a jail or group home.

Biochemical examination of liver function is used to diagnose hepatitis. Initial laboratory tests should include total and direct bilirubin, ALT (alanine transaminase), AST (aspartate aminotransferase), alkaline phosphatase, prothrombin time, total protein albumin, globulin, complete blood count, and coagulation studies (Hollinger et al., 2001).

Specific antigens and/or antibodies must be present to validate the diagnosis. There is currently no treatment for acute HBV infection, but it is vaccine-preventable.

Several vaccines have been used to prevent this illness, the most well-known of which are Lamivudine, Adefovir, Dipivoxil, Famvir, FTC, Ritonavir, Theradigm-HBV, and Ganciclovir.

1.1 Objectives.

Hepatitis B virus infection is a global concern. More importantly, it is a national concern, with over 23 million Nigerians infected with HBV.

The incidence of infection in South-Western Nigeria is as significant, given the region’s high rate of immunisation issues. The majority of texts have focused on HBsAg, although other markers are just as significant. The goal of this investigation is, therefore,

1. To detect the presence of Hepatitis B envelope antibodies in patients who have previously been tested for the surface antigen.

2. Determine which group of people is most affected.