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1.1     Background of Study

Viral hepatitis is an inflammation of the liver affecting millions of people every year. Five different types of hepatitis viruses (A-E) are responsible for viral hepatitis (Prescott et al., 2002; WHO, 2002). Of these five viruses, hepatitis C virus (HCV) is the second most common type of virus (after hepatitis B virus) that infects the liver. HCV is a small single-stranded ribonucleic acid (RNA) virus that belongs to the Flaviviridae family. HBV and HCV can both be transmitted by exposure to infectious semen, blood, also other body fluids. They can also be transmitted from infected mothers to infants (Lam et al., 2010). Other routes of transmission could be in the course of unsafe sexual intercourse, injections, transfusions through contaminated blood, and sharing of needles as well as syringes among injecting drug users (Averhoff et al., 2012; Lai et al., 2013). About 75 – 85% of patients with HCV develops chronic infection and about 10 – 15% of patients with HCV develops liver cirrhosis (Chen and Morgan, 2006). The risk of vertical transmission of HCV depends on positivity of the mother for HCV RNA and if the mother is HCV RNA positive, the rate of vertical transmission becomes about 4.3%. On the other hand, in mothers co-infected with HIV the rate of vertical transmission increases up to 19.4% (Lam et al., 2010; Navabakhsh et al., 2011). Viral hepatitis during pregnancy is associated with high risk of maternal complications; they include premature contractions, vaginal bleeding, placental separation, premature rupture of membranes, preterm delivery, gestational diabetes mellitus and mortality (Safir et al., 2010; Reddick et al., 2011). The prevalence of HCV infection varies greatly in different regions of the world and it is highly endemic in areas such as Asia, sub-Saharan Africa, the Middle East, the Pacific Basin, and the Amazon Basin (Walle et al., 2008). In Nigeria, the prevalence rates of HCV in pregnant women differ from one locality to another. Oladeinde et al (2013) reports a rate of 0.8% of HCV infections amongst pregnant women in Benin City, Nigeria. Pregnant women are regarded a sentinel population because they are a comparatively unselected population, for whom prevalence data may be extended to the general sexually active heterosexual population ((Saphonn et al., 2012). Failure to diagnose and treat these overwhelming disease agents at an early stage may lead to serious complications and sequelae, they include infertility, ectopic pregnancy, fetal wastage, anogenital cancer, premature death, and also as neonatal and infant infections (W H O, 2003).

1.2     Aim and Objectives

The primary aim of the present study is to survey the hepatitis C virus prevalence among pregnant women attending antenatal in Federal Teaching Hospital, Abakaliki, Ebonyi State south eastern part of Nigeria. To realize this aim, the objectives include:

  1. To establish the HCV occurrence rate among the subjects with respect to age.
  2. To establish the HCV occurrence rate among the subjects with respect to trimester.
  3. To establish the HCV occurrence rate among the subjects with respect to gravidity.

1.3     Significance of Study

Although different studies on the prevalence of HCV have been conducted in different parts of Africa, most of them focused on investigating the prevalence among blood donors, HIV infected individuals, health care workers and medical waste handlers. There is very limited data about the magnitude of HCV prevalence among pregnant women in Ebonyi towns and the adjacent administrative areas. Hence, the main aim of this research is to assess prevalence and predictors of HCV infections among pregnant women attending antenatal in Federal Teaching Hospital Abakaliki.



2.1     Virology of Hepatitis C Virus (HCV)

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus (Rosen, 2011). It is a member of the Hepacivirus genus in the family Flaviviridae (Ray and Thomas, 2009). There are seven major genotypes of HCV, which are known as genotypes one to seven (Nakano et al., 2011). The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes (Wilkins et al., 2010). Genotype 1 is also the most common in South America and Europe (Rosen, 2011).

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes (Lerat and Hollinger, 2004). In an infected person, about 1012 virus particles are produced each day (Lerat and Hollinger, 2004). In addition to replicating in the liver the virus can multiply in lymphocytes (Lerat and Hollinger, 2004).


2.1.1  Viral Replication

Replication of HCV involves several steps. The virus replicates mainly in the hepatocytes of the liver, where it is estimated that daily each infected cell produces approximately fifty virions (virus particles) with a calculated total of one trillion virions generated. The virus may also replicate in peripheral blood mononuclear cells, potentially accounting for the high levels of immunological disorders found in chronically infected HCV patients. HCV has a wide variety of genotypes and mutates rapidly due to a high error rate on the part of the virus’ RNA-dependent RNA polymerase. The mutation rate produces so many variants of the virus it is considered a quasispecies rather than a conventional virus species (Lindenbach and Rice, 2005). Entry into host cells occurs through complex interactions between virions and cell-surface molecules CD81, LDL receptor, SR-BI, DC-SIGN, Claudin-1, and Occludin (Lindenbach and Rice, 2005).

Once inside the hepatocyte, HCV takes over portions of the intracellular machinery to replicate (Lindenbach and Rice, 2005). The HCV genome is translated to produce a single protein of around 3011 amino acids. The polyprotein is then proteolytically processed by viral and cellular proteases to produce three structural (virion-associated) and seven nonstructural (NS) proteins. Alternatively, a frameshift may occur in the Core region to produce an Alternate Reading Frame Protein (ARFP) (Syed et al., 2010). HCV encodes two proteases, the NS2 cysteine autoprotease and the NS3-4A serine protease. The NS proteins then recruit the viral genome into an RNA replication complex, which is associated with rearranged cytoplasmic membranes. RNA replication takes places via the viral RNA-dependent RNA polymerase NS5B, which produces a negative strand RNA intermediate. The negative strand RNA then serves as a template for the production of new positive strand viral genomes. Nascent genomes can then be translated, further replicated or packaged within new virus particles. New virus particles are thought to bud into the secretory pathway and are released at the cell surface.

The virus replicates on intracellular lipid membranes (Dubuisson et al., 2012). The endoplasmic reticulum in particular is deformed into uniquely shaped membrane structures termed ‘membranous webs’. These structures can be induced by sole expression of the viral protein NS4B (Dubuisson et al., 2012). The core protein associates with lipid droplets and utilizes microtubules and dyneins to alter their location to a perinuclear distribution (Lindenbach and Rice, 2005). Release from the hepatocyte may involve the very low density lipoprotein secretory pathway (Syed et al., 2010).

2.2     Risk factors/Mode of Transmission

Hepatitis C virus is predominantly a blood-borne virus, with very low risk of sexual or vertical transmission (Shepard et al., 2005). Because of this mode of spread the key groups at risk are injecting drug users (IDUs), people who are transfused blood, recipients of blood products and sometimes patients on haemodialysis. Common setting for transmission of HCV is also intra-hospital (nosocomial) transmission, when practices of hygiene and sterilization are not correctly followed in the clinic (Alter, 2011). A number of cultural or ritual practices have been proposed as a potential historical mode of spread for hepatitis C virus, including circumcision, genital mutilation, ritual scarification, traditional tattooing and acupuncture.[34] It has also been argued that given the extremely prolonged periods of persistence of HCV in humans, even very low and undetectable rates of mechanical transmission via biting insects may be sufficient to maintain endemic infection in the tropic, where people receive large number of insect bites (Pybus et al., 2007).

2.2.1  Intravenous drug use (IDU)

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80% (Pondé, 2011). Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment (Imperial, 2010).

2.2.2  Healthcare exposure

Transfusion of blood and blood products or organ transplants without HCV screening is associated with significant risks of infection. The United States instituted universal screening in 1992 and Canada instituted universal screening in 1990. This decreased the risk from one in 200 units to between one in 10,000 to one in 10,000,000 per unit of blood (Pondé, 2011). This low risk remains as there is a period of about 11–70 days between the potential blood donor’s acquiring hepatitis C and the blood’s testing positive depending on the method (Pondé, 2011).

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