CHAPTER ONE

INTRODUCTION

Hepatitis C virus (HCV) was discovered in 1989 and the first

blood test was available in May; 1990 (Jean-Jacquces et al.,

2004). Hepatitis C is a spherical, enveloped, single

stranded RNA virus of the family Flaviviridae, Genus Hepacivirus

(Kapoor et al., 2011). It is spread primarily through direct

contact with blood or body fluids of infected individuals.

It is also genetically diverse and divided into at least six

different clones (1 to 6) which include eleven types and

numerous subtypes (Jean-Jacquces et al., 2004). The diversity

depends on mutation on the genome of the virus. The N

terminus of E2 protein, the first hyper variable region

(HVR), has the highest diversity in studies of chronically

infected adults. Higher diversity of this region has been

associated with progression of liver disease (Zhi et al.,

2004).

Hepatitis C virus is an intracellular pathogen that takes

over replication machinery within an infected cell (mostly

hepatocytes), effectively turning the cell into a factory.

People who control HCV before it becomes chronic mount a

vigorous T-cell response. But while most people’s T-cell can

recognize and attack HCV infected cells, this response is

usually not enough to keep up with HCV replication and

1

protect other liver cells from being infected (Jeffery et al.,

2003).

Antibody response appears to be less important. Studies have

shown that neutralizing antibodies are produced during HCV

infection, but do not appear to be protective against re-

infection in human or in chimpanzees (Jeffery et al., 2003).

If the initial immune response following infection is not

sufficiently strong, persistent viral replication leads to

mutant strains, which are no longer detected by the immune

cells (San Diego, 1999). The possible strategies for HCV to

escape immune elimination may include decrease in visibility

to the immune system, decrease in the effectiveness of

antiviral cytokines, infection of immunologically privileged

sites, induction of immunologic tolerance and immunologic

evasion (Jeffery et al., 2003).

Hepatitis caused by the HCV is a leading cause of liver

failure and liver transplantation in adults (Karen et al.,

2003). The typically newly diagnosed patient is usually

young, healthy and has few or no symptoms that can be

attributed to the HCV infection. Because of these some

doctors and many patients do not consider Hepatitis C to be

a very serious illness (Karen et al., 2003). Clearly Hepatitis

C is a progressive liver disease which eventually leads to

cirrhosis with its attendant risks of liver cancer

(hepatocellular carcinoma), liver transplantation and death

2

(Dale et al., 2004 and Michael and Alexander, 2004). HCV may

take years in some persons to severely damage the liver. The

younger the person when the infection is acquired, the

higher it is likely that progression to cirrhosis may occur

during the person’s life time.

While the primary site of clinical infection with HCV is the

liver, a significant number of people develop disease

symptoms at sites other than the liver, referred to as extra

hepatic manifestations of chronic hepatitis C virus

infection. These include arthralgia, paresthesia, myalgia, pruritia and

sicca syndrome (Jeffery-Schouten, 2000).

The main risk factors for HCV transmission are maternal

infection and transfusion of blood products. Other risk

factors for hepatitis C virus infection include, intravenous

drug use, exposure, intranasal drugs use, multi-sexual

partners, history of sexually transmitted disease,

tattooing, hemodialysis, working in patient care or a

clinical laboratory, and low socioeconomic level (Ala et al.,

1996 and Karen et al., 2003). In 1970s and 1980s post

transfusion non A, non B hepatitis and HCV is the primary

etiologic agent of parenterally transmitted non A, non B,

hepatitis worldwide (Giancarlo et al., 2001 and Maria et al.,

2004).

Currently, unlike Hepatitis A and Hepatitis B, there is no

vaccine to protect people from Hepatitis C as little is

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known about the variability of HCV genome and how the immune

system interacts with the virus (Maria et al., 2004).

The key to the early diagnosis of HCV infections is to

identify and test those individuals at risks for having

hepatitis C or when liver enzymes (e.g. alanin amino

transferees) are found to be elevated on routine testing

(Dale et al., 2004.). Detection of HCV requires not only the

measurement of levels of liver enzymes, but also testing for

the hepatitis C antibodies in the blood and testing for the

viral genome as some people with hepatitis C infection may

have normal levels of liver enzymes (Dale et al., 2004).

Antibody to hepatitis is detected by the use of 3rd or 4th

generation recombinant enzyme linked immune sorbent assay

(ELISA) which is found to have high sensitivity and

specificity (Dale et al., 2004). Both quantitative and

qualitative RNA tests are used to detect viral genome in the

blood to access therapeutic effectiveness and management of

patient with hepatitis C (Linda et al., 2004). Viral

eradication, however, should not be the only end point in

all HCV patients. Achieving significant reductions in viral

load usually results in marked improvement of the liver

inflammation and will retard progression to more severe

liver damage (Linda et al., 2004). The cornerstone of

hepatitis C treatment is the use of interferon. Interferons

are proteins normally produced by the body’s immune system

in response to a viral infection and the human body produces

4

over 20 different types of interferons. There are four types

of interferons licensed in the USA for the treatment of HCV

namely, interferon alfa2b (intron -A) interferon alfa2a

(Roferon-A), consensus interferon (intergen) and interferon

alpha n-1 (ellferon) (Ala et al., 1996). Studies have shown

the efficiency of the combination of paginated interferon

and ribavirin in the treatment of patients with chronic

Hepatitis C (Jean-Jacque et al., 2004).

Preventive measures are used to reduce the burden of HCV

infection. These measures include primary prevention

activities that reduce risks for contracting HCV infection

and secondary prevention activities that reduce risks for

liver and other chronic diseases in HCV infected persons.

The primary preventive activities include, screening and

testing of blood, plasma, organ, tissue and semen donors,

virus inactivation of plasma derived products, risk

reduction counseling and implementation and maintenance of

infection control practices, while secondary prevention

activities include, identification, counseling and testing

of persons at risk and medical management of infected

persons.

1.1 Statement of the Problem

Egah et al (2004) reported Hepatitis C Virus seroprevalence

of 6.0% among blood donors in Jos. Ayolabi et al (2006) in

Lagos reported a HCV seroprevalence of 8.4% all among blood

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donors. It is estimated that 130–200 million people, or 3%

of the world's population, are living with chronic Hepatitis

C (Gravitz, 2011 and WHO, 2010). About 3–4 million people

are infected per year, and more than 350,000 people die

yearly from Hepatitis C-related diseases (WHO, 2010). HCV

infection may ultimately lead to cirrhosis and

hepatocellular carcinoma (Karen et al., 2003). HCV is the most

important cause of post transfusion non A and B hepatitis

worldwide (Maria et al., 2004).

1.2 Justification

Hepatitis C virus (HCV) poses a significant threat to health

worldwide (Dale et al., 2004). Although the transmission of

Hepatitis C virus through the transfusion of blood and blood

products has nearly disappeared since the introduction of

approved screening measures worldwide among blood donors,

studies have shown its prevalence in some parts of Nigeria,

viz; Lagos (Lesi and Kehinde, 2003) and Jos (Egah et al.,

2004). The prevalence of chronic HCV among blood donors has

also been noted in some West African countries (Jean-

francois et al., 2001) these include Ghana (Wansbrough et al.,

1998), Senegal, Mauritania and Benin (Jean-francois et al.,

2001). In most parts of Nigeria, the screening for Hepatitis

C among blood donors is not practiced despite the fact that

it can lead to serious sequelae. As a result, the actual

burden of the disease is not known. There is therefore the

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need for studies to check its prevalence especially in this

part of the Country so as to have a clue to its spread which

can help healthcare policy makers and care givers in

providing measures of controlling the disease.

1.3 Aim and Objectives

Aim:

To determine the prevalence of hepatitis C virus among blood

donors attending General Hospital Minna

Objective:

To determine the risk factors associated with HCV

seropositivity.

CHAPTER TWO

LITERATURE REVIEW

2.1 History of Hepatitis C Virus

In the mid-1970s, Harvey J. Alter, Chief of the Infectious

Disease Section in the Department of Transfusion Medicine at

the National Institutes of Health, and his research team

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demonstrated how most post-transfusion hepatitis cases were

not due to hepatitis A or B viruses. Despite this discovery,

international research efforts to identify the virus,

initially called nonA-non-B hepatitis (NANBH), failed for the

next decade. In 1987, Michael Houghton, Qui-Lim Choo, and

George Kuo at Chiron Corporation, collaborating with Dr.

D.W. Bradley at the Centers for Disease Control and

Prevention, used a novel molecular cloning approach to

identify the unknown organism and develop a diagnostic test

(Boyer, 2001). In 1988, the virus was confirmed by Alter by

verifying its presence in a panel of NANBH specimens. In

April 1989, the discovery of HCV was published in two

articles in the Journal Science (Choo et al., 1989 and Kuo et al.,

1989). The discovery led to significant improvements in

diagnosis and improved antiviral treatment (Boyer, 2001). In

2000, Drs. Alter and Houghton were honored with the Lasker

Award for Clinical Medical Research for pioneering work

leading to the discovery of the virus (Winner, 2008).

2.2 Biology of Hepatitis C Virus: The hepatitis C virus

(HCV) is a small, enveloped, single, positive-sense RNA

virus (Rosen, 2011).

2.2.1 Genome of Hepatitis C Virus:

The HCV genome carries a single long open reading frame

(ORF) encoding a polyprotein that is proteolytically cleaved

into a set of distinct products. Translation of the HCV ORF8

is directed via a ∼340 nucleotide long 5′ non-translated

region (NTR) functioning as an internal ribosome entry site

(IRES) and permitting the direct binding of ribosomes in

close proximity to the start codon of the ORF (Tsukiyama-

Kohara et al., 1992; Wang et al., 1993). The first ∼40

nucleotides of the RNA genome are not required for

translation but, based on analogy with other plus-strand RNA

viruses, are involved most likely in RNA replication (Boyer

& Haenni, 1994). The 3′ NTR was only recently discovered

(Kolykhalov et al., 1996; Tanaka et al., 1995, 1996; Yamada et al.,

1996). It has a tripartite structure composed of a variable

sequence following the stop codon of the ORF, a poly (U)

tract of heterogeneous length and a highly conserved 98

nucleotide sequence essential for replication in vivo (Yanagi

et al., 1999; Kolykhalov et al., 2000).

The HCV polyprotein is cleaved co- and post-translationally

by cellular and viral proteinases into ten different

products, with the structural proteins located in the amino-

terminal one-third and the nonstructural replicative

proteins in the remainder (Bartenschlager, 1999; Reed et al.,

1998). The first cleavage product of the polyprotein is the

highly basic core protein, forming the major constituent of

the nucleocapsid (Yasui et al., 1998). In addition, a number

of other functions like modulation of several cellular

processes or induction of hepatocellular carcinoma in

transgenic mice have been described (Chang et al., 1998; Chen

9

et al., 1997 and Matsumoto et al., 1997). Envelope proteins (E1

and E2) are highly glycosylated type 1 transmembrane

proteins, forming two types of stable heterodimeric

complexes: a disulfide-linked form representing misfolded

aggregates and a non-covalently linked heterodimer

corresponding most likely to the pre-budding complex

(Deleersnyder et al., 1997). In addition, E2 was shown to

interact with the IFN-induced double-stranded RNA-activated

protein kinase PKR. Upon induction by IFN-α, this enzyme

reduces protein synthesis via phosphorylation of translation

initiation factor eIF2-α, but in cells containing E2, PKR is

inhibited, allowing continuation of translation in the

presence of IFN (Taylor et al., 1999). Protein p7, located at

the carboxy terminus of E2, is a highly hydrophobic

polypeptide of unknown function. Most of the nonstructural

(NS) proteins 2–5B (the term indicates that these proteins

are not expected to be constituents of the virus particle)

are required for replication of the viral RNA (Lohmann et al.,

1997). NS2 and the amino-terminal domain of NS3 constitute

the NS2–3 proteinase, catalysing cleavage at the NS2/3 site

(Grakoui et al., 1993). NS3 is a bifunctional molecule

carrying in the amino-terminal ∼180 residues, a serine-type

proteinase responsible for cleavage at the NS3/4A, NS4A/B,

NS4B/5A and NS5A/B sites and, in the carboxy-terminal

remainder, NTPase/helicase activities essential for

translation and replication of the HCV genome (Gwack et al.,

10

1996; Kim et al., 1995; Suzich et al., 1996; Bartenschlager et al.,

1993; Eckart et al., 1993; Grakoui et al., 1993; Tomei et al.,

1993; Kolykhalov et al., 2000). In addition, NS3 may have

other properties involved in interference with host cell

functions like inhibition of protein kinase A-mediated

signal transduction or cell transformation (Borowski et al.,

1996). NS4A is an essential cofactor of the NS3 proteinase

and is required for efficient polyprotein processing

(Bartenschlager et al., 1994; Failla et al., 1994; 1994; Tanji et

al., 1995). The function of the hydrophobic NS4B is so far

unknown. NS5A is a highly phosphorylated protein and, at

least with some HCV isolates, the level of phosphorylation

is influenced by NS4A via direct interaction with NS5A or it

requires the expression of NS5A in the context of a NS3–5A

polyprotein (Asabe et al., 1997; Tanji et al., 1995., Kaneko et

al., 1994; Koch & Bartenschlager, 1999; Neddermann et al.,

1999;). NS5A phosphorylation is mediated by an as yet

unknown cellular kinase (Tanji et al., 1995;Ide et al., 1997;

Reed and Rice, 1999). For the HCV-H isolate the major

phosphorylation site has been mapped to serine residue 2321

of the polyprotein and the proline-rich nature of the

flanking sequence suggests that a proline-directed kinase is

responsible for NS5A phosphorylation (Reed & Rice, 1999).

The role NS5A may play in RNA replication is so far not

known, but based on analogy with other RNA viruses, where

phosphoproteins are important regulators of replication; one

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could assume that NS5A plays a similar role. Apart from such

a function, NS5A appears to be involved in resistance of the

infected cell to the antiviral effect of IFN. At least for

some HCV isolates NS5A is able to bind to PKR, blocking the

translational reduction in the IFN-treated cell (Gale et al.,

1997, 1998). Interestingly, an alanine substitution for the

major phosphorylation site at serine residue 2321 did not

affect the NS5A: PKR interaction, showing that

phosphorylation at this particular site is not required for

complex formation with PKR (Reed & Rice, 1999). NS5B was

identified as the RNA-dependent RNA polymerase (RdRp) (Al et

al., 1998; Behrens et al., 1996; Lohmann et al., 1997; Yamashita et

al., 1998; Yuan et al., 1997).

2.3 Classification of Hepatitis C Virus (HCV):

HCV has been classified as the sole member of a distinct

genus called Hepacivirus in the family Flaviviridae, which

includes the Flaviviruses, the animal pathogenic

pestivivruses and although this awaits official

confirmation, the recently cloned GB virus A (GBV-A), GBV-B

and GBV-C/ hepatitis G viruses (Ray et al., 2009). There are

seven major genotypes of HCV, which are indicated

numerically from 1-7 (Nakano et al., 2011). 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

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(Wilkins et al., 2011). Genotype 1 is also the most common in

South America and Europe (Rosen, 2011).

2.4 Mode of Replication:

HCV nonstructural proteins and viral RNA have been detected

in livers of infected patients or experimentally inoculated

chimpanzees, confirming that the liver is a site of HCV

replication (Blight & Gowans, 1995). Unfortunately, the

amounts of viral proteins and RNA in infected tissues are

very low, necessitating the use of highly sensitive but also

less reliable detection methods. This may in part explain

why the reported number of HCV-positive cells detected in

infected liver tissue is contradictory and estimates vary

between less than 5% and up to 100% (Blight & Gowans, 1995).

Apart from liver cells, there is strong evidence that HCV

can also replicate in peripheral blood mononuclear cells

(PBMCs) both in vivo and ex vivo or in experimentally infected

B- and T-cell lines (see below). Such a lymphotropism may

account for the numerous immunological disorders, in

particular type II and type III cryoglobulinaemia, observed

in more than 50% of chronic hepatitis C patients (Esteban et

al., 1998).

The dynamics of HCV replication can be deduced from the

rapid rates of virus production and emergence of mutants.

13

Owing to the lack of a convenient animal model and an

efficient cell culture system our current understanding of

the molecular mechanisms of HCV replication is based

primarily on analogies to the closely related flavi- and

pestiviruses and on the characterization of recombinant HCV

proteins. Using this limited information the HCV replication

cycle can be summarized as follows:

i. Penetration of the host cell and liberation of the

genomic RNA from the virus particle into the cytoplasm

ii. Translation of the input RNA, processing of the

polyprotein and formation of a replicase complex associated

with intracellular membranes

iii. Utilization of the input plus-strand for synthesis of a

minus-strand RNA intermediate

iv. Production of new plus-strand RNA molecules which in

turn can be used for synthesis of new minus strands, for

polyprotein expression or packaging into progeny virions

v. Release of virus from the infected cell.

2.5 Life Cycle:

The first step in a virus life-cycle is the attachment of

the infectious particle to the host cell, for which a

specific interaction between a receptor on the cell surface

and a viral attachment protein on the surface of the

particle is required. CD81 was identified as a putative HCV

receptor based on its strong interaction with E2 as well as14

with virus particles in vitro (Pileri et al., 1998). Furthermore,

preincubation of the HCV-containing plasma used for the

binding studies with sera from chimpanzees that were

protected from HCV challenge by vaccination with recombinant

E1 and E2 also blocked in vitro binding of HCV to CD81 (Pileri

et al., 1998). However, whether virus binding to CD81 is

followed by internalization of the virus particle is not

known.

Apart from this route, HCV as well as other members of the

Flaviviridae family may enter the cell by binding to low-

density lipoprotein (LDL) receptors. Based on the

observation that HCV particles are associated with beta-

lipoproteins (Thomssen et al., 1992 and Agnello et al.,1999),

analysed whether endocytosis of HCV is mediated by LDL

receptors. Using in situ hybridization to determine HCV-RNA-

positive cells, a direct correlation between the level of

cell surface-expressed LDL receptor and the number of

positive cells was found. This result and the finding that

HCV does not bind to COS-7 cells unless they have been

transfected with the LDL receptor gene (Monazahian et al.,

1999) suggest that HCV particles associated with LDL bind to

this receptor. Whether interaction with the LDL receptor or

CD81 leads to a productive infection remains to be

determined.

15

While the nature of the HCV receptor is not known currently,

the major envelope glycoprotein E2 is thought to be

responsible for initiating virus attachment to the host cell

because E2-specific antisera can block binding to cells

(Rosa et al., 1996 and Farci et al., 1996). The role of E1 is

less clear but the presence of a stretch of hydrophobic

amino acids tentatively called the E1 fusion peptide,

displaying similarities to the fusion peptides of

Paramyxovirus and Flavivirus suggests that E1 is involved in

membrane fusion (Flint et al., 1999). To study the early steps

in the HCV life-cycle, generated vesicular stomatitis virus

(VSV) pseudotypes. They expressed chimeric envelope proteins

composed of the HCV E1 or E2 ectodomains fused to the

transmembrane and cytoplasmic domains of the VSV G protein.

As indicated by the formation of plaques, a baby hamster

kidney cell line (BHK-21), the human T-cell line MOLT4 and

the human hepatoma cell line HepG2 were susceptible to

infection with the pseudotypes, but the human cervical

carcinoma cell line HeLa and the human embryonic lung cell

line L-132 were not. However, only pseudotypes carrying

either the E1 or the E2 ectodomain were used, not

pseudotypes with both chimeric HCV proteins. This is

surprising, because E2 acts as a chaperone for E1, which in

the absence of E2 forms misfolded aggregates (Michalak et al.,

1999). Furthermore, E1 and E2 form stable heterodimers that

most likely represent the native form found in the HCV

16

envelope (Dubuisson et al., 1994). Finally, studies with

engineered cell surface-expressed E2 glycoproteins folded in

a manner comparable to authentic E2 demonstrated that this

protein alone did not enable cell fusion (Flint et al., 1999).

2.6 Hepatitis C Virus Infection:

HCV is a blood borne liver disease caused by hepatitis C

virus. HCV infection is a leading cause of chronic liver

disease, including cirrhosis of the liver. Chronic hepatitis

C is marked by the persistence of HCV RNA in the blood for

at least six months after onset of acute infection. HCV is

self limiting in only 15% to 25% of patients in whom HCV RNA

in their serum becomes undetectable and the patients possess

normal liver enzymes (Alanine amino transferase (ALT) and

normal liver histology (Michael and Alexander, 2004).

Progression of chronic hepatitis C is slow in the patients

and they can remain asymptomatic for several years. Chronic

HCV infection is caused by many factors including alcohol

abuse, the duration of infection, age at time of infection,

gender, ethnicity, and development of jaundice during acute

infection (Michael and Alexander, 2004).

2.7 MODE OF TRANSMISSION

2.7.1 Intravenous drug use

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IDU is a major risk factor for hepatitis C in many parts of

the world (Xia et al., 2008). 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% ( Nelson et al., 2011 and Xia et al.,

2008).Twelve countries had rates greater than 80% (Nelson et

al., 2011). 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 (Nelson et al., 2011).

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 and Vescio, 2008).

2.7.2 Healthcare exposure

Blood transfusion, transfusion of blood products, or organ

transplantation without HCV screening carry significant

risks of infection (Wilkins et al., 2010). The United States

instituted universal screening in 1992 (Marx, 2010), and

Canada instituted universal screening in 1990 (Day et al.,

2009).This decreased the risk from one in 200 units (Marx

and John, 2010) to between one in 10,000 to one in

10,000,000 per unit of blood (Springer Verlag , 2011 and

Ponde, 2010). This low risk remains as there is a period of

18

about 11–70 days between the potential blood donor acquiring

hepatitis C and their blood testing positive depending on

the method (Ponde, 2010). Some countries do not screen for

hepatitis C due to the cost (Alter, 2007).

2.7.3 Sexual intercourse

Whether hepatitis C can be transmitted through sexual

activity is controversial (Tohme, 2010). While there is an

association between high-risk sexual activity and hepatitis

C, it is not known whether transmission of the disease is

due to drug use that has not been admitted to or sex as a

risk factor (|Wilkin et al., 2010).The majority of evidence

supports there being no risk for monogamous heterosexual

couples (Tohme, 2010). Sexual practices that involve higher

levels of trauma to the anogenital mucosa, such as anal

penetrative sex, or that occur when there is a concurrent

sexually transmitted infection, including HIV or genital

ulceration, do present a risk ( Ponde, 2010) .

2.7.4 Body modification

Tattooing is associated with two to threefold increased risk

of hepatitis C (Jafari et al., 2010). This can be due to

either improperly sterilized equipment or contamination of

the dyes being used (Jafari et al., 2010). Tattoos or

19

piercings performed either before the mid-1980s,

"underground," or nonprofessionally are of particular

concern, since sterile techniques in such settings may be

lacking. The risk also appears to be greater for larger

tattoos (Jafari et al., 2010). It is estimated that nearly

half of prison inmates share unsterilized tattooing

equipment (Jafari et al., 2010). It is rare for tattoos in a

licensed facility to be directly associated with HCV

infection (CDC, 2012).

2.7.5 Shared personal items

Personal-care items such as razors, toothbrushes, and

manicuring or pedicuring equipment can be contaminated with

blood. Sharing such items can potentially lead to exposure

to HCV (Lock et al., 2006 and CDC, 2012). Appropriate caution

should be taken regarding any medical condition that results

in bleeding, such as cuts and sores (CDC, 2012). HCV is not

spread through casual contact, such as hugging, kissing, or

sharing eating or cooking utensils (CDC, 2012). Neither is

it transmitted through food or water (Wong and Lee, 2006).

2.7.6 Vertical transmission

Vertical transmission of hepatitis C from an infected mother

to her child occurs in less than 10% of pregnancies (Lam et

20

al., 2010). There are no measures that alter this risk (Lam et

al., 2010). It is not clear when during pregnancy

transmission occurs, but it may occur both during gestation

and at delivery (Ponde, 2011). A long labor is associated

with a greater risk of transmission (Alter, 2007). There is

no evidence that breast-feeding spreads HCV; however, to be

cautious, an infected mother is advised to avoid

breastfeeding if her nipples are cracked and bleeding (Mast,

2004), or her viral loads are high (Ponde, 2011).

2.8 Pathogenesis:

Hepatitis C being a blood borne disease is transmitted

through blood and body fluids. Route of infection vary among

infected individual. They include blood, IVDU, blood

transfusions, sexual activities, among others as discussed

earlier. The virus replicates in the cytoplasm of

hepatocytes but is not directly cytopathic (Lau, et al.,

1995). Persistence infection appears to rely on rapid

production of the virus and continuous cell to cell spread

along with a lack of virgeous T.cell. Immune response to HCV

antigens. The HCV turnover rate can be quite high with

replications ranging from 1010-1212 virions per day and a

product viral half life of 2-3 hours. The rapid viral

replication and lack of error proof reading by the viral RNA

polymerase are reasons why the HCV RNA mutates frequently

(Nahum et al., 2004).

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2.9 Progression of Liver Fibrosis:

During persistence hepatitis C viremia the rate of

progression of liver fibrosis varies widely (Colina, et al.,

1999). There have been extensive studies focusing on the

natural cause of disease progression from chronic hepatitis

C to cirrhosis, Hepatocellular carcinoma HCC and death.

The liver biopsy is the gold standard for the granding and

staging of chronic hepatitis C (Colina, et al., 1999). The

activity of liver disease or grade is gauged by the number

of mononuclear inflammatory cells present in and around the

portal entry areas, and by the number of dead dying

hepatocytes. The structural liver damage, also known as

Filorosis is variable in chronic HCV infection to cirrhosis.

In mild cases, fibrosis is limited to the portal and

periportal areas.

Multipliers of studies have shown that chronic alcohols use

a major external risk. Factors include gender, co-infection

with HCV and HBV, the degree of inflammation and fibrosis

present on the liver biopsy, and co-morbid conditions such

as immune suppression, insulin resistance, non-alcoholic

steatohepatitis, hemochromatosis and schistosomies.

2.10 Clinical Manifestation:

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Chronic HCV infection is marked by the persistence of HCV

RNA in the blood for at least 6 months after a set of acute

infection. HCV infection is self-limiting in 15-25% of

patients in whom HCV RNA in serum becomes undetectable and

ALT level return to normal. Approximately 75-85% of infected

individuals do not clear the virus by 6 months and chronic

HCV infection develops (Colina, et al., 1999). The sequence of

chronic HCV infection includes cirrhosis of liver as well as

hepatocellular carcinoma HCC. Chronic HCV infection has been

associated with numerous extra hepatic manifestations

involving multiple organ system including renal,

dermatological, hematological and rheumatological systems

(Colina, et al., 1999). Approximately 1-2% of HCV infected

individuals will develop extra hepatic manifestation (San

Diego, 1999).

2.3 Laboratory Diagnosis

2.3.1 Anti HCV Anti-Body Detection:

The detection of anti-HCV Ab in plasma or serum is based on

the use of third generation EIAS (enzymes immunoassay) that

detect mixtures of Ab directed against various HCV epitopes.

Recombinant antigens are used to capture circulating anti-

HCV antibodies into the wells of a micro-titer plates, micro

beads or specific holder adapted to closed automated

devices.

23

The optical density (OD) ratio of the reaction is

proportional to the amount of Ab in the serum or plasma

sample (Colina et al., 1999). The specificity of third-

generation EIAS for anti-HCV is greater than 99% (Peter et

al., 2003). Their sensitivity is more difficult to determine,

given the lack of a good standard method, but it is

excellent in HCV infected immunocompromised patients.

EIAS can be fully automated and are well adapted to large

volume testing. Immunoblot tests are nowadays clinically

obsolete given the performance of third generation anti-HCV

EIAS (Peter et al., 2003).

2.3.2 Acute Hepatitis C:

Patients with a suspicious acute hepatitis C should be

tested for both anti-HCV Abs by EIA and HCV RNA with a

sensitive techniques, i.e. an HCV RNA assay with a lower

limit of detection of 50 Iuml or less (Colina et al., 1999).

Four marker profiles can be observed according to the

presence of anti-HCV Ab is strongly indicative of acute HCV

infection, which will be confirmed by sera conversion (i.e.

the appearance of anti-HCV Abs) a few day to weeks later.

Acutely infected patients can also have both HCV RNA and

anti-HCV Abs at time of diagnosis. It is difficult in this

case to distinguish acute hepatitis C from an acute

exacerbation of chronic hepatitis C or an acute hepatitis C

cause of another cause in a patient with chronic hepatitis24

C. Acute hepatitis C is very unlikely if both anti-HCV Abs

and HCV RNA are absent. (Christian et al., 2004).

2.4. Signs and Symptoms

2.4.1 Acute infection:

Hepatitis C infection causes acute symptoms in 15% of cases

(Maheshwari et al., 2008). Symptoms are generally mild and

vague, including a decreased appetite, fatigue, nausea,

muscle or joint pains, and weight loss (Wilkins et al., 2010),

and rarely does acute liver failure result(Bailey and

Caittin, 2010). Most cases of acute infection are not

associated with jaundice (Stringer Verlage, 2011). The

infection resolves spontaneously in 10-50% of cases, which

occurs more frequently in individuals who are young and

females (Stringer Verlage, 2011).

2.4.2 Chronic infection

About 80% of those exposed to the virus develop a chronic

infection (Nelson et al., 2011). Most experience minimal or

no symptoms during the initial few decades of the infection,

(Stringer Verlage, 2011), although chronic hepatitis C can

be associated with fatigue (Ray, 2009). Hepatitis C after

many years becomes the primary cause of cirrhosis and liver

cancer (Rosen, 2011). About 10–30% of people develop

cirrhosis over 30 years (Rosen, 2011 and Wilkin et al., 2010).

25

Cirrhosis is more common in those co-infected with hepatitis

B or HIV, alcoholics, and those of male gender (Rosen, 2011

and Wilkin et al., 2010). Those who develop cirrhosis have a

20-fold greater risk of hepatocellular carcinoma, a rate of

1–3% per year, (Rosen, 2011 and Wilkin et al., 2010), and if

this is complicated by excess alcohol the risk becomes 100

fold greater (Mueller et al., 2009). Hepatitis C is the cause

of 27% of cirrhosis cases and 25% of hepatocellular

carcinoma worldwide (Alter, 2007).

Liver cirrhosis may lead to portal hypertension, ascites

(accumulation of fluid in the abdomen), easy bruising or

bleeding, varices (enlarged veins, especially in the stomach

and esophagus), jaundice, and a syndrome of cognitive

impairment known as hepatic encephalopathy. It is a common

cause for requiring a liver transplant (Ozaras and Tahan,

2009).

2.4.3 Extrahepatic

Hepatitis C is also rarely associated with Sjögren's

syndrome (an autoimmune disorder), thrombocytopenia, lichen

planus, diabetes mellitus, and B-cell lymphoproliferative

disorders (Zignego et al., 2007). Thrombocytopenia is

estimated to occur in 0.16% to 45.4% of people with chronic

hepatitis C (Louie et al., 2011). Putative associations with

Hyde's prurigo nodularis (Lee and Shumach, 2005), and

membranoproliferative glomerulonephritis have been reported26

(Ray et al., 2009). Hepatitis C infection is also associated

with a condition called mixed cryoglobulinemia, which is

inflammation of small and medium sized blood vessels (or

vasculitis) caused by deposition of immune complexes

involving cryoglobulins (Iannuzzela et al., 2010).

2.5 Treatment

HCV induces chronic infection in 50–80% of infected persons.

Approximately 40-80% of these clear with treatment (Torresi

et al., 2011 and Ilyas and Vierling, 2011). In rare cases,

infection can clear without treatment (Stringer Verlag,

2011). Those with chronic hepatitis C are advised to avoid

alcohol and medications toxic to the liver, (Wilkins, 2010),

and to be vaccinated for hepatitis A and hepatitis B

(Wilkins, 2010). Ultrasound surveillance for hepatocellular

carcinoma is recommended in those with accompanying

cirrhosis (Wilkins, 2010).

In general, treatment is recommended in those with proven

HCV infection liver abnormalities (Wilkins, 2010). As of

2010, treatments consist of a combination of pegylated

interferon alpha and the antiviral drug ribavirin for a

period of 24 or 48 weeks, depending on HCV genotype

(Wilkins, 2010). When combined with ribavirin, pegylated

interferon-alpha-2a may be superior to pegylated interferon-

alpha-2b, though the evidence is not strong (Awad et al.,

2010). Improved outcomes are seen in 50–60% of people27

(Wilkins, 2010).Combining either boceprevir or telaprevir

with ribavirin and peginterferon alfa improves antiviral

response for hepatitis C genotype 1 (Foote et al., 2011; Smith

et al., 2011 and Ghany et al., 2011). Adverse effects with

treatment are common, with half of people getting flu like

symptoms and a third experiencing emotional problems

(Wilkins, 2010). Treatment during the first six months is

more effective than once hepatitis C has become chronic

(Ozaras and Tahan, 2009). If someone develops a new

infection and it has not cleared after eight to twelve

weeks, 24 weeks of pegylated interferon is recommended

(Ozaras and Tahan, 2009). In people with thalassemia,

ribavirin appears to be useful but increases the need for

transfusion (Alavian and Tabatabaei, 2010).

2.6. Prevention and Control

As of 2011, no vaccine protects against contracting

hepatitis C. However, a number are under development and

some have shown encouraging results (Hagan et al., 2011). A

combination of harm reduction strategies, such as the

provision of new needles and syringes and treatment of

substance use, decrease the risk of hepatitis C in

intravenous drug users by about 75% (Hagan et al., 2011). The

28

screening of blood donors is important at a national level,

as is adhering to universal precautions within healthcare

facilities (Ray et al., 2009). In countries where there is an

insufficient supply of sterile syringes, medications should

be given orally rather than via injection (when possible)

(Alter, 2007). The United States government only recommends

condom use to prevent hepatitis C transmission in the use

with multiple partners (United state department of veteran

affairs).

2.6.1 Primary Prevention Activities

Primary prevention activities reduce potential risk for HCV

transmission from such high risk activities as injecting

drug use, sex with multi-partners and precutaneous exposures

to blood in health care, blood, blood components, plasma

derivatives, tattooing and body piercing (Ala et al., 1996).

Practices that exclude blood, plasma, organ, tissue or serum

from donors who are associated public health policies aimed

at reducing HIV transmission, such as the promotion of

sexual barrier protection and inhabitation of needle

exchange programs are likely to decrease transmission of HCV

in high risk groups (Ala et al., 1996). Counseling and

education to prevent initiation of drug injecting or high

risk sexual practices is important. Persons who inject drug

or who are at risk for STDs should be counseled regarding

what they can do to minimize their risk for infection or

29

transmission to other persons who inject illegal drugs

should be advised to stop using and injecting drugs or never

to re-use or share syringes, needles and to use only sterile

syringe obtained from a reliable source e.g. pharmacies,

clean the injection site with a new alcohol to swab before

inject and to safety dispose syringe after one use.

Health and emergency medical and public safety workers

should be educated on the risk and prevention of blood borne

infection. Standard barrier precautions and engineering

control should be implemented to prevent exposure to blood

(Ala et al., 1996).

As recommended for all healthcare workers those who are HIV

positive should follow strict aseptic techniques and

standard precautions including appropriate use of hand

washing, protective barrier and care in the use and disposal

of needles and other sharp instrument (Ala et al., 1996).

2.6.2 Secondary Prevention Activities

Secondary prevention activities can reduce risks for

chronic disease by identifying HCV infected persons through

diagnostic testing and by providing appropriate medical

management and antiviral therapy. Identification of HCV-

infected persons must be a major focus of currents

prevention programs since their number is significant.

Identification of person at risk for HCV infection provides

30

opportunity for testing to determine their disease status if

infected, and antiviral therapy, if appropriate.

Identification also provides infected persons opportunities

to obtain information concerning how they can be prevented

further to their liver and prevent transmitting HCV to

others.

2.7 Epidemiology:

Hepatitis C Virus (HCV) continues to be a major disease

burden on the world. In 1999 World Health Organization

(WHO), it is estimated that 130–200 million people, or ~3%

of the world's population, are living with chronic hepatitis

C (WHO, 2010 and Gravitz, 2011) About 3–4 million people are

infected per year, and more than 350,000 people die yearly

from hepatitis C-related diseases (WHO, 2010). Rates have

increased substantially in the 20th century due to a

combination of IDU and intravenous medication or poorly

sterilized medical equipment (Alter, 2007).

Among those chronically infected, the risk of cirrhosis

after 20 years varies between studies but has been estimated

at ~10%-15% for men and ~1-5% for women. The reason for this

difference is not known. Once cirrhosis is established, the

rate of developing hepatocellular carcinoma is ~1%-4% per

year (Yu and Chuang, 2002).

31

Between central and south America, a recent community based

study San Juan, Puerto Rocco, should that estimated HCV

prevalence in 2001-2002 was 6.3% (Peter et al., 2003). In

Mexico, the prevalence reported was 1.2% (Nahum et al., 2004).

Among blood donor in Chile and Brazil, prevalence of HCV

antibodies (Abs) was low 0.3% 1.14% respectively (Marshal et

al., 2005 and Munox et al., 1998). Prevalence of HCV antibodies

is 0.87% (1993-1994) in Belgium (Bellentani and Tiribellic,

2001).in U.K, at least 200,000 adult carry HCV (hapetitis C

strategy for England). In Northern Italy prevalence of HCV

Abs was 3.2% (Stroffolini et al., 1995). Three studies in

central and southern Italy showed a higher rate of HCV

(8.4%-22.4%) especially in the order population (Monica et

al., 2003). Among patients of general practitioners in

Lyon, France, the prevalence of HCV was estimated to be

1.3%, very similar to the French population (Peter et al.,

2003) within the Russian army, frequency of anti-HCV was

1.5% among service men and donors with increased prevalence

in the Northern countries, far east and Siberia (3.1-3.8%)

compared to the transikal region (0.70%) (Ogarkov et al.,

2004). Low rates were found in Hungary (0.73% of 15, 864

blood donors) (Egah et al., 2004). Recently, HCV prevalence

studies have come out of Pakistan in the middle east, 751

out of 16,400 patients (4.57%) were found to be positive for

HCV Abs from 1998-2002 (Muhammad and Jan, 2005). Among male

blood donors in Karachi, Pakistan, the seroprovalence of HCV

32

was 1.8% with a trend of increasing proportion of positive

donors from 1998-2002 (Attar et al., 2004) there have been

very high prevalence rates of HCV reported in Egypt in the

past (28%) (Heidi et al., 2003). This was confirmed among 90

blood donors in Cairo, where 14.4% were anti-HCV positive

for RIBA test (Darwish, 1992). Then 26.6% among 188 blood

donors and 22% among 163 donors were positive with both

studies done in Cairo (Bassily et al., 1995 and Darwish et al.,

1993). Rates were lower in Saudi Arabia (1.8%) and semen

(2.1%). Intermediate rates of HCV have been reported out of

Asia from 1995- 2000, 0.49% anti HCV Ab was detected among

3,485,648 blood donors in Japan (Tanak et al., 2004). This was

lower than the 0.98% out of 10,905,489 blood donor reported

in 1992 (Yamaguchi et al., 1994). In China prevalence low with

rate around 1% among blood donor in Beijing and Wuhan (Zhang

et al., 1992 and Wang et al., 1994). However rate may be higher

in certain areas such as the hubei provincs, (30.1%) and

Inner Mongolia autonomous region (31.86%) (Soni et al.,

2004). Low rates have been found in Malaysia (around 1.6%)

and Singapore (0.54%) (Koff, 1997). Higher rate has been

reported in Thailand (3.2-5.6%) (Songsivilar et al., 1997and

Apichartpiyakul et al., 1999) within a smaller community of

103 residences in sherpas, Nepal, only one person had

borderline reaction in 2004 (Chba et al., 2004) in new Delhi,

India, 1.85% of blood donor were positive (Panigrali et al.,

1997). There have been fewer studies out of Africa but lower

33

rate have been reported; 1.6% among blood donors in Ethiopia

and 0.9% in Kenya (Frommel et al., 1993 and Ilako, 1995).

CHAPTER THREE

MATERIALS AND METHODS

3.1 Study Area:

34

The study was conducted at the Laboratory unit of the

General Hospital Minna, in Niger state where patients are

referred for blood donation.

3.2 Study Population:

These include all adult blood donors, aged 18 and above, of

all sexes (male and female) and of all social classes.

3.3 Materials:

These included:

i. Serum from fresh blood samples

ii. Plain blood bottles

iii. One step Hepatitis C virus test strip (Serum/Plasma)

made by Gold Diagnostics for in vitro diagnostics use

only. One package contains 50 strips.

3.4 Methods

i. Blood sample was collected from each subject by vene-

puncture of the median

veins.

ii. The site was cleaned using 70% isopropyl alcohol for

one minute and allowed to

dry.

iii. The blood was allowed to clot.

iv. The clotted blood samples were centrifuged to obtain

serum.

35

v. Using sterile Pasteur pipette, six drops of the serum

were transferred into sterile

plain bottles.

vi. Test for HCV antibodies was carried out using one step

Hepatitis C Virus test

strip (serum/plasma) made by gold diagnostics for

in vitro diagnostics.

vii. Testing was carried out immediately after the transfer.

3.5 Screening of Sera For Anti-HCV Antibodies

3.5.1 Principle of Assay:

The one step HCV test strip (serum/plasma) is a qualitative

membrane based immunoassay for the detection of antibodies

to HCV in serum or plasma. The membrane is coated with

recombinant HCV antigen on the test line region of the

strip. The mixture migrates upwards on the membrane

chromatographically by capillary action to react with the

recombinant HCV antigen on the membrane and generate a

colored line. Presence of this colored line indicates a

positive result. To serve as procedural control, a colored

line would always appear at the control line region

indicating that proper volume specimen has been added and

membrane wicking has occurred (Nahum et al., 2004).

3.6.2 Test Procedure

i. Bring the test kit to room temperature

ii. Cut the foul paper and bring out the test strip

36

iii. Immerse the test strip vertically into the serum

sample with the arrows pointing towards the serum for

fifteen seconds and the test strip not immersed beyond the

line indicated on it.

iv. Immediately after fifteen (15) seconds bring the test

strip out from the sample and allow standing for 25minutes

and observing for red lines each test result was read.

3.7.2 Interpretation of Result

Positive: Test was considered positive when two distinct red

lines appear; one line in the control region and another in

the test region (T). The intensity of the red line on the

test strip varies and this was as a result of concentration

of HCV antibodies presents in the specimen.

Negative: Test was considered negative when only one

distinct red line appeared in the control region © and none

at the test region (T).

Invalid: Test was considered invalid when control line fades

to appear. This may be as a result of insufficient specimen

volume or incorrect procedural techniques.

3.7. Statistical Analysis

The results were subjected to statistical analysis using

graph pad prism software. X2 test was carried out to find

out if there is significant difference between the different

37

age groups and occurrence of Hepatitis C, as well as between

sex and occurrence of Hepatitis C.

38

CHAPTER FOUR

RESULTS

4.1. The results showed that of the 200 samples screened for

Hepatitis C Virus antibodies among Blood donors in General

Hospital, Minna four (4) tested positive giving a prevalence of

2.0%

Table 4.1 shows the seroprevalence of HCV antibodies in relation

to sex of the subjects. The study comprises 181 males and 19

females. Three (1.7%) out of the 181 males were seropositive for

HCV antibodies while 1(5.3%) out of the 19 female blood donors

were seropositive. This is as shown in Table 4.1. The results

showed that females had the higher prevalence of 5.3% for HCV as

compared to the 1.7% for the males. The distribution across sex

is shown in Table 4.1.

Table 4.1 Percentage distribution of HCV by sex of the blood

donors attending General Hospital Minna

Sex No screened No positive %prevalenceMales 181 03 1.7Females 19 01 5.3Total 200 04 2.0

39

Based on the age group, blood donors within the age group of 20-

29 constituted the majority of the population screened (57%)

while those of age group 50 and above constituted the least

(2.5%). Distribution across age group showed that those of age

group 20-29 had the highest prevalence rate of 2.6% while age

groups 30-39 had 1.8% prevalence for HCV infection. The age

groups of 10-19 and 50 and above recorded zero (0) prevalence

rate. The distribution of HCV infections is shown in Table 4.2.

Table 4.2 Distribution of HCV By Age Among Blood Donors

Attending General

Hospital Minna

Age (yrs) NoScreened

NoPositive

% prevalence

10-19 09(4.5) 00 0.020-29 114(57.0) 03 2.630-39 56(28.0) 01 1.8

40

40-49 16(8.0) 00 0.0≥ 50 05(2.5) 00 0.0Total 200 04 2.0

CHAPTER FIVE

DISCUSSION

The prevalence of Hepatitis C Virus was determined to be 2.0%

among blood donors in General Hospital Minna. This rate though

lower, compares to prevalence studies carried out in Jos, Plateau

state where 6.0% was found for anti HCV antibodies (Egah et al.,

2004), and 8.4% found in Lagos (Ayolabi et al., 2006). This low

rate compares to the findings in other parts of the world. For

instance, Ethiopia reported 1.6% among blood donors and Kenya

reported 0.9% among blood donors (Frommel et al., 1993 and Ilako,

41

1995). Nigeria and Africa in general have no well documented

prevalence of Hepatitis C as fewer studies have originated out of

Africa (Janny et al., 2004 and Jordan, 2005).

In Minna General Hospital where this study was conducted, both

male and female donors are received though most are males. This

is corroborated by the study in Jos, Plateau state, in which most

of the donors were males (Egah et al., 2004).

Based on the age group, blood donors within the age group of 20-

29 constituted the majority of the population screened (56%)

while those of age group 50 and above constituted the least

(2.5%). Distribution across age group showed that those of age

group 20-29 had the highest prevalence rate of 2.6% for HCV

infection. They are followed by those of age group 30-39 with

prevalence rate of 1.8% for HCV infection. This may be due to the

sharing of personal-care items such as razors, toothbrushes, and

manicuring or pedicuring equipment which may be common among

members of this age group, and these items can be contaminated

with blood. Sharing such items can potentially lead to exposure

to HCV (Lock et al., 2010 and CDC, 2012). HCV is not spread through

casual contact, such as hugging, kissing, or sharing eating or

cooking utensils (CDC, 2012). Neither is it transmitted through

food or water (Wong and Lee, 2006).

The results showed that sero-prevalence of Hepatitis C Virus

among male Blood donors in General Hospital, Minna was (1.7%) and

42

(5.3%) for females blood donors. This showed that females had

higher prevalence than the males.

In the transfusion setting where the acute onset is best

documented, 70-80% are asymptomatic and only 20-30% develop

symptoms (Chihiro et al., 2004) and this occurs 3-12 weeks after

exposure. In a place like Minna and most probably Nigeria in

general where the awareness of hepatitis is very low, given the

few studies carried out and the little significance given to it

in the transfusion setting, prevalence could be higher than

determined.

Awareness about the disease, its complication and risk factors

among others, should be created mainly among public health

workers in Minna and in Nigeria as a whole in other to reduce the

risk of transmission through transfusion in particular and other

ways in general. Approximately, 75-85% of HCV infected person are

surely going to progress to chronic HCV infection, and are at

risk of developing extra-hepatics manifestation, compensated and

decompensated cirrhosis, and hepatocellular carcinoma (Colina et

al., 1999 and Munox et al., 1998). With most people acutely

infected being asymptomatic and chance of diagnosis in Minna and

Nigeria in general being limited, rate of transmission through

the known risk factors especially sexual inter-course, vertical

transmission, intravenous drug use in particularly among others

is likely to be high.

43

The use of blood donors as prevalence source under-estimates the

real prevalence of the virus because donors are highly selected

population (Alter et al., 1997). In Nigeria social-economic

situation is likely to play important and sometimes positive

roles in checking the prevalence rate of the disease where it is

tested. The incidence or role of commercial donor and free donor

as well come into play. Some hospitals and blood bank centers are

known to offer monetary benefits for blood donation, although it

is known that the knowledge of tests being carried out on blood

before acceptance scares away potential donors.

The Hospital where this study was done, offer such benefits. It

was discovered in the course of this study that regular or well

known blood donors are not regularly tested before bleeding. This

is likely to be a possible risk since blood donated are used

either immediately or sold to other hospitals in need, who are

less likely to re-test the blood on the presumption that it has

already been tested before collection.

Prevalence rate of Hepatitis C across the world has changed with

more countries being aware of transfusion related to Hepatitis C.

The prevalence rate is high as well as intermediate in mainly

developing countries of Asia, where documentation has been

attempted such as Pakistan where rates range from 1.8-4.57%

(Attar et al., 2004), Egypt (22-28%) (Darwish et al., 1992 and

Darwish et al, 1993; Heidi et al., 2003), New delhi, India (1.85%)

(Panigrali et al., 1997).

44

Statistical analysis, however, showed no significant difference

(P=0.299) between the prevalence rates of the male and female

individuals. There was, however, no statistical association (P

=0.299) between age group and prevalence of HCV antibodies. It is

conformity with that of Udeze et al., 2009, who found that there

was no statistically significant difference (P=0.05) between the

different age groups considered in their study. Also, of the two

factors of age and sex considered, there was no association

(P=0.05) between them and occurrence of Hepatitis C. This is also

in line with the finding of Udeze et al., 2009.

5.1 CONCLUSION

The prevalence of Hepatitis C Virus among Blood donors in General

Hospital, Minna was 2.0%. The overall seroprevalence of HCV

antibodies in the study group is 1.7%. Three (1.7%) out of 181

males were female seroprevalence for HCV antibodies while 1 (5.3)

out of 19 females blood donors were seropositive for HCV

antibodies. This showed that females had the higher prevalence of

5.3 % compared to the 1.7% for the males. Based on the age group,

blood donors within the age group of 20-29 constituted the

majority of the population screened (57%) while those of age

group 50 and above constituted the least (2.5%). Distribution

across age group showed that those of age group 20-29 had the

higher prevalence rates of 2.6% while age groups 30-39 1.8% for

HCV infection. The age group of 10-19 and 50 and above recorded

zero (0) prevalence rate. The distribution of HCV

45

infections.Statistical analysis, however, showed no significant

difference (p=0.299) between the prevalence rates of the male and

female individuals. There was, however, no statistical

association (p =0.299) between age group and prevalence of HCV

antibodies.

5.2 Recommendation

Hepatitis C is an emerging disease. There is an urgent need to

introduce HCV screening of blood donors for the disease where it

is not currently practiced, and a radical awareness campaign

about the disease should be introduced to reduce the risk of

transfusion associated with hepatitis C as well as other risk

factors and its complication in Minna and Nigeria in general.

Prevention is the only safeguard against spread of viral

hepatitis infection, thus, careful screening of blood, blood

products, and adequate sterilization of reusable surgical or

dental instruments should be done. Professional and public health

education and implementation of infection control practices in

all health facilities is of utmost importance.

Appropriate caution should be taken regarding any medical

condition that results in bleeding, such as cuts and sores.

Also, appropriate caution should be taken regarding personal-care

items such as razors, toothbrushes, and manicuring or pedicuring

equipment avoid sharing of these items.

46

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