Research Key

The Impact of Antiretroviral Therapy On haemoglobin, Cd4 Cell and Liver Enzyme Function Test in HIV Patients in Boyo Health District

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International: $20
No of pages
Qualitative method
Analytical tool
Descriptive Statistics
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A study was carried out in FundongDistrict Hospital from January 2013 to July 2013 to assess the impact of ART on Hb, CD4 cell and liver enzyme function test in HIV patients.

Blood specimens were collected from 150 patients and their HIV status determined using Alere determine HIV 1/2 rapid test and the Bioline test was used as a confirmatory and also to determine the HIV serotype. 

Also, Hb was tested using the Uritmachine (urit 3300), CD4 cell count determine using the Pima machine and AST and ALT were also determined using the urit1880 machine.

Upon registration, the patient’s demographic information such as age and sex were obtained. The clients were classified in the following age groups; 10-20, 21-30, 31-40, 41-50, 51-60, >60

The impact of antiretroviral therapy was greater in the age group 21-20years.

However, the difference was significant (P < 0.05).ALT and AST increase in the age group 10-20 age from 48.36 to 49.19 and 27.12-27.80 units per litre respectively compare with the other age group which was rather decreasing. However, this difference was significant (P<0.05).

The increase in AST and ALT shows that ART can be hepatotoxic if taken for a long period.  Furthermore, it was observed that ART has a positive impact on HIV patients as there is a general increase in CD4 cell count and haemoglobin.

For CD4 cells the increase was maximum in female (from 192.32- 292.84cells per microliter) than in male (from 152.17-247.03 cells per microliter). Similarly, this increase was higher in the age group 21-30years (from 352.77-361.11 cells per microliter). However, this difference was significant (P<0.05).


The human immunodeficiency virus (HIV) is the cause of acquired immunodeficiency syndrome (AIDS). This disease has continued to spread in the population killing people of every age group, making this infection one of the public health issues with great concern (UNAIDS, 2008).

The introduction of Antiretroviral (ARV) drugs sometimes calls Highly Active Antiretroviral Therapy (HAART), or Antiretroviral Therapy (ART) in the management of HIV/AIDS brought hope to people infected with this disease (Nwankwoet al., 2014).

HAART is a combine action of medications known to be efficacious in the treatment of HIV viral infections regardless of the viral subtype. These drugs have dramatically altered the natural progression of HIV infection and significantly improved the quality of life of infected people (Seseen, 2009), resulting in about 80% decline in the AIDS death rate between 1990 and 2003 in the united states (WHO, 2014).

However HAARTs require strict adherence for the attainment of optimal clinical survival benefits (North, 2011). Despite the advances in antiretroviral therapy resistance development still poses a major challenge in HIV management because 70 to 95% adherence to ART regimen is required to achieve optimal results and to prevent the emergence of resistance strains (Nachegaet al., 2010).

Medication adherence in general could be defined as the patient’s conformance with the providers’ recommendations with respect to timing, dosage and frequencies of medication-taking within the specified length of time. It is therefore estimated that 50% of patients do not take medication as prescribed and increasing adherence may have a greater effect on health than improvement in specific medical therapy especially in HIV/AIDS patients (Brown and Bussell, 2011).

ART is very important because it increases the CD4+ cell count and reducing the viral load. The drugs also reduce the rate of morbidity and mortality rate of HIV patients making the disease a chronic disease (Nwankwoet al., 2014). Antiretroviral therapy reduces the risk of sexual transmission of the disease as the drugs reduce the plasma viral load (CDC, 2009). Reduction in viral load also reduces the risk of transmission from mother to child during delivery (CDC, 2009).

However, these drugs can also bring about serious side effects and also increase the risk of liver diseases. HAART can inhibit the replication of HIV in the body (CDC, 2009). They are also important because the bring about an increase in Hb values. Though some of the drugs can suppress the bone marrow bringing about a decrease in Hb and may lead to anaemia in some HIV patients ( Nkwankwoet al., 2014)


HIV  is one of  WHO  public health concern due to the high morbidity and mortality rates recorded around the world and especially in  Sub  Saharan  Africa and Since the discovery of antiretroviral drugs, people with the disease have been given hope as morbidity and mortality rates has been reduced ( Nwankwoet al., 2014). Though the drugs do not completely eliminate HIV, they can inhibit the virus replication thereby reducing viral load.

Although little work has been done on the impact of the drug on HIV patient on the immunological response in other parts of the country this information is lacking in Cameroon and so this study is intended to compare the impact of ART on Hb, CD4 cell and liver enzyme function test in HIV patients within six months of treatment from the time of initiation in Fundong.

This study will therefore provide information on the impact of the ART on Hb, CD4 cell count and liver enzyme function test in HIV patients and will therefore help in the management of the patients. 


Literature review

Virus classification

            Group:             Group VI (ssRNA RT)

            Order:              Unassigned

            Family:            Retroviridae

            Subfamily:       Orthoretrovirinal

            Genus:             Lentivirus

            Species:           Human immunodeficiency virus 1

                                    Human immunodeficiency virus 2

The Parasite

HIV is a single-stranded RNA (ssRNA) virus containing a phospholipid envelope. The virus consists of three glycoproteins i.e., gp105 or 110 for HIV I and gp120 for HIV II (Lazagrumeet al., 1989). The virus consists of a dense cylindrical core that encases the RNA molecule and viral enzymes which have catalytic rules during replication. The enzymes include proteases, reverse transcriptase integrase.

The genome of HIV contains 3 major genes i.e. gag gene which coils for the core protein, the pol gene that codes for protein reverse transcriptase and the envelop gene that codes for the envelope glycoprotein of the virus (Hoffman et al., 2009).


HIV can be transmitted through exposure to contaminated body fluids such as blood, semen (Pilcher, 2007) or breast milk from mother to child (Salazar, 2011). Potential routes of transmission include blood transfusion (Salazar, 2011), intravenous drug use (Cohen 2008, Reguin 2011,) and unprotected oral and anal sexual intercourse (Body 2009), during delivery (Arya, 2010) or through breastfeeding (Liang, 2009).

HIV can be transmitted by;

Sexual transmission: This can either be by;

Heterosexual intercourse; between a man and a woman Homosexual intercourse; which involve anal sex and oral sex between the same-sex where anal sex presents with a relatively high rate of infection (Royce 1997, McGowan 2008) while oral sex presents with a relatively low risk of HIV transmission (Baggaley, 2010)

Mother to child transmission:

The virus can be transmitted from an infected mother to child during delivery, intrauterine infection, and perinatal transmission or through breastfeeding (Kayser, 2005)

Transmission through blood:

Through contact with infected blood i.e by sharing infected sharp objects such as needles of injection, blades, and through transfusion of infected blood. The transmission of HIV is dependent on the viral load as this predicts the transmission potential of the virus during sexual intercourse, as the higher viral load is associated with higher probabilities of HIV transmission (Hontelezet al., 2013).

Life cycle 

virus replicated in the following stages; Attachment and Entry, Replication and Transcription, Assembly and Release.

Viral entry to the cell:

The interaction between the gp120 on the HIV virion and its receptor, CD4 on the target cell, provokes conformational changes in gp120 that expose a previously buried portion of the transmembrane glycoprotein, gp41, and allows access of gp120 to the coreceptor (a chemokine receptor on the target cell).

A fusion peptide within gp41 causes the fusion of the viral envelope and the host-cell envelope, allowing the capsid to enter the target cell. The exact mechanism by which gp41 causes the fusion is still largely unknown (Chan and Kim, 1998; Wyatt and Sodroski, 1998).

Once HIV has bound to the CD4+ T-cell the HIV RNA and various enzymes including but not limited to reverse transcriptase, integrase and protease are injected into the cell (Chan and Kim, 1998; Wyatt and Sodroski, 1998).

Viral replication and transcription

Once the viral capsid has entered the cell, an enzyme called reverse transcriptase liberates the single-stranded (+)RNA from the attached viral proteins and copies it into a negatively sensed viral complementary DNA (cDNA). This process of reverse transcription is extremely error-prone and it is during this step that mutations (such as drug resistance) are likely to arise.

The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). This new vDNA is then transported into the nucleus. The integration of the proviral DNA into the host genome is carried out by another viral enzyme called integrase. This is called the latent stage of HIV infection (Zhenget al., 2005).

Viral assembly and release

The final step of the viral cycle is the assembly of new HIV virions, which begins at the plasma membrane of the host cell. The envelope polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120.

These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell.

The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begin to bud from the host cell.

Maturation either occurs in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases (proteinases) cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion (Gelderblom, 1997). This step can be inhibited by drugs. The virus is then able to infect another cell.

Research objectives

General objective

The aim of this study is to know the impact of antiretroviral therapy on HIV patients.

Specific objectives

This research is carried out to;

  • Evaluate the impact of the drug on the CD4+ cell counts.
  • Know the impact of the drug on the liver enzymes such as ALT and AST.
  • To assess the impact of the drug on haemoglobin.
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