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IMMUNE-STATUS OF HIV POSITIVE PATIENTS WITH AND WITHOUT P. FALCIPARUM MALARIA (HIV AND MALARIA)

                                                   CHAPTER ONE

1.0                                              INTRODUCTION                

 Plasmodium falciparum, the etiologic agent of malaria and Human immunodeficiency virus (HIV), the causative agent of  acquired immunodeficiency syndrome (AIDS), are co-endemic in many tropical and sub-tropical countries with the potential risk for  improved clinical, parasitological and hematological complications (Gregory et al., 2010). Malaria and HIV infections are the lead cause of morbidity and mortality in this region. Together they account for over 4 million deaths each year. Both infections affect those in poverty and contribute to poverty by hindering sustainable development (WHO, 2008).

                    Plasmodium falciparum malaria causes about 300-500 million clinical cases annually, of which 90% occur in sub-Saharan Africa. Approximately, more than one million deaths occur each year, primarily among children under five years of age (UNAIDS/ WHO, 2004). Apart from young children, also heavily affected are pregnant women, with resultant effects on maternal health, birth outcome and increased mother-to-child transmission (MTCT) of HIV in HIV positive mothers with placental malaria (UNAIDS/WHO, 2004). Sub-Saharan Africa is also a home to an estimated 25 million adults and children living with HIV/AIDS. Worldwide, 33 million people are living with HIV/AIDS (UNAID/WHO, 2004). In 2007, an estimated 2.1 million deaths were due to HIV infections, of which 1.6 million occurred in sub- Saharan Africa and over 1.9 million individuals mainly children were newly infected (WHO,2008). Given the overlap of their geographic distribution and resultant rates of co-infection, interactions between these two diseases pose major public health problems (WHO, 2008).

Early studies found little or no definitive interaction between malaria and HIV infections in either adult or children (Kublin et al., 2005). More recent research has shown that HIV infections predisposes to more frequent episodes of symptomatic, severe or complicated malaria including death in both children and adult (Grimwade et al., 2004) and it has also been associated with an increased rate of malaria treatment failure (Kamya et al., 2006). Malaria infection has been associated with an increase in plasma HIV viral load as well as a more rapid CD4+ T-cell decline (Mermin et al., 2006). Although, some of these interactions between malaria and HIV infections are known, these have not been extensively studied from an epidemiological viewpoint. Numerous aspects of the relationship between these interactions remain unanswered (Kalyesubula et al., 1997). Therefore examining the interactions between these all-too-common pathogens in the setting of immune cells would shed light on the effects on immune dysregulation, as different clinical manifestation of malaria has been associated with different states of immune dysregulation (Akanmori et al., 2000).

The mechanism used by the immune system to fight malaria and HIV co-infection is still not fully understood, although it’s clear that humoral and cell-mediated immunity (CMI) are involved and that various T-cell subsets are important for regulating the immune response (Akanmori et al., 2000). The immune system of parasitized individual in malaria endemic area is characterized by chronic immune activation (Mermin et al., 2006). The pathogenesis of HIV infection is also marked by generalized immune activation and depletion of CD4+T lymphocytes, an important component of cell-mediated immunity. HIV associated immune suppression may affect the prognosis of malaria by altering the immune response against P. falciparum (Hoffman et al., 1999). Knowledge of CD4+Tcell number and evaluation of the normal profile of immune cells in the peripheral blood in response to HIV and malaria antigens may provide better understanding of immune interactions between these infections for more proper management of a co-infected individual. More so, when CD4+ cell is central for determining the immune status of HIV/AIDS infected patient as well as establishing the efficacy of or commencement of ART (anti-retroviral therapy), (Hoffman et al., 1999).

Malaria parasite have been reported to perturb the normal profile of immune cells in the peripheral blood as shown in the case of P. falciparum infection, where the proportions of total-leukocyte (WBC), total lymphocyte, natural killer (NK) cell, B-cell and T-cell count was  affected (Kassa et al., 2006). Other works found no significant difference in the WBC count, the percentage of CD4+ and CD8+ cell in P. falciparum patient (Lisse et al., 1994). Therefore, in spite of the ample evidence showing the potential of malaria infection to affect the count of lymphocyte subpopulation in the peripheral blood, but this might not be predominant in all geographical locations, as the pathogenesis and the disease outcome of malaria have been reported to be highly dependent on local factors such as the level of endemicity, host genetics and parasite factors.

Besides immunological complications of HIV disease (Rudnicka et al., 2009), hematological abnormalities have been documented as strong independent predictors of morbidity and mortality in HIV-infected individuals (Anastos et al., 2004). Some studies have reported reduction in the following blood parameters: differential lymphocyte counts, hemoglobin concentrations, platelet count, erythrocyte sedimentation rates (ESR), packed cell volume (PCV)and CD4+ T cell counts in a co-infected patients compared to patients with single infections of either type (Suresh et al., 2008). These hematological changes could be understood in light of the mechanisms by which malaria and HIV individually impact hematological parameters: HIV can result in a general myelossupressive effect (Erhabor et al., 2006), while malaria could impact hematological parameters through its hemolytic effect on red blood cells as well as its immuno-inflammatory effects on white blood and platelet cell counts (Gosselle et al., 2009).

The growing burden and severity of HIV and malaria infections in Nigeria, has made the clinical management of both infections more difficult with hematological complications and high rate of drug failure. This study intends to examine the interactions between both infections in the setting of immune cells via enumeration of some hematological parameters in order to aid physicians caring for HIV/malaria co-infected patients in the management, as well as optimizing medical cost.

AIMS AND OBJECTIVS OF THE STUDY

1    To establish the correlation between immune-status of HIV positive patients infected with both P. falciparum malaria and without P. falciparum via enumeration of some hematological parameters.

2     To determine the prevalence rate of HIV patients co-infected with P. falciparum

malaria in Abakaliki.

3     To correlate CD4+T cell population in HIV positive patients with rate of

parasitaemia.

4     To determine the correlation between parasitaemia and some demographic data

(age /sex) of the co-infected individuals.

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