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Assessment of CD4 and CD8 Levels in Secretors and Non-Secretors of ABH Antigen among HIV Positive Patients


Sixty (60) patients with Human immunodeficiency disease attending Ebonyi State University Teaching Hospital (EBSUTH) Abakaliki were used for the study. Sixty (60) age and sex matched apparently healthy individual who were screened 3 months prior to study served as the control group. Secretor status of the group (test and control) was determined using neutralization and agglutination inhibition technique. Levels of CD4 and CD8 were determined using Partec cyflow 2.4 Microsoft. Results obtained were compared statistically based on secretors and non secretors of ABH antigen. CD8 count in: test non secretors, control non secretors, test male non secretors, control male non secretors, control female non secretors, control secretors, control female secretors, control male secretors;CD4 counts in: control secretors, control non secretors, control female secretors, control male non secretors, control male secretors; CD4 and CD8 count in: control secretors, control female secretors, control male secretors (p<0.05). There was no significant difference in mean values of CD8 count in: control non secretors, control male non secretors, control female non secretors; CD4 and CD8 count in: test female non secretors, control female non secretors; CD4 count in: test non secretors, control non secretors, test male non secretors, test female non secretors, control male non secretors, control female non secretors, control male non secretors, control female non secretors (p>0.05). Percentage distribution of secretors 95 (78.2%) non secretors 25 (20.8%). PLWHA secretors 41 (78.3%) non secretors 13 (21.7%). Secretors and non secretors of ABH antigen has health advantages over each other.    


1.0                            INTRODUCTION

Human immunodeficiency virus (HIV) disease is a chronic progressive infection caused by HIV Virus characterized by a depletion of CD4 lymphocyte. (Joseph et al., 2005).

The devastating demographic, social, and economic impact of the HIV/AIDS (human immunodeficiency virus/ acquired immunodeficiency syndrome). Pandemic continues to pose a huge challenge and burden to the world since its emergence over 29 years ago (Jay et al., 1996).

Cell death secondary to infection of CD4 cells causes a decline in immune function, resulting to neurological disorders, opportunistic infections and malignancies (Levy 2001). The human Immunodeficiency virus HIV-I establishes persistent infections in human which lead to acquired Immunodeficiency syndrome (AIDS) The HIV – I envelope glycoprotein gp120 and gp41, are assembled into a trimetric complex that mediates virus entry into target cells. HIV I entry depends on the sequential interaction of the gp120 exterior glycoprotein with the receptors on the cell (Pope et al; 2003). The gp120 glycoprotein can be shed from the envelope, it elicits both virus-neutralizing and non neutralizing antibodies during natural infection (Tane et al; 2008).

HIV enters macrophages and CD4 T- cells by the adsorption of glycoprotein on its surface to receptors on the target cell followed by fusion of the viral envelope with cell membrane and the release of the HIV capsid into the cell. entrance to the cell starts through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor either CCR5 or CXCR4 but others are known to interact on the cell surface. The gp120 binds to intergrin α4, β7 activating LFA-I the central intergrin involved in the establishment of virological synapses, which ease efficient cell to cell distribution of HIV-I (Surf and Sprent 2000). The gp160 spike contains binding domains for both CD4 and chemokine receptors (Bodman et al; 2002). The first step in the fusion involves the high affinity attachment of the CD4 binding domains of gp120 to the CD4. Immediately  gp120 is attached with the CD4 protein, the envelope complex takes a structural change, exposing the chemokine binding domain of gp120 and allowing them to attachment, which allows they N-terminal fusion peptide gp41 penetrate the cell membrane. (Ali et al; 2000, McGovern et al; 2002, Reeves and Dan 2002). After HIV has bound to the target cell, the HIV RNA and also various enzymes, including reverse transcriptase, protease, ribonuclease and integrase are injected into the cell. During the microtubulebased transport to the nucleus, the viral – strand RNA genome is transcribed into double-strand DNA which is then integrated into a host chromosome (Foli et al; 2002).


CD4 T helper cells are white blood cells that are an essential part of the human immune system. They are always called CD4 cells, T-helper cells or T4 cells. CD4 cells send the signal and CD8 cells destroy and kill the infection or virus (Cunningham et al 2010, Ray et al; 2006). CD4 is a co-receptor that assists the T cell receptor (TCR) in communicating with an antigen presenting cell using its intracellular domain.

Understanding the clinical significance of ABH secretor status affords a valuable view into seemingly unrelated aspect of physiology. This includes several generalized aspect of the immune function.

The term ABH secretors refers to secretion of ABO blood group antigens in fluids such as saliva, semen, sweat, tears and serum.

The ABH antigens are not primary gene products but instead they are enzymatic reaction products of enzymes called fucosyltransferases. The ABO system occurs as a result of polymorphism of complex carbohydrate structures of glycoproteins and glycolipids expressed at the surface of erythrocytes (Ali et al; 2000). Immunodorminant structure of A and B antigens are synthesized by series of reaction and A and B transferase encoded by the functional alleles (A and B allele) of a lone gene at the ABO locus, while transferase coded by the o allele is non- functional therefore the receptor substrate, (H antigen) remains without further modification and the A &B determinants are present (Kindberg et al., 2006). The carbohydrate moiety of ABH and Lewis glycoproteins consists primarily of four sugar, D- galactose, L-fucose, N-acetylgalactosamine and N-acetyl glucosamine (Dickey et al; 1994; Hein 2006). The ABH secretor systems vary widely. Secretor function continues around the action of a cluster of genes which controls the product of genes which controls the product of enzymes called fucosyltransferases. The genes are called ‘FUT’ and are numbered 1-7 (Mollicone et al; 1995). The majority of these are on chromosome number (19q 13.3). The enzymes help assemble the fucose strings which them become the H antigens, or are further glycosylated to A and or B antigens (Egesie et al; 2005).  Chromosome 19 does most of the secretor work.  It carries the code for FUT I & FUT 2 (fucusyl transferase enzymes) of which the null allele on FUT 2 codes for non secretor status. FUT 2 codes for fucusyltransferase activity in body exocrine.


Many authors recorded various health advantages the secretors have over non secretors of ABH antigen, but none was recorded for CD4 and CD8 to the best of our knowledge.


  1. To determine if there is any immunological advantage of secretors over non secretors of ABH antigen or vise versa.

To determine the percentage of secretors and non secretors including persons living with HIV/AIDS (PLWHA) in our environment.

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