**1. Introduction**

### **1.1 HIV and TB**

150 Biomedical Science, Engineering and Technology

Yamamoto, M.; Ozawa, K. & Tobe T. (1981). Roles of high blood glucose concentration

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during hemorrhagic shock in alloxan diabetic rats. *Circ Shock,* Vol. 8, No. 1, n.d., pp.

Scientific evidence has shown that HIV infection is caused by a retrovirus, the Human Immunodeficiency Virus (HIV) which is a ribonucleic acid (RNA) virus so designated because of its genome that encodes an unusual enzyme, reverse transcriptase (RT) that enables the virus to make copies of its own genome as DNA in its host's cells (human T4 helper lymphocytes) (Oguntibeju *et al.*, 2008).

The drastic increase in the number of people infected with HIV is not peculiar to a particular racial group, country or community despite multidimensional efforts which have been made to combat this scourge (Weiss, 1996; Oguntibeju *et al.*, 2007a). It is reported that the virus selectively attacks and depletes T-lymphocyte bearing CD4+ cells (T-helper cells) causing a predisposition to opportunistic infections and malignancies (Weiss, 1996) and ultimately resulting in Acquired Immunodeficiency Syndrome (AIDS).

The cellular receptors to HIV are cells that express the CD4+ T cell receptor (CD4+ T-cells or T4-cells) as well as other white blood cells including monocytes and macrophages. Glial cells in the central nervous system, chromaffin cells in the intestine and Langerhans cells in mucous membranes and skin that express CD4+ T cell receptors can also be infected (Paxon *et al.*, 1996). The possibility that there are other cellular targets apart from CD4+T-cells is proved by the likelihood of neurons that can be infected. This creates the possibility of the presence of co-receptors in addition to CD4+ T cells to mediate fusion between HIV and its target cells (Grossman and Heberman, 1997).

Recognition of the CD4+ T-cells by HIV-1 envelope glycoprotein (gp120) to which the virus binds and enters host cells to initiate rapid replication cycles (Oguntibeju *et al.*, 2007b) depicts significant cytopathic consequences of HIV infection of CD4+ T-cells (Bartlett, 1998) and is an important factor in the initiation of HIV infection. The shed virions which are immunogenic, stimulate B cells to produce humoral antibodies and plasma cells through lymphoid hyperplasia that ultimately results in decreased number of infected cells as the CD4+ T-cells migrate through the germinal cells. The depletion in the number of CD4+ T-cells exceeds the formation of new cells and may maintain this phase for many years resulting in general disorganization of the lymphoid nodes, loss of lymphoid function and integrity.
