ABSTRACT
Human immunode‰ciency virus (HIV) infection is characterized by progressive immunosuppression leading to acquired immunode‰ciency syndrome (AIDS). The effects of HIV on the immune system are multifold. The cascading effects are principally due to the direct lytic effect on CD4 T-cells and follicular dendritic cells (nursemaid cells). This affects the inductive phase of the immune system by lowering the ef‰ciency of antigen presenting cells and CD4 afferent functions. Sustained loss of this activity in untreated individuals is followed eventually by effector function loss of the cellular limb viz. CD8 effector function. This process results over a period of time; hence, there is an adverse effect on several levels of both innate and acquired immunity. The selective depletion of CD4 lymphocytes is the ‰rst observable abnormality related to HIV infection. The HIV infection in its natural course was well studied before the introduction of antiretroviral therapy (ART). These early studies focused on the natural history of infection, which clearly showed the association with several pathological changes affecting multiple organs including the endocrine system. The circulating cytokine levels and more importantly the observations at the lymph node sites based on messenger ribonucleic acid (mRNA) expression revealed interesting changes (Graziosi et al. 1994). It was documented that during HIV disease progression, there was an observable shift from a Th1 to a Th2 cytokine pro‰le (Maggi et al. 1994). The interaction between the endocrine and immune system is well documented. One of the possible reasons for this shift in cytokine pro‰le may be the increase in the production of cortisol and the reduction of dehydroepiandrosterone (DHEA) (Clerici et al. 1997; Clerici et al. 2000).
