Re: How does the immune system react when the African Sleeping Sickness attacks

African sleeping sickness, also known as human African trypanosomiasis 
(HAT), is usually caused by the parasites trypanosomes. The trypanosomes 
are important pathogenic protozoa. Protozoa are unicellular eukaryotic 
microorganisms that lack cell walls. Protozoa usually obtain food by 
ingesting other organisms or organic particles. In humans, the trypanosomes 
live and grow primarily in the bloodstream, but in the later stages of the 
disease, invasion of the central nervous system occurs, causing an 
inflammation of the brain and spinal cord that is responsible for 
neurological symptoms of African sleeping sickness. As you may know, our 
body has two kinds of immunity, cell-mediated (T cell-mediated) immunity 
and humoral (antibody) immunity, to help us resist infection. The 
specificity of the antigen-antibody interaction in humoral immunity or 
antigen-T cell interaction in cell-mediated immunity is very critical in 
our immune response. Our immune response occurs only AFTER a microorganism 
interacts with the immune system. The specific immune effectors, either T 
cells or antibodies, then interact with the invader and destroy it. This 
capacity for responding to challenge after additional exposure to the same 
microorganism is known as "memory". Therefore, the antigen is critical in 
the whole immune recognition.  However, trypanosomes have the ability to 
evade the immune responses by periodically switching their major surface 
antigens, variant surface glycoprotein (VSG), a phenomenon called antigenic 
variation. Antigenic variation, we believe, is the major mechanism for the 
trypanosomes survival in the human body.  In some recent studies, 
scientists showed that several other mechanisms might also help 
trypanosomes survive. The ability to grow in high levels of 
interferon-gamma and to avoid complement-mediated destruction may 
facilitate the parasite's infection.