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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.

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