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\( { }_{80} \) Vaccines often contain agents derived from the surface proteins of foreign pathogens that cause disease. These agents stimulate the immune system of the host, allowing the host to recognize and destroy the pathogen in any future encounters. However, \( { }^{\text {a }} \)-some pathogens have developed mechanisms to alter their surface proteins and evade the immune system, making it difficult or :Gimpossible to develop effective vaccines against them. How do mutations that affect the viral protein coat allow human immunodeficiency virus (HIV) to evade the immune system? The virus alters the viral protein coat to mimic host cells. Mutant viral coat proteins attract macrophages to the pathogen. Mutations can alter the antigenic determinant on the protein coat. Changes to the viral protein coat enable the bound virus to leave the antigen-binding site. A protozoan called Trypanosoma brucei, carried by the tsetse fly, causes African sleeping sickness. One variable surface glycoprotein (VSG), or surface coat protein, dominates the trypanosome surface. The trypanosome genome encodes over 1000 different versions of VSGs. All of the cells in an initial infection feature the same VSG coat on their surfaces, and the immune system readily recognizes this protein as foreign. However, an individual trypanosome cell in the broader population will switch and randomly begin expressing a different variant of the VSG coat. All the descendants of that cell will have the new and different protein on their surface. As the population with the second VSG coat increases, an individual cell will then switch to a third VSG coat, and so on. How does expressing a different VSG allow T. brucei to evade the immune system? Some VSG variants allow the protozoan to strongly bind host immune cells, preventing an immune response. Random chance produces some VSG variants that bind and inactivate the antibody variable domains. The switch to a different VSG variant prevents host antigens from recognizing protozoan antibodies. The pathogen expresses a new VSG variant and evades the host antibodies against the earlier VSG variant.

\( { }_{80} \) Vaccines often contain agents derived from the surface proteins of foreign pathogens that cause disease. These agents stimulate the immune system of the host, allowing the host to recognize and destroy the pathogen in any future encounters. However, \( { }^{\text {a }} \)-some pathogens have developed mechanisms to alter their surface proteins and evade the immune system, making it difficult or :Gimpossible to develop effective vaccines against them.
How do mutations that affect the viral protein coat allow human immunodeficiency virus (HIV) to evade the immune system?
The virus alters the viral protein coat to mimic host cells.
Mutant viral coat proteins attract macrophages to the pathogen.
Mutations can alter the antigenic determinant on the protein coat.
Changes to the viral protein coat enable the bound virus to leave the antigen-binding site.
A protozoan called Trypanosoma brucei, carried by the tsetse fly, causes African sleeping sickness. One variable surface glycoprotein (VSG), or surface coat protein, dominates the trypanosome surface. The trypanosome genome encodes over 1000 different versions of VSGs. All of the cells in an initial infection feature the same VSG coat on their surfaces, and the immune system readily recognizes this protein as foreign.
However, an individual trypanosome cell in the broader population will switch and randomly begin expressing a different variant of the VSG coat. All the descendants of that cell will have the new and different protein on their surface. As the population with the second VSG coat increases, an individual cell will then switch to a third VSG coat, and so on.
How does expressing a different VSG allow T. brucei to evade the immune system?
Some VSG variants allow the protozoan to strongly bind host immune cells, preventing an immune response.
Random chance produces some VSG variants that bind and inactivate the antibody variable domains.
The switch to a different VSG variant prevents host antigens from recognizing protozoan antibodies.
The pathogen expresses a new VSG variant and evades the host antibodies against the earlier VSG variant.

Added by Philip M.

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