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WAGUSTIN t1_j942f2t wrote

In many instances, pathogens display antigenic variation. Your immune system makes antibodies in response to pathogenic antigens, but some pathogens display a survival technique wherein they swap out their antigens so that the antibodies your body just made don’t work anymore. Sometimes this is a built-in mechanism, such as in relapsing fever. The pathogens in this instance are some species of Borrelia, where it can rearrange its DNA to dodge your immune system. Plasmodium, the family of protozoa responsible for malaria, also displays this strategy, and also has a characteristic presentation of cycling fever (which is two or three days depending on the specific species). In other cases it can simply be random mutations that result in cycles of fever due to selective pressure, wherein your immune system kills off pathogens with one antigen, leaving the pathogens with other antigens to proliferate. The Hepatitis C virus is good example, which even has an RNA polymerase that can't proofread gene copies, effectively encouraging mutations. Your body therefore goes through periods where it makes antibodies against a certain antigen (which can take a few days), kills off pathogens with that antigen, leading to reduced symptoms, but then leaves a few that switched antigens. The survivors proliferate and force your immune system to have to make different antibodies, repeating the process.

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malefiz123 t1_j951ofy wrote

> Plasmodium*, the family of protozoa responsible for malaria, also displays this strategy, and also has a characteristic presentation of cycling fever (which is two or three days depending on the specific species).

An infectious disease specialist at my hospital said he never saw this kind of precise cycling in malaria patients, even though he treated hundreds of them. It seems to be one of the text book myths that float around medicine since forever.

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