The success of any pathogen depends upon its ability to evade host immunity.

The development of cancer is determined by a variety of factors such as host immunity and mutations in the host.

TH1 helper cell is the host immunity against intracellular bacteria and protozoa.

TH2 helper cell is the host immunity against multicellular helminths.

TH17 helper cells mediate host immunity against extracellular bacteria and fungi.

THαβ helper cells provide the host immunity against viruses.

In these cases, it is thought that short host lifespans prevent the build-up of host immunity necessary to effectively drive antigenic drift.

The rate of antigenic drift is dependent on two characteristics: the duration of the epidemic, and the strength of host immunity.

Eventually, when host immunity develops, the virus persists by turning off most (or possibly all) of its genes, only occasionally reactivating to produce fresh virions.

The reason is unknown but may be due to the development of larvae which were arrested in their development as a result of host immunity.