Error catastrophe

Error catastrophe refers to the cumulative loss of genetic information in a lineage of organisms due to high mutation rates. The mutation rate above which error catastrophe occurs is called the error threshold. Both terms were coined by Manfred Eigen in his mathematical evolutionary theory of the quasispecies.[1]

The term is most widely used to refer to mutation accumulation to the point of inviability of the organism or virus, where it cannot produce enough viable offspring to maintain a population. This use of Eigen's term was adopted by Lawrence Loeb and colleagues to describe the strategy of lethal mutagenesis to cure HIV by using mutagenic ribonucleoside analogs.[2][3]

There was an earlier use of the term introduced in 1963 by Leslie Orgel in a theory for cellular aging, in which errors in the translation of proteins involved in protein translation would amplify the errors until the cell was inviable.[4] This theory has not received empirical support.[5]

Error catastrophe is predicted in certain mathematical models of evolution and has also been observed empirically.[6]

Like every organism, viruses "make mistakes" (or mutate) during replication. The resulting mutations increase biodiversity among the population and can confer advantages such as helping to subvert the ability of a host's immune system to recognise it in a subsequent infection. The more mutations the virus makes during replication, the more likely it is to avoid recognition by the immune system and the more diverse its population will be (see the article on biodiversity for an explanation of the selective advantages of this). However, mutations are not, as a general rule, beneficial, and if it accumulates too many harmful mutations, it may lose some of its biological features which have evolved to its advantage, including its ability to reproduce at all.

The question arises: how many mutations can occur during each replication before the population of viruses begins to lose the ability to survive?

  1. ^ Eigen M (October 1971). "Selforganization of matter and the evolution of biological macromolecules". Die Naturwissenschaften. 58 (10): 465–523. Bibcode:1971NW.....58..465E. doi:10.1007/BF00623322. PMID 4942363. S2CID 38296619.
  2. ^ Hizi, A; Kamath-Loeb, AS; Rose, KD; Loeb, LA (1997). "Mutagenesis by human immunodeficiency virus reverse transcriptase: incorporation of O6-methyldeoxyguanosine triphosphate". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 374 (1): 41–50. doi:10.1016/S0027-5107(96)00217-5. PMID 9067414. Retrieved 3 October 2021.
  3. ^ Loeb, LA; Mullins, JI (2000). "Perspective-Lethal Mutagenesis of HIV by Mutagenic Ribonucleoside Analogs". AIDS Research and Human Retroviruses. 16 (1): 1–3. doi:10.1089/088922200309539. PMID 10628810. Retrieved 3 October 2021.
  4. ^ Orgel, Leslie E. (1963). "The maintenance of the accuracy of protein synthesis and its relevance to ageing". Proc. Natl. Acad. Sci. USA. 49 (4): 517–521. Bibcode:1963PNAS...49..517O. doi:10.1073/pnas.49.4.517. PMC 299893. PMID 13940312.
  5. ^ Michael R. Rose (1991). Evolutionary Biology of Aging. New York, NY: Oxford University Press. pp. 147–152.
  6. ^ Pariente, N; Sierra, S; Airaksinen, A (2005). "Action of mutagenic agents and antiviral inhibitors on foot-and-mouth disease virus". Virus Res. 107 (2): 183–93. doi:10.1016/j.virusres.2004.11.008. PMID 15649564.