ArticleImmunogenetics2014
Parallel evolution of a self-signal: humans and new world monkeys independently lost the cell surface sugar Neu5Gc.
Article in Immunogenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 85 citations in OpenAlex.
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- Mutations Inactivating Biosynthesis of Dispensable Carbohydrate-Antigens Prevented Extinctions in Primate/Human Lineage Evolution.Journal of molecular evolution · 2025Review
- Inactivation of the CMAH gene and deficiency of Neu5Gc play a role in human brain evolution.Inflammation and regeneration · 2025Review
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- Evolutionary constraint and innovation across hundreds of placental mammals.Science (New York, N.Y.) · 2023Article
- N-glycolylated carbohydrates in nature.Glycobiology · 2022Review
- Wild and domestic animals variably display Neu5Ac and Neu5Gc sialic acids.Glycobiology · 2022Article
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- GANAB andInternational journal of molecular sciences · 2022Review
- Respiratory mucus as a virus-host range determinant.Trends in microbiology · 2021Review
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human sialic acid biology is unusual and thought to be unique among mammals. Humans lack a functional cytidine monophosphate-N-acetylneuraminic acid hydroxylase (CMAH) protein and cannot synthesize the sugar Neu5Gc, an innate mammalian signal of self. Losing this sugar changed how humans interact with some of our deadliest pathogens: malaria, influenza, and streptococcus among others. We show that the New World monkeys, comprising the third of all primate species, have human-like sialic acid biology. They have lost Neu5Gc because of an independent CMAH inactivation ~30 million years ago (mya) (compared to ~3 mya in hominids). This parallel loss of Neu5Gc opens sialic acid biology to comparative phylogenetic analysis and reveals an unexpected conservation priority. New World monkeys risk infection by human pathogens that can recognize cells in the absence of Neu5Gc. This striking molecular convergence provides a mechanism that could explain the long-standing observation that New World monkeys are susceptible to some human diseases that cannot be transmitted to other primates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.