ArticlePLoS pathogens2014
Larger mammalian body size leads to lower retroviral activity.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Different Host-Endogenous Retrovirus Relationships between Mammals and Birds Reflected in Genome-Wide Evolutionary Interaction Patterns.Genome biology and evolution · 2024Article
- Evolutionary conservation of an ancient retroviralJournal of virology · 2023Article
- Between the Devil and the Deep Blue Sea: Non-Coding RNAs Associated with Transmissible Cancers in Tasmanian Devil, Domestic Dog and Bivalves.Non-coding RNA · 2021Article
- Article
- Viral Causality of Human Cancer and Potential Roles of Human Endogenous Retroviruses in the Multi-Omics Era: An Evolutionary Epidemiology Review.Frontiers in oncology · 2021Review
- What Animal Cancers teach us about Human Biology.Theranostics · 2021Review
- Interferon-Inducible Protein 16 (IFI16) Has a Broad-Spectrum Binding Ability Against ssDNA Targets: An Evolutionary Hypothesis for Antiretroviral Checkpoint.Frontiers in microbiology · 2019Article
- Variable BaselineFrontiers in immunology · 2019Article
- Distribution, Diversity, and Evolution of Endogenous Retroviruses in Perissodactyl Genomes.Journal of virology · 2018Article
- Human Endogenous Retrovirus-K HML-2 integration withinProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Body mass index and survival from amyotrophic lateral sclerosis: A meta-analysis.Neurology. Clinical practice · 2018Review
- Degradation and remobilization of endogenous retroviruses by recombination during the earliest stages of a germ-line invasion.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- All's well that ends well: why large species have short telomeres.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Article
- Making a virtue of necessity: the pleiotropic role of human endogenous retroviruses in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Epigenetic Control of Human Endogenous Retrovirus Expression: Focus on Regulation of Long-Terminal Repeats (LTRs).Viruses · 2017Review
- Article
- Importance of metabolic rate to the relationship between the number of genes in a functional category and body size in Peto's paradox for cancer.Royal Society open science · 2016Article
- Evolutionary constraints over microsatellite abundance in larger mammals as a potential mechanism against carcinogenic burden.Scientific reports · 2016Article
- Human endogenous retrovirus (HERV) expression is not induced by treatment with the histone deacetylase (HDAC) inhibitors in cellular models of HIV-1 latency.Retrovirology · 2016Article
- Viral fossils.Nature reviews. Microbiology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Retroviruses have been infecting mammals for at least 100 million years, leaving descendants in host genomes known as endogenous retroviruses (ERVs). The abundance of ERVs is partly determined by their mode of replication, but it has also been suggested that host life history traits could enhance or suppress their activity. We show that larger bodied species have lower levels of ERV activity by reconstructing the rate of ERV integration across 38 mammalian species. Body size explains 37% of the variance in ERV integration rate over the last 10 million years, controlling for the effect of confounding due to other life history traits. Furthermore, 68% of the variance in the mean age of ERVs per genome can also be explained by body size. These results indicate that body size limits the number of recently replicating ERVs due to their detrimental effects on their host. To comprehend the possible mechanistic links between body size and ERV integration we built a mathematical model, which shows that ERV abundance is favored by lower body size and higher horizontal transmission rates. We argue that because retroviral integration is tumorigenic, the negative correlation between body size and ERV numbers results from the necessity to reduce the risk of cancer, under the assumption that this risk scales positively with body size. Our model also fits the empirical observation that the lifetime risk of cancer is relatively invariant among mammals regardless of their body size, known as Peto's paradox, and indicates that larger bodied mammals may have evolved mechanisms to limit ERV activity.
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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.