Ancient Viruses: How infectious diseases arrived in the colonial Americas
When European colonisers arrived in the Americas in the 16th and 17th centuries, they brought with them multiple infectious diseases which led to massive outbreaks that killed millions of indigenous people. However, it is unclear which pathogens were responsible for these devastating epidemics that are generally referred to as the Cocoliztli, meaning ‘pest’ in the Nahuatl language (Acuna-Soto et al., 2004).
Most research in this area has focused on diseases that arrived in the Americas from Europe, and do not factor in another horrific part of European colonial history: the transatlantic slave trade that forcibly transported West Africans – who carried unique genotypes of the disease-causing pathogens – to the Americas (Diamond, 1998). Now, in eLife, María C. Ávila-Arcos from Universidad Nacional Autónoma de México and colleagues – including Axel A Guzmán-Solís as first author – report the first likely evidence of viruses that originated in Africa circulating in Mexico during the colonial period (Guzmán-Solís et al., 2021).
The team (who are based in Mexico, Denmark and the United States) studied human remains that were found in two burial sites in Mexico City: one was associated with a colonial hospital and chapel, and the other a hospital that treated Native Americans during the 1576 Cocoliztli outbreak. Archaeological analysis of the remains from the latter site suggested that 21 of the individuals studied were of West African ancestry, despite their presence in a hospital associated with the treatment of indigenous people. Viral DNA was then extracted from these remains and analysed using various genetic sequencing tools.
The data identified an ancient strain of parvovirus B19 in three of the individuals studied, and an ancient strain of hepatitis B in one other individual. The genome of the discovered parvovirus was highly similar to a strain called genotype 3, which is sporadically found in Africa and is extremely rare in modern Europe and the Americas. This suggests that the transatlantic slave trade imposed by European colonization may have introduced new viral pathogens or genotypes into colonial Mexico.
Guzmán-Solís et al. also found the genotype 3 strain in the human remains of an indigenous person, suggesting that the virus may have spread to local individuals and contributed to the disease outbreaks that affected millions of people. The researchers then carried out genealogical DNA testing of the four individuals to study whether being infected with a specific pathogen genotype was associated with their genetic ancestry. These data helps build on a previous study revealing how different viral genotypes are distributed among modern Native Americans with African ancestry related to European colonial history (Lopera et al., 2014).
Although the study provides an important glimpse into the existence of these ancient viral strains in the colonial Americas, there are some limitations. First, the historical global distribution of the genotypes discovered is still largely unknown. Second, the conclusions are based on pathogens isolated from only four individuals, although it is common for these kinds of studies to have small amounts of genetic data due to limited number of samples.
Nevertheless, a global dataset with more genotype 3 sequences needs to be retrieved and analysed to confirm or refute the hypothesis that B19 genotype 3 was first brought to the Americas by enslaved Africans during the transatlantic slave trade. Indeed, a previous study found this strain of B19 in the remains of North European soldiers from the Second World War (Toppinen et al., 2015), and the genotype has also been observed in India (Jain et al., 2015) and the Brazilian Amazon (Freitas et al., 2008). Lastly, very few viral strains of African origin have been isolated from modern or ancient remains of African individuals, which will be needed to fully understand the genetic history and genotype distribution of these human infecting pathogens (Figure 1).
Previous studies have found other ancient pathogens in the human remains of individuals who were alive during the colonial period in Mexico, some of whom were buried in a manner associated with an epidemic event. The work by Guzmán-Solís et al. suggests that parvovirus B19 can be added to this growing list of microbes, which includes the viruses and bacteria responsible for the skin disease yaws, hepatitis B, syphilis, salmonella and paratyphoid fever (Barquera et al., 2020; Schuenemann et al., 2018; Vågene et al., 2018). The study also provides historical evidence of viruses being transmitted between geographically distant human populations, which likely led to the emergence of related infectious diseases in populations that were previously naïve to the pathogen.
References
-
When half of the population died: the epidemic of hemorrhagic fevers of 1576 in MexicoFEMS Microbiology Letters 240:1–5.https://doi.org/10.1016/j.femsle.2004.09.011
-
Historic Treponema pallidum genomes from Colonial Mexico retrieved from archaeological remainsPLOS Neglected Tropical Diseases 12:e0006447.https://doi.org/10.1371/journal.pntd.0006447
-
Bones hold the key to DNA virus history and epidemiologyScientific Reports 5:17226.https://doi.org/10.1038/srep17226
-
Salmonella enterica genomes from victims of a major sixteenth-century epidemic in MexicoNature Ecology & Evolution 2:520–528.https://doi.org/10.1038/s41559-017-0446-6
Article and author information
Author details
Publication history
Copyright
© 2021, Pimenoff and Houldcroft
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 1,732
- views
-
- 113
- downloads
-
- 2
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
The transatlantic slave trade introduced dangerous human pathogens into Mexico
-
- Developmental Biology
- Genetics and Genomics
Paternal obesity has been implicated in adult-onset metabolic disease in offspring. However, the molecular mechanisms driving these paternal effects and the developmental processes involved remain poorly understood. One underexplored possibility is the role of paternally-induced effects on placenta development and function. To address this, we investigated paternal high-fat diet-induced obesity in relation to sperm histone H3 lysine 4 tri-methylation signatures, the placenta transcriptome and cellular composition. C57BL6/J male mice were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age. Males were timed-mated with control-fed C57BL6/J females to generate pregnancies, followed by collection of sperm, and placentas at embryonic day (E)14.5. Chromatin immunoprecipitation targeting histone H3 lysine 4 tri-methylation (H3K4me3) followed by sequencing (ChIP-seq) was performed on sperm to define obesity-associated changes in enrichment. Paternal obesity corresponded with altered sperm H3K4me3 at promoters of genes involved in metabolism and development. Notably, sperm altered H3K4me3 was also localized at placental enhancers. Bulk RNA-sequencing on placentas revealed paternal obesity-associated sex-specific changes in expression of genes involved in hypoxic processes such as angiogenesis, nutrient transport, and imprinted genes, with a subset of deregulated genes showing changes in H3K4me3 in sperm at corresponding promoters. Paternal obesity was also linked to impaired placenta development; specifically, a deconvolution analysis revealed altered trophoblast cell lineage specification. These findings implicate paternal obesity-effects on placenta development and function as one potential developmental route to offspring metabolic disease.