Archive | aDNA RSS feed for this section

The Bone Ages: MOSI on Down to the Manchester Science Festival, Sunday 2nd Nov 2014

3 Oct

A date for the diary for all bone and science lovers!  Skeletal researchers from the University of Sheffield and Manchester Metropolitan University will be at the Manchester Museum of Science & Industry (MOSI) on Sunday 2nd of November 2014 (from 10.30 am to 4 pm) helping to present an event called The Bone Ages to the public.  The Bone Ages will bring together the social sciences and lab based research in helping to present the wonders of studying the human skeleton, detailing how bones can teach us about the history, health and society of past populations and individuals using live demonstrations.  The event will include interactive showcases and activities for children and adults of all ages, from learning about how to age and sex the skeleton to understanding what DNA testing of skeletal material can reveal.

The Bone Ages event is being run at MOSI as a part of the Manchester Science Festival (which runs from 23rd October to 2nd November), which is aimed at engaging the whole family in understanding the wonders of cutting edge science and ground shaking research.  The Manchester Science Festival is free to attend and will be running a whole host of events to do with innovative scientific topics in a variety of locations across Manchester.


A flyer from the website advertising the Bone Ages open day. Image credit: MOSI.

So what is actually happening at the Bone Ages event?

Well there will be a host of hands on demonstrations and live shows by the researchers of the Manchester Metropolitan University and the University of Sheffield staff.  There will be four staff from MMU who each specialise in different areas of skeletal research including:

  • Dr Craig Young (human geography), who will be discussing the importance of human remains as a part of the socio-political processes linked to cultural identity.
  •  Dr Seren Griffiths (archaeology), who will provide a live demonstration of 3D laser scanning and talk about the importance of the technique to accurately digitally record excavated specimens.
  • Dr Kirsty Shaw (molecular biology), who will be demonstrating the application of miniaturized technology that allows the DNA sampling of remains in the field.
  • Dr Alex Ireland (health science), who’ll be demonstrating how scanning bones can reveal the permanent record of previous activity, to help prevent health risks in the present day population.

On top of this researchers from the University of Sheffield, including doctoral candidate Jennifer Crangle, will be discussing and highlighting the value of analysing the human skeleton, from how to age and sex remains (using casts and examples) to talking about the nature of archaeological bone, from complete to fragmented remains.  I will also be there, helping to engage the public how and why osteoarchaeologists analyse bones and generally helping out.  Alongside this I’ll also be assisting with the exciting ‘exploding skeleton’, a fun and interactive way to learn about the skeletal anatomy of the body by having members of the pubic trying to figure out what piece goes where in the human body.

The demonstrations for The Bone Ages will be taking place at the new purpose built PI: Platform for Investigation arena at the museum, which is part of a new monthly contemporary science program aimed at the bold, innovative presentation and engagement of science with the public.  I, for one, am thoroughly looking forward to this, so I hope to see you there!

Learn More

  • Look out for the #boneages hashtag on twitter for further information and updates.  There will also be a number of guest blogs produced for the Manchester Science Festival, which will also appear on the Institute of Humanities & Social Sciences Research, run by Manchester Metropolitan University.
  • The Manchester Science Festival runs from 23rd October to the 2nd of November, with events being ran all day, and for free, during these dates.  The festival will fuse art and science together in an intoxicating mix for all of the family, with topics ranging from industrial archaeology to 3D printing, from film showings to computer coding.  Find out more here.

Infectious Disease Part 2: Malaria and Associated Anaemic Conditions

5 Oct

This second post, and the first part, deal with biomolecular approaches and research studies in detecting  the presence of infectious diseases in human bone from archaeological material.  The recent coming of age of biomolecular techniques, as applied to archaeological material, has provided a rich and complex source of information in helping to uncover how infectious diseases spread in the historic and prehistoric past.  The second post, here, describes recent research focused on Malaria and associated anaemic conditions, including Sickle Cell Anaemia and Thalassaemia.  The first post can be found here.


It has long been realised that malaria can only be recognised in skeletal remains via indirect evidence of presentation of the following pathological lesions- porotic hyperostosis, cribra orbitalia and marrow hypertrophy- which are taken as evidence of the presence of anaemia, the main contributor of mortality in malarial victims (Roberts & Manchester 2010).  However there is no pathognomonic bone lesion for either Plasmodium vivax or P. falciparum, the main human species of malaria causing Plasmodium genus  (Gowland & Western 2012: 303, Roberts & Manchester 2010: 233), and the above skeletal lesions have varying aetiologies including anaemia, osteitis, parasitic infection, and other interrelated deficiency diseases which are still not clearly understood (Gowland & Western 2012: 302).  To securely diagnose malaria in skeletal material, DNA identification of the Plasmodium genus must take place, and even then current Polymerase Chain Reaction (PRC) tests ‘do not appear to be able to amplify routinely the DNA of malaria pathogens from ancient bones’ (Gowland & Western 2012: 302).

Recent immunological techniques to identify antigens have also been used to isolate and identify P. falciparum, although false positives can occur as a result of contamination or diagenetic factors(Gowland & Western 2012: 302).  Gowland & Western (2012) have recently proposed a spatial epidemiological model for malarial spread in Anglo-Saxon England, which highlights the re-surging interest in malaria in the modern context as well as one affecting a past population.  This holistic approach used GIS data with diagnosed porotic hyperostosis in skeletal remains, mosquito (Anopheles atroparvus) habitat information and historical data in presenting a locality data set for malaria infected individuals (Gowland & Western 2010: 304-305).  The modelling of palaeopathological, climatic, and historical data, provides new information on disease range, mechanism of transmission, and infection localities.  However, there are also complicating factors in assessing and diagnosing malaria from other diseases, as noted below (Roberts & Manchester 2010: 234).

Particularly important are two inherited haemolytic anaemia’s, thalassaemia and sickle-cell anaemia, who are characterised by abnormal haemoglobin and increased destruction of red blood cells (Jurmain et al. 2011: 312, Roberts & Manchester 2010: 232).  Thalassaemia is a genetically determined disorder which is caused by a ‘problem of haemoglobin synthesis’ (Roberts & Manchester 2010: 233).  This results in failure or depression of synthesis of the chain, this leads to pale cells with low hemoglobin content which are then rapidly destroyed once formed.  There are three grades of the disease, minor, intermediate and major, the last of which includes severe anemia and possible bone changes; the range of the disease is typically centered in the Mediterranean, Middle East and Far East (Roberts & Manchester 2010: 233).  The importance is that it is seen as an adaptive response to malaria infection through the development of this heritable disease; that the high red blood cell turnover stalls and negates any effect of malarial infection.  Archaeological evidences comes from Greek, Turkish and Cypriot populations deriving from marshy contexts, which are ideal breeding grounds for mosquitoes, the prime vector for malaria (Roberts & Manchester 2010: 233).

Sickle-cell anaemia occurs as a result of the deformation and destruction of red blood cells which leads to over enlargement of bony centres (centered on the skull, pelvis, vertebrae) and over-activity of marrow production as the body produces more red blood cells (Waldron 2009).  This inheritable disease range is mainly located in Central and Eastern African populations who have high rates of the disease, but also affects Indian, Middle Eastern, and Southern European populations (Roberts & Manchester 2010: 234).  Jurmain et al. (2011: 312) remark that the sickle-cell allele hasn’t always been effective in malarial negation in human populations, and primarily came to prominence during the advent of agriculture, and in particular during the last 2000 years in Africa.  The origin of the mutation of the allele responsible, HB5 in haemoglobin, has been dated to 2100 to 1250 years ago in African populations (Jurmain et al. 2011: 312).  Although malaria infection has only relatively recently affected human populations, it has become a powerful selective force that still affects large portions of the world’s population today.

In conclusion, biomolecular approaches to archaeological and osteological remains are vital in unraveling past populations and the natural world (Jurmain et al. 2011).  The interactions between wild and domesticated animals, humans, insects and the environment are a prerequisite for understanding the mode of transmission and virulence of infectious diseases (Barnes et al. 2011, Gowland & Western 2012, Jurmain et. al 2011).  Yet, we must take into consideration the difficulties in understanding infectious disease; examples of the osteological paradox are ever present, understanding the aetiology of bone changes, and the context of genetic differences between populations must be noted whilst PCR amplification, aDNA detection and genome explorations methods must be continually improved for clearer results (Li et al. 2011, Schurch et al. 2011, Spigelman et al. 2012, Tran et al. 2011); this approach must be multidisciplinary in understanding past and present populations (Jurmain et al. 2011, Roberts & Manchester 2010, Waldron 2009).

The modern world has changed, and the boundaries that once protected various human populations has changed dramatically with cheap air travel and vast population movement; this is unprecedented in both history and prehistory, and in population density and scale, but also at the genetic level in human genetic variation (Hawks et al. 2007, Jurmain et al. 2011: 311).  The eradication of smallpox, the Bill and Melinda Gates foundation in fighting malaria, and the ongoing WHO (World Health Organisation) case against polio (Branswell 2012: 50) are strong examples of what can be achieved worldwide.  By building a past population profile of the effects of infectious disease, we are better prepared for the fight tomorrow.


Barnes, I., Duda, A., Pybus, O. G. & Thomas, M. G. 2011. Ancient Urbanization Predicts Genetic Resistance to Tuberculosis. Evolution. 65 (3): 842-848.

Branswell, H. 2012. Polio’s Last Act. Scientific American. 306 (4): 50-55.

Gowland, R. L., & Western, A. G. 2012. Morbidity in the Marshes: Using Spatial Epidemiology to Investigate Skeletal Evidence for Malaria in Anglo-Saxon England (AD 410- 1050). American Journal of Physical Anthropology. 147: 301-311.

Hawks, J., Wang, E. T., Cochran, G. M., Harpending, H. C. & Moyzis, R. K. 2007. Recent Acceleration of Human Adaptive Evolution. Proceedings of the National Academy of Sciences. 104 (52): 20753-20758.

Jurmain, R., Kilgore, L. & Trevathan, W. 2011. The Essentials of Physical Anthropology, International Edition. Belmont: Wadsworth.

Li, Y., Carroll, D. S., Gardner, S. N., Walsh, M. C., Vitalis, E. A. & Damon, I. K. 2007. On the Origin of Smallpox: Correlating Variola Phylogenics with Historical Smallpox Record. Proceedings of the National Academy of Science. 104 (40): 15787-15792.

Roberts, C. & Manchester, K. 2010. The Archaeology of Disease. Stroud: The History Press.

Schurch, A. C., Kremer, K., Kiers, A., Daviena, O., Boeree, M. J., Siezen, R. J., Smith, N. H., & Soolingen, D. V. 2010. The Tempo and Mode of Molecular Evolution of Mycobacterium Tuberculosis at Patient-to-Patient Scale. Infection, Genetics and Evolution. 10 (1): 108-114.

Spigelman, M., Shin, D. H., & Gal, G. K. B. 2012. The Promise, the Problems and the Future of DNA Analysis in Palaeopathology Studies. In Grauer, A. L. (ed). A Companion to Palaeopathology. Chichester: Blackwell Publishing Ltd.  pp.133-151.

Tran, T., Aboudharam, G., Raoult, D., & Drancourt, M. 2011. Beyond Ancient Microbial DNA: Nonnucleotidic Biomolecules for Palaeomicrobiology. BioTechniques. 50: 370-380.

Waldron, T. 2009. Palaeopathology. Cambridge: Cambridge University Press.

Infectious Disease Part 1: Treponemal Disease & Smallpox

5 Oct

The following two posts deal with biomolecular approaches and research studies in detecting the presence of infectious diseases in human bone from archaeological material.  The recent coming of age of biomolecular techniques, as applied to archaeological material, has provided a rich and complex source of information in helping to uncover how infectious diseases spread in the historic and prehistoric past.  Whilst it has help clear some mysteries up, it has unleashed others.  The first post, here, describes recent research focused on Treponemal diseases (including Yaws, Syphilis and Pinta) and Smallpox.  The second post can be found here.


Treponemal Diseases

Roberts & Manchester (2010: 216) note that infectious diseases are ‘not solely microbiological entities but are a composite reflection of individual immunity, social, environmental, and biological interaction’.  The study of treponemal disease, in particular, is fraught with controversy and stigma, both in the modern and historical contexts (Lucas de Melo et al. 2010: 1, Roberts 2000), and in the nature of its spread and transmission.  However the combination of molecular pathology, phylogenetics, and palaeopathological studies, are helping to produce a clearer genetic origin of the disease and the impacts that this disease had, and continues to have, on the world at large (Hunnius et al. 2007: 2092).  Typically the bacterial diseases of the genus Treponema are split into different forms; pinta (T. carateum), yaws (T. pallidum subspecies pertenue), endemic syphilis (T. pallidum subspecies edemicum) and venereal/congenital syphilis (T. pallidum subspecies pallidum) (Table 1; Lucas de Melo et al. 2010: 2).  The four forms were, until recently, indistinguishable in physical and laboratory characteristics (Roberts & Manchester 2010: 207), whilst the pinta strand does not affect bone (Waldron 2009: 103).  DNA analysis of the bacteria of venereal syphilis has shown a difference between it and the non-venereal types; although it is noted that there is no change in the clinical presentation of the disease (Roberts & Manchester 2010: 207).

Table 1. Geographic location, transmission and whether bone is affected for treponemal disease (after Waldron 2009: 103).

Yaws was likely the first disease to emerge, probably from an ape relative in Central Africa, whilst the endemic form of syphilis derived from an ancestral form in the Middle East and the Balkans at a later date, whilst T. pallidum was the last to emerge, probably from a New World progenitor, although the issue is still highly contentious (Roberts & Manchester 2010: 212, Waldron 2009: 105).  Gaining virulence at a dramatic rate in the 15th and 16th centuries AD in Europe, venereal syphilis affected a large section of the population due to its mode of transmission.  It should be noted, however, that bone changes in syphilis are rare in the early stages but common in the tertiary stage of the disease (Roberts & Manchester 2010).  It has also been noted that there could be a back and forth transmission, from one treponemal disease to another, within intra-population groups changing from one environment to another; that ultimately it’s possible that each social group, or population, has its own treponemal disease suited to its ‘geographic and climatic home and its stage of cultural development’ (Roberts & Manchester 2010: 213).

However, this infectious disease, in its venereal form, is particularly hard to locate and identify in archaeological populations; the limitations of biomolecular palaeopathology have become clear (Bouwman & Brown 2005: 711, Hunnius et al. 2007, Lucas de Melo et al. 2010: 10).  Bouwman & Brown’s (2005) experiment, and Hunnius et al. (2007) subsequent paper, have highlighted the difficulties in amplifying T. pallidum subspecies T. pallidum, even in highly suspected bone samples.  Bouwman & Brown (2005: 711) tested 9 treponemal samples using the Polymerase Chain Reaction (PCR) tests, optimized to highlight ancient treponemal DNA.  This resulted in poor amplification of  treponemal ancient DNA (aDNA) from human bone, even with bone of varying origins (geographic, social and climatic samples).  3 outcomes where postulated; the bones were either not suitable for aDNA retrieval, treponemal aDNA was present but the PCR was not sensitive enough to be pick it up, or there was no treponemal DNA in the bones (Bouwman & Brown 2005: 711-712).  Subsequent investigations and phylogenetic approaches have highlighted that the disease invades different parts of the body at impressive rates, but in the later stages of the disease, the organism’s DNA is not present in the actual bone itself, just at the stage when an osteologist can identify it macroscopically (Hunnius et al 2007: 2098).  Phylogenetic evidence supports evidence of variations in the virulence of syphilis, and the support of a more distant origin, possibly around 16,500 to 5000 years ago, but where exactly remains unsolved (Lucas de Melo et al. 2010: 2).  Interestingly, in the early 20th century P. Vivax (the main causer of malaria) was used as a treatment for patients with neurosyphilis in a procedure by the physician Julius Wagner-Jauregg; it was injected as a form of pyrotherapy to introduce high fevers to combat the late stage syphilitic disease by killing the causative bacteria (Wagner-Jauregg 1931).


The Smallpox virus is particularly devastating and disfiguring disease, but thankfully no longer an active infection in the modern world (Manchester & Roberts 2010: 180).  Although kept only in laboratory samples now, there is an ongoing concern regarding whether it could be a danger to modern archaeologists dealing with infected material (Waldron 2009: 110).  The disease, once contracted, either leads to recovery with lifelong immunity or death.  The severe form is called variola major and is documented in the Old World with a 30% death rate once contracted, whilst its less virulent form, named variola or alastrim minor, is found in Central America and has a mortality rate of 1% (Hogan & Harchelroad 2005, Li et al. 2007: 15788).  Smallpox, the strictly human variola virus pathogen, is found in literature and documentary records during the last 2000 years (Larsen 1997), yet an osteological signature is not present or identifiable in infected individuals (Waldron 2009: 110).  Therefore to find out the origins of the disease, Li et al. (2007) used correlated variola phylogenetics with historical smallpox records to map the evolution, origin and transportation of smallpox between human populations.

Li et al. (2007: 15787) state that no credible descriptions of the variola virus have been found on the American continent or sub-Saharan Africa before the advent of westward European exploration in the 15th century AD; suggesting that with European exploration and expansion came the virulent waves of smallpox that helped to decimate the existing Native American populations, who previously had no contact or natural immunization with such a highly virulent disease.  It is worth noting here the disease has been used in warfare as a chemical weapon surprisingly early.  During the 18th century American colonial wars between the French, British and the Native Americans, the British forces stationed in America actively infected items of clothing that were given to the Native population to help aid the spread of the disease among the Native Americans , who at that time were largely allied to the French.  This weakened the Native American population dramatically during the various colonial wars and subsequent colonial expansion westward; it’s estimated nearly half of the American Native population died from smallpox alone and its naturally rapid commutable spread of smallpox through human populations (Hogan & Harchelroad 2005).

Li et al. (2007: 15787) note that there are ambiguous gaps in the evolution of smallpox disease itself however.  Li et al. (2007) initiated a systematic analysis of the concatenated Single Nucleotide Polymorphisms (SNP’s) from the genome sequences of 47 variola major isolates from a broad geographic distribution to investigate its origins.  Variola major has a slowly evolving DNA genome, which means a robust phylogeny of the disease is possible (Hogan & Harchelroad 2005).

Firstly, the results showed that the origin of variola was likely to have diverged from an ancestral African rodent–borne variola like virus, either around 16,000 or 68,000 thousand years ago dependent on which historical records are used to calibrate the molecular clock (East Asian or African) (Li et al. 2007: 15791).  Taterapox virus is associated with terrestrial rodents in West Africa, and provides a close relationship with the variola virus.  It is entirely possible that variola derived from an enzootic pathogen of African rodents, and subsequently spread from Africa outwards (Li et al. 2007: 15792).  Secondly, evidence points towards two primary clades of the variola virus, both from the same source as above, but each represent a different severity and virulence of the variola virus.

The first primary clade is represented by the Asian variola major strains, which are the more clinically severe form of smallpox;  the molecular study of its natural ‘clock’ suggests it spread from Asia either 400 or 1600 years ago (Li et al. 2007: 15788).  Included in this first primary clade is the subclade of the African minor variation of the main Asian variola major disease.  The second primary clade compromises two subclades, of which are the South American alastrim minor and the West African isolates (Li et al. 2007: 15788).  This clade had a remarkably lower fatality rate in comparison to the above clade.  The importance of phylogeny analysis is that it highlights areas of disease prevalence and virulence that can be missed, or indeed entirely absent, from the osteological and archaeological record (Brown & Brown 2011).


Bouwman, A. S. & Brown, T. A. 2005. The Limits of Biomolecular Palaeopathology: Ancient DNA cannot be used to Study Venereal Syphilis. Journal of Archaeological Science. 32: 703-713.

Brown, T. & Brown, K. 2011. Biomolecular Archaeology: An Introduction. Chichester: Blackwell Publishing.

Hogan, C. J. & Harchelroad, F. 2005. Smallpox. Emedicinehealth. Accessed at on the 29th of April 2012.

Hunnius, T. E., Yang, D., Eng, B., Waye, J. S. & Saunders, S. R. 2007. Digging Deeper into the Limits of Ancient DNA Research on Syphilis. Journal of Archaeological Science 34: 2091-2100.

Larsen, C. S. 1997. Bioarchaeology: Interpreting Behaviour from the Human Skeleton. Cambridge: CambridgeUniversity Press.

Li, Y., Carroll, D. S., Gardner, S. N., Walsh, M. C., Vitalis, E. A. & Damon, I. K. 2007. On the Origin of Smallpox: Correlating Variola Phylogenics with Historical Smallpox Record. Proceedings of the National Academy of Science. 104 (40): 15787-15792.

Lucas de Melo, F., Moreira de Mello, J. C., Fraga, A. M., Nunes, K. & Eggers, S. 2010 Syphilis at the Crossroad of Phylogenetics and Palaeopathology. PLoS Neglected Tropical Diseases.4 (1): 1-11.

Mitchell, P. 2003. The Archaeological Study of Epidemic and Infectious Disease. World Archaeology. 35 (2): 171-179.

Roberts, C. & Manchester, K. 2010. The Archaeology of Disease. Stroud: The History Press.

Wagner-Jouregg, J. 1931. Verhutung und Behandlung der Progressiven Paralyse durch Impfmalaria.  Handbuch der Experimentellen Therapie, Erganzungsband Munchen.

Waldron, T. 2009. Palaeopathology. Cambridge: Cambridge University Press.