Scientists believe the invading Romans caused the loss of a genetic shield that makes some people resistant to infection by the Aids virus, HIV.It's hard to envision a disease that would be limited to the territory of the Roman Empire. The Roman frontier was fluid, with both Romans trading beyond it, and barbarians moving into Roman territory; it's hard to imagine how a disease could be "contained" within the territory of the Empire. Moreover, I don't really see a good candidate for a really dramatic Empire-wide epidemic, which would surely have been noticed by historians.
The gene variant, called CCR5-Delta32, impairs the ability of HIV to enter white blood cells.
People with the mutation are not as easily infected by the virus and take longer to develop full-blown Aids.
Generally, only Europeans and western Asians carry the variant, which becomes less widespread as you move south.
More than 15% of people in some parts of northern Europe have CCR5-Delta32, compared with fewer than 4% of Greeks.
He does not think the Romans spread a different version of the gene into their colonies by breeding with the natives.
A more likely explanation, he believes, is that they introduced a fatal disease to which carriers of the CCE5-Delta32 variant were unusually susceptible.
New Scientist magazine reported: "As the Romans moved north, this disease killed people with the variant.
Via the BBC:Infection, Genetics and Evolution doi:10.1016/j.meegid.2008.08.007
In countries inside the borders of the empire for longer periods, such as Spain, Italy and Greece, the frequency of the CCR5-delta32 gene, which offers some protection against HIV, is between 0% and 6%.
Countries at the fringe of the empire, such as Germany, and modern England, the rate is between 8% and 11.8%, while in countries never conquered by Rome, the rate is greater than this.
However, some researchers believe that infections may have played a role - but in reverse -increasing rather than decreasing the frequency of the variant.
Researchers at the University of Liverpool suggested that the variant may have offered protection against pandemics such as the Black Death which swept Europe on a regular basis during and after the Roman era.
These, said the Liverpool researchers, were illnesses which may have been lethal to people without the gene variant, raising its frequency from one in 20,000 people to approximately 10% in Northern Europe.
Is the European spatial distribution of the HIV-1-resistant CCR5-Delta32 allele formed by a breakdown of the pathocenosis due to the historical Roman expansion?
Eric Faure and Manuela Royer-Carenzi
We studied the possible effects of the expansion of ancient Mediterranean civilizations during the five centuries before and after Christ on the European distribution of the mutant allele for the chemokine receptor gene CCR5 which has a 32-bp deletion (CCR5-Delta32). There is a strong evidence for the unitary origin of the CCR5-Delta32 mutation, this it is found principally in Europe and Western Asia, with generally a north-south downhill cline frequency. Homozygous carriers of this mutation show a resistance to HIV-1 infection and a slower progression towards AIDS. However, HIV has clearly emerged too recently to have been the selective force on CCR5. Our analyses showed strong negative correlations in Europe between the allele frequency and two historical parameters, i.e. the first colonization dates by the great ancient Mediterranean civilizations, and the distances from the Northern frontiers of the Roman Empire in its greatest expansion. Moreover, other studies have shown that the deletion frequencies in both German Bronze Age and Swedish Neolithic populations were similar to those found in the corresponding modern populations, and this deletion has been found in ancient DNA of around 7000 years ago, suggesting that in the past, the deletion frequency could have been relatively high in European populations. In addition, in West Nile virus pathogenesis, CCR5 plays an antimicrobial role showing that host genetic factors are highly pathogen-specific. Our results added to all these previous data suggest that the actual European allele frequency distribution might not be due to genes spreading, but to a negative selection resulting in the spread of pathogens principally during Roman expansion. Indeed, as gene flows from colonizers to European native populations were extremely low, the mutational changes might be associated with vulnerability to imported infections. To date, the nature of the parasites remains unknown; however, zoonoses could be incriminated.