An international team of scientists investigating African human tissue
samples preserved for nearly 50 years have suggested that the HIV/AIDS
pandemic
started around 100 years ago, between 1884 and 1924, at the same time as
urbanization started growing in west central Africa.
The finding is published in the 2nd October issue of the journal Nature and was the work of Dr Michael Worobey, an assistant professor of ecology and evolutionary biology at The University of Arizona in Tucson, and colleagues at research centres in Australia, Belgium, France, Democratic Republic of Congo, Denmark and the USA.
Worobey and colleagues suggested that the growing urbanization of colonial Africa around the dawn of the 20th century, characterized by the growth of cities and a rise in high risk behaviours, set the stage for the HIV/AIDS pandemic and created the conditions that allowed the most pervasive strain of HIV, the HIV-1 group M, to spread among humans.
This is some 30 years before previous estimates, which suggested HIV started spreading around 1930.
For the study, Worobey and colleagues spent 8 years screening endless quantities of tissue samples until they discovered a genetic sequence of HIV-1 group M. Dating from 1960, this is the second oldest ever found. It came from a lymph-node tissue biopsy from a woman who lived in present day Kinshasa in the Democratic Republic of the Congo.
The oldest genetic fragment of HIV-1 group M came from a 1959 blood sample from another Kinshasa resident, this time a man.
First the researchers created a range of plausible family trees for the HIV-1 group M, using the 1960 sample and other known HIV-1 genetic sequences. From this it was possible to make time estimates of when the strains diverged from their ancestors, and the rates at which the branches of the trees grew. By projecting backwards the researchers then estimated when the trees took root, that is when the HIV-1 M strain began, which they put at around the beginning of the 20th century.
They then compared the same genetic region in the 1959 virus to the 1960 virus and found more evidence that their common ancestor existed around 1900; it took more than 40 years for the genetic divergence between them to evolve, said the researchers.
Worobey said:
"Previous work on HIV sequencing had been done on frozen samples and there are only so many of those samples available. The 1959 and 1960 samples are presently the oldest links to the HIV epidemic."
"From that point on," explained Worobey, "the next oldest sequences that anyone has recovered are from the late 1970s and 1980s, the era when we knew about AIDS. Now for the first time we have been able to compare two relatively ancient HIV strains."
That helped us to calibrate how quickly the virus evolved and make some really robust inferences about when it crossed into humans, how quickly the epidemic grew from that time and what factors allowed the virus to enter and become a successful human pathogen," he added.
Previous research has shown that HIV started in chimps and spread to humans in southeastern Cameroon.
The present day city of Kinshasa, in the Democratic Republic of the Congo, was once Léopoldville, the centre of a Belgian colony that went through rapid urban growth at the turn of the 19th century, as did the neighbouring regions of Central African Republic, Congo, Gabon and Equatorial Guinea. This coincides with the spread of HIV among humans, said Worobey.
The genetic diversity of the virus suggests that a lot of people in the area were already infected with HIV by 1960, and from there it spread to the rest of the world, until 1981 when it came to public awareness.
The technical preparation that went into researching the ancestry of the HIV strains was "extraordinarily painstaking" said Worobey, who described the condition of the RNA and the DNA in the near 50 year old samples as a "really sorry state". In those days, tissue samples were preserved rather indelicately. First they were treated with chemicals, then embedded in paraffin wax, and there was no refrigeration, so these samples will have been at room temperature for decades.
Instead of a "nice, pearl-strand of DNA or RNA, you have a jumbled mass that's all jammed together," said Worobey.
The research team's next step will be to recover more samples, get more DNA and RNA fragments, and try to piece together more of the jigsaw of the history of HIV. This study has done a lot to "snap everything into sharp focus and allows us to understand the timing of these events and the growth of the epidemic," said Worobey.
Drawing a broader conclusion from the research, Worobey said it would seem HIV was encouraged to spread because of changes in human population, and therein lies the clue to its demise, by making changes in human population to reverse the epidemic.
"If HIV has one weak spot, it is that it is a relatively poorly transmitted virus. From better testing and prevention, to wider use of antiretroviral drug therapy, there are a number of ways to reduce transmission and force this virus back into extinction. Our results suggest that there are reasons for such optimism," said Worobey.
"Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960."
Click here for Abstract.
Source: Nature, The University of Arizona .
The finding is published in the 2nd October issue of the journal Nature and was the work of Dr Michael Worobey, an assistant professor of ecology and evolutionary biology at The University of Arizona in Tucson, and colleagues at research centres in Australia, Belgium, France, Democratic Republic of Congo, Denmark and the USA.
Worobey and colleagues suggested that the growing urbanization of colonial Africa around the dawn of the 20th century, characterized by the growth of cities and a rise in high risk behaviours, set the stage for the HIV/AIDS pandemic and created the conditions that allowed the most pervasive strain of HIV, the HIV-1 group M, to spread among humans.
This is some 30 years before previous estimates, which suggested HIV started spreading around 1930.
For the study, Worobey and colleagues spent 8 years screening endless quantities of tissue samples until they discovered a genetic sequence of HIV-1 group M. Dating from 1960, this is the second oldest ever found. It came from a lymph-node tissue biopsy from a woman who lived in present day Kinshasa in the Democratic Republic of the Congo.
The oldest genetic fragment of HIV-1 group M came from a 1959 blood sample from another Kinshasa resident, this time a man.
First the researchers created a range of plausible family trees for the HIV-1 group M, using the 1960 sample and other known HIV-1 genetic sequences. From this it was possible to make time estimates of when the strains diverged from their ancestors, and the rates at which the branches of the trees grew. By projecting backwards the researchers then estimated when the trees took root, that is when the HIV-1 M strain began, which they put at around the beginning of the 20th century.
They then compared the same genetic region in the 1959 virus to the 1960 virus and found more evidence that their common ancestor existed around 1900; it took more than 40 years for the genetic divergence between them to evolve, said the researchers.
Worobey said:
"Previous work on HIV sequencing had been done on frozen samples and there are only so many of those samples available. The 1959 and 1960 samples are presently the oldest links to the HIV epidemic."
"From that point on," explained Worobey, "the next oldest sequences that anyone has recovered are from the late 1970s and 1980s, the era when we knew about AIDS. Now for the first time we have been able to compare two relatively ancient HIV strains."
That helped us to calibrate how quickly the virus evolved and make some really robust inferences about when it crossed into humans, how quickly the epidemic grew from that time and what factors allowed the virus to enter and become a successful human pathogen," he added.
Previous research has shown that HIV started in chimps and spread to humans in southeastern Cameroon.
The present day city of Kinshasa, in the Democratic Republic of the Congo, was once Léopoldville, the centre of a Belgian colony that went through rapid urban growth at the turn of the 19th century, as did the neighbouring regions of Central African Republic, Congo, Gabon and Equatorial Guinea. This coincides with the spread of HIV among humans, said Worobey.
The genetic diversity of the virus suggests that a lot of people in the area were already infected with HIV by 1960, and from there it spread to the rest of the world, until 1981 when it came to public awareness.
The technical preparation that went into researching the ancestry of the HIV strains was "extraordinarily painstaking" said Worobey, who described the condition of the RNA and the DNA in the near 50 year old samples as a "really sorry state". In those days, tissue samples were preserved rather indelicately. First they were treated with chemicals, then embedded in paraffin wax, and there was no refrigeration, so these samples will have been at room temperature for decades.
Instead of a "nice, pearl-strand of DNA or RNA, you have a jumbled mass that's all jammed together," said Worobey.
The research team's next step will be to recover more samples, get more DNA and RNA fragments, and try to piece together more of the jigsaw of the history of HIV. This study has done a lot to "snap everything into sharp focus and allows us to understand the timing of these events and the growth of the epidemic," said Worobey.
Drawing a broader conclusion from the research, Worobey said it would seem HIV was encouraged to spread because of changes in human population, and therein lies the clue to its demise, by making changes in human population to reverse the epidemic.
"If HIV has one weak spot, it is that it is a relatively poorly transmitted virus. From better testing and prevention, to wider use of antiretroviral drug therapy, there are a number of ways to reduce transmission and force this virus back into extinction. Our results suggest that there are reasons for such optimism," said Worobey.
"Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960."
Click here for Abstract.
Source: Nature, The University of Arizona .
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