Dating the origin of the ccr5
To infect immune cells, HIV must first bind to chemokine receptors.
Researchers discovered in 1996 that people who had a naturally occurring mutation in their genes for one of these, CCR5, were strongly protected from developing AIDS—or even becoming infected in the first place—and suffered no ill effects from lacking the receptor.
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Background: The CCR5 is a chemokine receptor that serves as a co-receptor for HIV-1 attachment and entry to T lymphocytes.
To avoid confusion, we have named this disease haemorrhagic plague.
in 1600 (fig 1, line A); extrapolation of the line shows that the overall mortality in the Black Death was around 40%.
The number of places in Europe reporting plague epidemics each year is shown in fig 2 Line A (dashed line, solid circles): estimates of the population of Europe (ordinate, log scale) from 1000 to 1800.19 The single epidemic of the Black Death caused 40% mortality.
deletion; the average frequency of this allele is 10% in European populations.
A mathematical model based on the changing demography of Europe from 1000 to 1800 AD demonstrates how plague epidemics, 1347 to 1670, could have provided the selection pressure that raised the frequency of the mutation to the level seen today.
Sangamo specializes in developing enzymes called zinc finger nucleases that can bind to genes, clip their DNA, and repair mutations (, 23 December 2005, p. But for the HIV gene therapy, they’ve created a nuclease to specifically disrupt the CCR5 gene in the same manner as the natural mutation.
In the new trial, researchers will put the gene for this zinc finger nuclease into an adenovirus vector, transduce harvested CD4 A reader alerted us to the fact that at least one drawback associated with this mutation has been found.