A deletion in the CCR5 gene has been
shown to protect humans against HIV infection (and also against the plague).
This is because the CCR5 protein, a chemokine receptor, is a co-receptor along
with CD4 antigen for HIV entry into a cell. This was discovered because certain
chemokines are able to block the binding of HIV to the cell surface. If the CCR5
protein is missing, the cell cannot be infected. It has therefore been proposed
that molecules that block interaction of HIV with the CCR5 protein might prove
useful in inhibiting infection of human cells. Several CCR5-blocking drugs
have been tested that might have this mode of action. However, in 2006, Patrick
Murphy and his colleagues showed that a genetically-engineered mouse that lacks
CCR5 mouse is very sensitive to infection by West Nile Virus. In fact, while
most wild type mice survived a West Nile Virus infection, the virus was usually
fatal to the CCR5-deficient mice. This seemed to be because CCR5 is essential
for the entry of immune cells into the brain where they protected against the
encephalitis that occurs after West Nile Virus infection. Without CCR5, no such
protection occurs. When the researchers looked at the correlation between West
Nile Virus infection in the population and the occurrence of the homozygous CCR5
mutation, they found that a much larger proportion of West Nile Virus-infected
people had the homozygous CCR5 mutation than the population as a whole. It would
thus seem that if CCR5 blocking drugs are used in patients, they should be
advised to avoid situations that might lead to West Nile Virus infection such as
contact with mosquitoes.