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Researchers Debunk Theory That Bubonic Plague Mutation Confers HIV Resistance

NEW YORK, Feb. 16 (GenomeWeb News) -  Researchers at the Scripps Research Institute have uncovered "strong evidence" that debunks the theory that Caucasians of Northern European descent - specifically, descendents of people who had been resistant to bubonic plague - may carry a gene mutation that protects against HIV.

 

The hypothesis under question suggests that the mutation in question, the C-C chemokine receptor 5-32, or CCR5-32, is the same mutation that made individuals resistant to bubonic plague in the late Middle Ages.

 

Using mice infected with Yersinia pestis, the bacteria believed to have caused bubonic plague, Donald Mosier, a professor of immunology at Scripps Research Institute, suggested that the mutation "does not protect" against the plague in mice today, and that "it is unlikely to have offered any protection" against the plague in humans during the Middle Ages. Therefore, it is unlikely to protect against HIV today.

 

It is widely known that the CCR5 gene encodes the production of the human receptor protein by the same name. In turn, the protein, a seven trans-membrane-spanning protein comprising 332 amino acids, is found on the cell membranes of human CD4+ T- helper cells.

 

The CCR5 32 mutation, which represents a deletion of 32 bases from the CCR5 gene, was first identified eight years ago in people who appeared to be protected against HIV despite multiple "high-risk exposures" to the virus, the authors wrote.

 

Every one of the individuals had the 32-base pair mutation in their CCR5 genes, leaving them with CD4+ T cells "with no CCR5 receptors, conferring resistance to HIV infection." (The authors wrote that subsequent research showed that individuals who were heterozygous for the mutation had "lower CCR5 expression levels, less cell-to-cell infection, and brighter clinical prognoses than those who were homozygous negative.)

 

To test the so-called HIV/plague hypothesis, Mosier and colleagues infected mice both with and without the CCR5 32 mutation with an attenuated, non-transmissible form of Y. pestis. They found "no difference in susceptibility between the two groups," Mosier wrote in his team's findings, which appear as a brief communication to be published this week in the journal Nature.

 

However, he said, "the possibility still exists ... that the CCR5 32 mutation arose due to the influence of some other disease that was prevalent in the Middle Ages, such as smallpox." He said he intends to study this potential link.

 

His team's research appears as a brief communication to be published this week in the journal Nature.

 

 

This article first appeared in  SNPtech Pharmacogenomics Reporter.