Researchers retract key finding in HIV long-term survivors study
January 24 2004 1:00 AM ET
David Ho of the Aaron Diamond AIDS Research Center and colleagues have retracted a key finding of a study of HIV long-term survivors that suggested a particular family of proteins blocked HIV replication, the San Francisco Chronicle reports. The researchers published a study in the September 2002 edition of the journal Science that said they had identified a family of three proteins called alpha-defensins present in the CD8 cells of HIV nonprogressors that blocked viral replication. Researchers had previously observed a protective antiviral factor associated with CD8 cells but hadn't been able to isolate the compound creating the added protection. Ho's team performed a series of procedures to deactivate alpha-defensins cultured from the cells, which eliminated the antiviral effect. They concluded that the compounds in the CD8 cells were the mystery chemicals providing a defense against the virus.
But in a letter titled "Retraction of an Interpretation" published in the January 23 edition of Science, Ho and his team write that the antiviral factor they had identified did not come from the CD8 cells of the study subjects. Instead, the factor likely came from a protein produced by a mixture of blood cells routinely used in the laboratory to make CD8 cells mature. The retraction came after two other research projects were unable to find alpha-defensins in CD8 cells. Ho and his team continue to back the remainder of the study, including the fact that alpha-defensins have a role in HIV suppression, noting that only their conclusion of where the compounds came from was incorrect.
Researchers have long been working to determine why between 1% and 5% of people infected with HIV can live untreated with the disease and never develop AIDS. Most scientists believe there is a compound or compounds in the bodies of these individuals that work to slow HIV replication so that the virus cannot severely damage the immune system, but research to date has been unable to identify the precise cause of the antiviral effect.
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