Addiction could stem from ancient retrovirus, study suggests

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An ancient retrovirus that predates modern humans may explain why people suffer from addiction, scientists have said.

Researchers studied drug users in two cities and found they were up to about three times more likely than the general population to have remnants of the HK2 virus within a particular gene in their DNA.

The virus dates back at least to Neanderthals and is present in the RASGRF2 gene — which a researcher called the “pleasure gene” because it increases the activity of dopamine in the brain — in about 5% to 10% of people.

That proportion of the population could therefore be more disposed to addictive behavior, the scientists said.

The team, from the universities of Oxford and Athens, found the virus in 34% of drug users tested in Glasgow, Scotland, compared to 9.5% of the local population, and in 14% of Greek patients, compared to 6% of that country’s population.

Retroviruses are viruses that have the capacity to inject their DNA into the genome of the host.

This is the third time they have been strongly linked with a harmful effect in humans, after the discoveries of the human immunodeficiency virus (HIV) and the human T-lymphotropic virus (HTLV), according to the researchers.

HK2 is present in all humans, but appears in the RASGRF2 gene in up to one in 10 people. The study suggests that these people “could be prone to any sort of addictive behavior, even beneficial in some sense,” Gkikas Magiorkinis of the University of Athens told CNN.

The same gene was linked to binge-drinking in an earlier study in 2012.

And the researchers said that studying the rarely analyzed, “dark” part of the genome that they looked at “will unlock more genomic secrets.”

“Human endogenous retroviruses comprise 8% of the genome and have not been linked with human disease until now,” Magiorkinis said.

“I believe that a significant part of this unexplained disease diversity will be understood by studying this difficult-to-understand ‘dark’ genome,” he added.

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