Scientists have cured living animals of HIV using CRISPR gene-editing, a new study claims.

The virus remains elusive due to the its ability to hide away in latent reservoirs.

But now, in new research published this week, US scientists showed they could completely remove HIV DNA from human cells implanted into mice – preventing further infection.

It is the first time scientists have ever achieved complete elimination in animal models – paving the way to a human clinical trial.

Most exciting, the study by at the Lewis Katz School of Medicine at Temple University and the University of Pittsburgh involved a ‘humanized’ model in which mice were transplanted with human immune cells and infected with the virus.

The new work, led by Dr Wenhui Hu at LKSOM, builds on the same team’s previous research, in which they managed to delete HIV-1 from the genome of most tissues.

A year later, they have been able to eliminate the virus from every tissue.

‘Our new study is more comprehensive,’ Dr. Hu said.

‘We confirmed the data from our previous work and have improved the efficiency of our gene editing strategy. We also show that the strategy is effective in two additional mouse models, one representing acute infection in mouse cells and the other representing chronic, or latent, infection in human cells.’

The team tested three groups of mice.

In the first, they infected mice with HIV-1.

In the second, they infected mice with a severe case of EcoHIV (the mouse equivalent of human HIV-1).

The third used a ‘humanized’ mouse model, engrafted with human immune cells, that was infected with HIV-1.

Treating the first group, they managed to genetically inactivate HIV-1, reducing the RNA expression of viral genes by up to 95 percent, confirming their earlier findings.

The second group has an added challenge: the virus is more prone to vociferously spread and multiply.

‘During acute infection, HIV actively replicates,’ Dr Khalili explained.

‘With EcoHIV mice, we were able to investigate the ability of the CRISPR/Cas9 strategy to block viral replication and potentially prevent systemic infection.’