A Cure For Aids?

Image Credit: AIDs.gov

Scientists at the Queensland Institute of Medical Research have turned HIV on itself suggesting the possibility of a cure, or at least a management system, for the AIDS virus. Scientists have stipulated that this is not a cure, but rather that it will keep the virus latent and not allow it to progress into the AIDS virus.

The exact text of the findings by Ann Apolloni, Haran Sivakumaran, Mr. Min-Husan Lin, Dr. Dongsheng Li, Dr. Michael H Kershaw, and Dr. David Harrich reads as follows: 

Here we show potent inhibition of HIV-1 replication in a human T cell line and primary human CD4+ cells by expressing a single antiviral protein. Nullbasic is a mutant form of the HIV-1 Tat protein that was previously shown to strongly inhibit HIV-1 replication in non-hematopoietic cell lines by targeting three steps of HIV-1 replication: reverse transcription, transport of viral mRNA and transactivation of HIV-1 gene expression. Here we investigated gene delivery of Nullbasic using lentiviral and retroviral vectors. While Nullbasic could be delivered by lentiviral vectors to target cells, transduction efficiencies were sharply reduced primarily due to negative effects on reverse transcription mediated by Nullbasic. However Nullbasic did not inhibit transduction of HEK293T cells by an MLV-based retroviral vector. Therefore, MLV-based VLPs were used to transduce and express Nullbasic-EGFP or EGFP in Jurkat cells, a human leukaemia T cell line, and Nullbasic-ZsGreen1 or ZsGreen1 in primary human CD4+ cells. HIV-1 replication kinetics was similar in parental Jurkat and Jurkat-EGFP cells, but was strongly attenuated in Jurkat-Nullbasic-EGFP cells. Similarly, virus replication in primary CD4+ cells expressing a Nullbasic-ZsGreen1 fusion protein was inhibited by approximately 8 to 10-fold. These experiments demonstrate the potential of Nullbasic, which has unique inhibitory activity, as an antiviral agent against HIV-1 infection.

The success is due to a mutant Tat protein according to the publication. You can read their full release here.