Tuesday, 28 August 2012

Recruiting AIDS to Combat Cancer


Recruiting AIDS to Combat Cancer


Using the AIDS Virus to fight Cancer? Yes, that’s right; as this may appear as a strange medical endevor to get your head around, recent genetic research conducted by a CRNS team at the RNA Architecture and Reactivity laboratory has found a certain mutant protein in HIV that posses incredible replication properties which can be used with aniticancer drugs to fight cancer. The uniqueness of this newly developed treatment is said to be able to treat patents with toxic drug doses up to 300 times lower than without the addition of the HIV virus.



The human immunodeficiency virus (HIV-1), which causes AIDS, uses human cells to replicate itself by inserting its genetic information into the host cell. What has scientists interested is that HIV mutates constantly and spreads from cell to cell at a fast rate. This enables the virus to adapt to avoid many treatments that are used against the virus today.



Although, why would anyone want to risk contracting the HIV virus when they are receiving treatment for a cancer tumour? This is not apparent; effects of the retrovirus are rechanneled for therapeutic applications, indeed the treatment of cancer. Scientists have improved the HIV genome by adding a gene for deoxycytidine kinase (dCK), which is a human protein that’s involved in the activation of drugs inside cells (PLoS Genetics, 2012). Through the manipulation of the HIV genome, the CNRS team has ran tests of over 80 mutant proteins and tested them with anticancer drugs on tumour cells. Out of the 80 proteins tested the team found a deoxycytidine kinase variant that is more effective than a protein in which isn’t mutated. This protein showed great effectiveness in inducing death to cancer cells (PLoS Genetics, 2012).

CNRS scientists have labelled this process as ‘The Retrovolution system’. In this system the replication genetics of HIV-1 are utilised to run the evolution of cellular genes. This continuously occurs by successive infection cycles with HIV-1 viral vectors, which are a tool that molecular biologists use to deliver genetic material into target cells. These viral vectors contain a target sequence of the evolved genetic material inserted into their RNA.  Therefore French scientists wanted to mutate many variants of the deoxycytidine kinase (dCK) gene; while isolating an enzyme that was able to increase the sensitivity to therapeutic drugs, such as anticancer compounds known as deoxycytidine analogues (PLoS Genetics, 2012). In a simpler form, after the HIV ridden drugs ‘enters the target cell, the viral polymerase converts the viral genomic RNA, throughout an error-prone process that generates genetic diversity, into double-stranded DNA, which is then integrated in the genome of the cell’ (PLoS Genetics, 2012).


Many studies still need to be conducted with this genetic discovery before it can be passed as a viable cancer treatment since some properties of the deoxycytidine kinase aren’t predictable on a rational basis. However, reducing patent doeses of anticancer medicines would provide great help in the overall effectiveness of the treatment, since these drugs produce negative side effects. Thus, using a deadly virus for therapeutic treatment is likely to lead into great medical advances in the future.

                                    References 

Paola Rossolillo, Flore Winter, Etienne Simon-Loriere, Sarah Gallois-Montbrun, Matteo Negroni. Retrovolution: HIV–Driven Evolution of Cellular Genes and Improvement of Anticancer Drug Activation. PLoS Genetics, 2012; 8 (8): e1002904 DOI:

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002904?imageURI=info:doi/10.1371/journal.pgen.1002904.g001

HIV picture: http://24.media.tumblr.com/tumblr_lsh0rbzaUV1qc6n7jo1_500.png
Lab Picture : http://www.medgenetics.ru/english/Laboratories/Evolutionary_Genetics/

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