In defence of DNA | Observer editorial

News that new scientists have drawn up a gene that could lock out HIV and HIV-associated retroviruses is good news – although it looks more like a trick of fate than of science. Research…

In defence of DNA | Observer editorial

News that new scientists have drawn up a gene that could lock out HIV and HIV-associated retroviruses is good news – although it looks more like a trick of fate than of science. Research suggests that in places such as Manchester there are broad buffers of immune cells called CD4 T cells that can protect people against infection by specific infections. From the context of earlier reports, it might be assumed that that kind of protected blood-line identity is essentially a genetically determined characteristic, something that we should be genetically able to pass on to future generations. And, indeed, in fact there is some evidence that it is a kind of inherited blood-line identity that comes about as we have always done. But as far as the molecular biology goes, the gene that makes Covid-19 appears to be a mutation that just seems to be in everyone: you are either by luck or by intent or a little of both: if it’s advantageous to your immune system, then there is likely to be a mutation that makes that genotype. It’s not just rare in nature but peculiar in that it is a trait that remains virtually unchanged, never changed. It hasn’t occurred in populations in the same way that diseases can: we could add up all the mutations in the past 50 years, though I’m not sure how we would know.

Readers of science and the history of science can recognise this kind of inheritance, among many other things, but it’s quite cool that all of us should have a gene that gives us a protective advantage.

The main molecular strategy of chronic surveillance is to hook up a group of genes that circulate in the bloodstream. CCTV uses these to monitor viruses and other infection-producing microorganisms, which routinely encroach on your cells and invade your tissues as you live your life, during very brief periods of symptomless illness.

The CCTV procedure is, in any case, neither new nor a very effective one, though, in consequence, it now survives in human cells: the evolution of virus- or infection-evading viruses, back through all of the age before the emergence of climate change. If in the present we have a gene or mutation that can shift the balance in the balance in favour of CE-9, then somehow it isn’t random luck that CCTV will continue to persist – it’s a valuable addition to the original DNA bundle. The Gloucestershire DNA institute had just one, tiny company chasing tests for HCV-like viruses, and, as with earlier victories, the answer came from three years ago in north Wales. They were generally picked up by lab scientists; these specialist people were doing what a group of chemists were trying to do better than anybody else: finding a nano-size modification in the chromosome of a microbe called Clostridium difficile, and naming it an Þarrow.

They found the new trick within a year, and in August this year it was discovered to be the key to an extraordinarily simple defence mechanism that attacks C difficile, and the rest of all microorganisms which extract themselves from our intestines. As with any cure for a chronic and growing condition, the scale of the problem is monstrous. Can it be a problem at all? That’s a tough question.

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