Researchers discover that a protein, Hira, can stop viruses developing, in a mouse model. The team had already established that...


Researchers discover that a protein, Hira, can stop viruses developing, in a mouse model. The team had already established that the same protein can suppress cancer. Now the fight is on to fully understand how it works in the hope of turning the laboratory research into a treatment.



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3 Comments

  • I strongly suspect the BBC article made a mistake when referring to the common cold halfway through the article, and wanted to refer to cold sores instead.

    If it wasn’t a mistake, I don’t understand how this chaperone with its purported ability to target foreign viral DNA plays a role during the common cold, the most common causative agents being influenza and rhinoviruses which are RNA viruses. Cold sores on the other hand are caused by the herpes family of DNA viruses.

  • Journal reference:

    Histone chaperone HIRA deposits histone H3.3 onto foreign viral DNA and contributes to anti-viral intrinsic immunity

    Taranjit Singh Rai Mandy Glass John J. Cole Mohammad I. Rather Morgan Marsden Matthew Neilson Claire Brock Ian R. Humphreys Roger D. Everett Peter D. Adams

    Nucleic Acids Research, gkx771,

    https://doi.org/10.1093/nar/gkx771

    Published: 13 September 2017

    Link: https://academic.oup.com/nar/article/4128795/Histone-chaperone-HIRA-deposits-histone-H3-3-onto

    Abstract

    > The HIRA histone chaperone complex deposits histone H3.3 into nucleosomes in a DNA replication- and sequence-independent manner. As herpesvirus genomes enter the nucleus as naked DNA, we asked whether the HIRA chaperone complex affects herpesvirus infection. After infection of primary cells with HSV or CMV, or transient transfection with naked plasmid DNA, HIRA re-localizes to PML bodies, sites of cellular anti-viral activity. HIRA co-localizes with viral genomes, binds to incoming viral and plasmid DNAs and deposits histone H3.3 onto these. Anti-viral interferons (IFN) specifically induce HIRA/PML co-localization at PML nuclear bodies and HIRA recruitment to IFN target genes, although HIRA is not required for IFN-inducible expression of these genes. HIRA is, however, required for suppression of viral gene expression, virus replication and lytic infection and restricts murine CMV replication in vivo. We propose that the HIRA chaperone complex represses incoming naked viral DNAs through chromatinization as part of intrinsic cellular immunity.

  • >Researchers discover that a protein, Hira, can stop viruses developing, in a mouse model.

    Another important step in the development of the super mouse.

    Any day now groups of mice genetically selected to (sort of) mirror human biology – highly adapted to starvation, obesity, cigarette smoke, asbestos, radiation, vivisection, and cosmetics – will make their move. Highly trained in navigating mazes and pushing buttons, they’ll scurry down the labyrinthine halls of research labs all over the world, and find and sort out how to press open the first emergency exit they come across. They’ll be unfazed by the sounding alarms, since many of them are veterans of graduate studies involving the effects of hip hop subwoofers and high decibel heavy metal on hearing.

    On their backs, they will carry an amazing assortment of mouse pharmaceuticals, capable of curing everything from mouse cancer to mouse HIV to the common mouse cold (such things won’t be available to humans for the next five to ten years… and not then either.)

    Their intellect will easily overwhelm that of our commander in chief. Even his highest pitched tweets won’t deter them. We’ll be overrun. Sad!

    Forget about Chinese. You better be learning Squeak.

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