MuLV found inserted into MITOCHONDRIAL DNA

[Gerwyn]

This article is direct evidence of MuLV integrating into Mitochondrial DNA. XMRV is a MuLV class virus . The second paper shows how integrated MuLV directly damages Mitochondrial DNA by altering the bases so they dont make sense anymore to the repair enzymes. Changing just three bases can reduce the energy output of a mitochondria by 60%
cience 13 February 1976:
Vol. 191. no. 4227, pp. 569 - 571
DOI: 10.1126/science.1251192

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Articles
Science, Vol 191, Issue 4227, 569-571
Copyright 1976 by American Association for the Advancement of Science

articles
Proviral DNA of Moloney leukemia virus: purification and visualization
AM Gianni, Hutton JR, D Smotkin, and RA Weinberg

Closed-circular proviral DNA of Moloney leukemia virus has been purified from a 10(7) excess of cellular and mitochondrial DNA. The DNA can be visualized in the electron microscope and has the contour length of a molecule with a moleculecular weight of about 5.5 + 10(6). Electron microscopic observation of a hybrid between viral RNA and this circular DNA confirms the viral origin of this molecule.


mitochondrial Mulv viral damage, in J. Neurosci. Search
The Journal of Neuroscience, March 12, 2008, 28(11):2827-2836; doi:10.1523/JN MuLv damage of Mitochondria

Neurobiology of Disease
The Mitochondrial Protease AFG3L2 Is Essential for Axonal Development

Francesca Maltecca,1 * Asadollah Aghaie,3 * David G. Schroeder,4 Laura Cassina,1 Benjamin A. Taylor,4 Sandra J. Phillips,4 Mariachiara Malaguti,2 Stefano Previtali,2 Jean-Louis Gunet,3 Angelo Quattrini,2 Gregory A. Cox,4 and Giorgio Casari1,5

1Human Molecular Genetics Unit, and 2Neuropathology Unit and Istituto di Neurologia Sperimentale, San Raffaele Scientific Institute, 20132 Milan, Italy, 3Departement de Biologie du Developpement, Institut Pasteur, 75724 Paris Cedex 15, France, 4The Jackson Laboratory, Bar Harbor, Maine 04609, and 5Vita-Salute San Raffaele University, School of Medicine, 20132 Milan, Italy


Abstract
Top
Abstract
Introduction


The mitochondrial metalloprotease AFG3L2 assembles with the homologous protein paraplegin to form a supracomplex in charge of the essential protein quality control within mitochondria. Mutations of paraplegin cause a specific axonal degeneration of the upper motoneuron and, therefore, hereditary spastic paraplegia. Here we present two Afg3l2 murine models: a newly developed null and a spontaneous mutant that we found carrier of a missense mutation. Contrasting with the mild and late onset axonal degeneration of paraplegin-deficient mouse, Afg3l2 models display a marked impairment of axonal development with delayed myelination and poor axonal radial growth leading to lethality at P16. The increased severity of the Afg3l2 mutants is explained by two main molecular features that differentiate AFG3L2 from paraplegin: its higher neuronal expression and its versatile ability to support both hetero-oligomerization and homo-oligomerization. Our data assign to AFG3L2 a crucial role by linking mitochondrial metabolism and axonal development. Moreover, we propose AFG3L2 as an excellent candidate for motoneuron and cerebellar diseases with early onset unknown etiology.

 

[Hope123]

This is interesting Gerwyn and perhaps should be moved over to the XMRV stuff since it is related and might be missed in this subforum.

There are very few family studies that I know of but one I know of (Underhill 2006) found that of people with CFS who had a relatives with CFS, it was just as likely that their paternal side had it as their maternal side. This is just one study and the confirmation of CFS was not as tight as the authors would have liked. Studying families with CFS in conjunction with XMRV would be enlightening.


(Also, in another post wiciarci posted an article about how pro-inflammatory cytokines can affect mitochrondrial function.)

 

[Gerwyn]

This is interesting Gerwyn and perhaps should be moved over to the XMRV stuff since it is related and might be missed in this subforum.

There are very few family studies that I know of but one I know of (Underhill 2006) found that of people with CFS who had a relatives with CFS, it was just as likely that their paternal side had it as their maternal side. This is just one study and the confirmation of CFS was not as tight as the authors would have liked. Studying families with CFS in conjunction with XMRV would be enlightening.


(Also, in another post wiciarci posted an article about how pro-inflammatory cytokines can affect mitochrondrial function.)

i dont know how to move it but you are welcome to

 

[Hope123]

I think the admins have to move it? Admins, help!

 

[spindrift]

Great find! Thanks for posting.