Judy Mikovits heeft onlangs een presentatie verzorgd over XMRV-opsporingsmethoden
in het kader van een lezingenserie over pathogenen (ziekteverwekkers) in de bloedvoorraad,
georganiseerd door The New York Academy of Sciences (29 maart 2011).
Relevant is vooral dat de variatie van "XMRV" groter blijkt te zijn dan gedacht.
Een samenvatting van de presentatie van Mikovits is hieronder weergegeven.
Onderaan deze pagina kunt U de video-opname van de presentatie (in drie delen) bekijken.
Disease Associations of XMRV and MLV-Related Viruses
Judy A. Mikovits, PhD,
Whittemore Peterson Institute for Neuro-Immune Disease
A new human retrovirus first associated with QQ variant RNaseL
a gene in the hereditary prostate cancer gene locus,
in prostate cancer in 2006.
Detection of integration sites in unmanipulated prostate tissue;
demonstration of neutralizing antibody and
in situ hybridization for XMRV,
supports XMRV as a human retroviral infection associated with prostate cancer.
Although in the absence of direct sequencing
it cannot be rule out the reactivity can be to related MLV viruses.
In 2009 using
a classical virology approach of viral isolation and transmission,
electron micropscopy, serology and PCR,
Lombardi et al demonstrated
the first isolation of XMRV
from blood from patients with chronic fatigue syndrome (CFS)
predominately from the west coast of the United States.
In 2010,
Lo et al. extended these studies
by detecting nucleic acids of MLV-related variants
in the peripheral blood mononuclear cells of CFS
from the northeastern United States
suggesting additional strains capable of infecting humans exist.
In a study of 300 CFS patients, 13 developed lymphoproliferative disorders.
Of those tested,
11/11 were positive for XMRV and 9/9 positive for clonalTCR gamma rearrangements.
Spontaneous development of four immortalized B cells lines
occurred during culture of cells from CFS patients.
Three developed from B cells
isolated from the peripheral blood
(two of whom had B cell lymphoma) and
one from a bone marrow biopsy.
The B cell lines have a mature CD20+, CD23+ phenotype and produce infectious XMRV.
Virus production occurred
despite extensive hypermutation of the proviruses in these cells by APOBEC3G.
Therefore,
XMRV infection may accelerate the development of B cell malignancies
by either indirect chronic stimulation of the immune system and/or by direct infection
of the B-cell lineage.
Since viral load in peripheral blood is low,
these data suggest that B cells in tissues
such as spleen and lymph nodes
could be an in vivo reservoir for XMRV.
We have also identified
an inflammatory cytokine and chemokine signature
that distinguishes XMRV infected CFS patients from healthy controls
with 94% sensitivity and specificity.
Monitoring immune dysfunction
affords the opportunity
to begin to understand
the pathogenesis of XMRVs.
In addition to these data,
recent advances in developing tests for detection and characterization of XMRVvariants
will be also be discussed
http://www.nyas.org/Events/Detail.aspx?cid=0918b8d8-9a46-4334-b194-23ade9c2a7aa
Strategies for Detection of XMRV in Blood.
Judy Mikovits
Pathogens in the blood supply.
Emerging Infectious Diseases & Microbiology Discussion Group.
New York Academy of Sciences.
March 29th, 2011.
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deel 3: vragen en antwoorden
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