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Referat fra XMRV-seminar i Spania 9. desember

Hentet fra Xand Xmrvs Facebookside:

«This Thursday, December 9, we had an event in Barcelona, in which the Spanish XMRV researchers explained their findings on XMRV in the Spanish CFS/ME population. This is a summary of what they said:

XMRV and CFS. WHAT SHOULD WE DO??

Controversy (scientific and social) has accompanied the retrovirus XMRV since it was identified in patients with chronic fatigue syndrome (CFS), a year ago. The disparity of results obtained by different laboratories and the scarce knowledge of this virus replication mechanism, have greatly limited scientific advances and therefore, their direct applicability to people affected. We need to reflect on the current situation so as to be able to define the steps that have to be taken by the various groups involved in the research of XMRV , whether they are health authorities, medical and research professionals, and of course, the people affected by CFS.

In the current situation, we should highlight these points:

1.- The lack of reliable detection methods for XMRV, that can be reproduced among different labs.

2.- The possibility that pollution is responsible for sporadic detection of XMRV in humans.

3.- The findings of new MLV-related virus in patients with CFS (polytrophic viruses).

4.- Indentify XMRV sensibility to different antiretrovirals.

Considering the evaluation of our data set in the context of the knowledge we have of other retrovirus, we can point out:

1.- Patients with CFS have no quantitative abnormalities of their lymphocytes, though they show alterations in B cells (antibody producers), and in the NK and T cells (responsible for the destruction of infected cells). The functional implications of these alterations remain to be defined.

2.- XMRV can infect human cells in vitro, but we do not know its viral persistence mechanism (for new infections or survival of infected cells). These data are vital to determine the potential efficiency of antiretroviral treatments.

3.- XMRV sequences can be found in patients with CFS but also in healthy donors or HIV+ patients. The copy numbers appear to be very low, and their pathogenic potential is unknown.

At this time we are facing a potential health problem of unknown magnitude. It is therefore necessary to provide different scenarios for the future (both positive and negative) and to maintain preventive measures, while waiting for contrasted results by different labs giving us information about the extent of infection by XMRV and its role in CFS and other pathologies.

Dr. Julià Blanco

Irsi Caixa Foundation»

Les det HER

 

3 responses to “Referat fra XMRV-seminar i Spania 9. desember

  1. Tone 10.12.10, kl. 10:08

    Slutten er bra. «At this time we are facing a potential health problem of unknown magnitude. It is therefore necessary to provide different scenarios for the future (both positive and negative) and to maintain preventive measures, while waiting for contrasted results by different labs giving us information about the extent of infection by XMRV and its role in CFS and other pathologies».
    Tipper vi hører mer fra dem innen få måneder. Dette er bra, selv om noen kanskje ventet noe mer slagkraftig, men snøballer ruller sent før de blir store….

  2. mhj 10.12.10, kl. 11:05

    Denne forskningsgruppen fra Spania hadde også poster presentasjon på XMRV Workshopen september 2010. Her er abstraktet fra denne:

    Abstract: P_18

    Chronic Fatigue syndrome/ neuro immune
    diseases

    Altered B, T and NK cell
    phenotype in chronic fatigue
    syndrome (CFS) individuals.

    M. Curriu1, M. Massanella1, J. Carrillo1, J. Puig2, J. Rigau1, B.
    Clotet1, C. Cabrera1, J. Blanco1

    1Fundació IrsiCaixa, Retrovirology laboratory, Badalona,
    Spain; 2Hospital Universitari Germans Trias i Pujol, Fundació
    Lluita contra la SIDA, Badalona, Spain

    Background: Several studies have reported
    controversial results on the dysfunction of the
    immune system in Chronic Fatigue Syndrome
    (CFS) affected individuals. Since the recently
    described Xenotropic murine leukemia virus-
    related virus (XMRV) can infect cells from the
    immune system (B, T or NK cells), we designed
    different panels of antibodies to deeply
    characterize the phenotype of B, T and NK
    lymphocytes populations in patients with CFS.

    Material and methods: We obtained blood
    samples from 12 individuals affected from CFS
    (fulfilling both Fukuda and Canadian criteria) and
    15 healthy donors (HD). B, T and NK cell
    populations were phenotyped in fresh blood
    samples and analyzed by multicolour flow
    cytometry. Fresh PBMCs were obtained to
    characterize spontaneous ex vivo apoptosis and
    NK cytotoxic activity against EGFP-K562 cells,
    both analyzed by flow cytometry.

    Results: No changes in the percentage or
    absolute numbers were observed in principal
    populations of B (CD19+), T (CD3+, CD3+CD4+,
    CD3+CD8+) or NK (CD56+ CD16+) cells.
    However, significant differences were observed
    in various subsets of these populations.

    B lymphocytes from CFS individuals showed a
    decrease in marginal-zone marker CD1c,
    especially in memory IgG population. The
    percentage of memory IgG+ cells, effector
    memory CD38high IgG+ cells and plasmatic B
    cells (CD38high/CD27high) was also reduced in
    CFS individuals. In contrast, CFS individuals
    showed an increase in transitional B cells
    (IgD+CD38highCD5+CD10+), which present
    lower spontaneous ex-vivo apoptosis.

    T-cells from CFS individuals presented
    increased CD25 levels mainly within CD8+
    population. Proliferation marker Ki67 was
    significantly diminished in CFS CD4 T-cells and
    a trend was also observed in CD8 T-cells. In
    addition, individuals with CFS showed increased
    CD5 levels within CD8 T-cells which could
    suggest an anergic state. No signs of altered
    senescence (CD57+ T cells) or activation
    (CD38+, HLA-DR+ or double positive cells) were
    observed in CD4 or CD8 subsets, although, CD8
    T cells from CFS individuals showed higher
    expression of FAS and PD-1 and a slightly
    higher spontaneous ex-vivo apoptosis.

    NK cells showed a significant decrease in
    CD57+ expression and expressed higher levels
    of CD69 and activating NK Cytotoxic Receptors
    (NCR) NKp30, NKp44 and NKp46.
    Nevertheless, this altered phenotype did not
    impact function, as we did not observe
    differences in NK cytotoxic activity in CFS
    patients compared with HD.

    Conclusions: CFS patients showed qualitative
    but not quantitative alterations in all major
    immune cell types. B cells presented a
    phenotype partially similar to some autoimmune
    disorders or viral infections. Interestingly, an
    anergic phenotype observed in T cells from CFS
    individuals could be related with an impaired
    control of viral infections and could explain the
    lack of increased activation and senescence
    observed in our patients. Finally, altered NK
    phenotype did not seem to significantly modify
    cytotoxic activity. On the whole, the results
    suggest a global immune dysfunction with an

    unknown aetiology as potential contributor to the
    mechanism of CFS.

    No conflict of interest

    ———————-

    Regner med at dette er bakgrunnen for presentasjonen i dette seminaret i Spania. kan ikke se at det fremkommer noe tall på hvor stor andel av befolkningen som er testet positivt, men det er mulig at de sparer tallene til senere publikasjoner.

    ja de setter spørsmålstegn med det sentrale her…. enkle pålitelige tester som allmenne labs kan bruke, men som noen andre presiserte i en kommentar over….. en vet ikke omfanget av retrovirus-spredning og konsekvens.

    😉 ellers må jeg si at *humre* litt mer romatisk å lese ting på spansk… da tenker vi bare palmer og bading og sol….. ikke kan æ spansk engang….

    😀 Kan jo ikke annet å si at det e bare helt enestående at forskere verden over tar fatt i dette og at forskning er intensivert og satt i prioritet *tommel opp folks*

    hmmm…. kan ikke se at det er vesentlige nytt fra abstraktet fra september, men det kan tenkes at de sitter inne med mer dybde i resultatene sine…. vi får vente å se….!!!!

    😉 trur jeg har en liten mini-oversettelse av denne…… skal skjekke…..

  3. mhj 10.12.10, kl. 11:13

    Jepp mini-oversettelsen med noen forklaringer???:

    P_18, s. 35: Endret B, T og NK celle fenotyper i CFS individer. Denne undersøkelsen er gjort av et retrovirus-forsker team i Spania.

    Det ble tatt blod fra 12 personer med CFS og 15 friske donorer (HD). Immunofenotypingen ac lympfocytter ble utført av flow cytometri.
    Resultaene viste: Ingen endring i den prosentvise eller det absolutte antallet av B-celler (CD19+), T-celler, T-hjelper og T-cyt/reg (CD3+, CD3+CD4+, CD3+CD8+) eller NK-celler (CD56+ CD16+).

    Men det ble funnet signifikante forskjeller i ulike subsets (CD variasjoner) innenfor disse cellene typene.
    – B-lymfocytter viste en nedgang i: CD1c, og særlig i «hukommelses» B-celler i IgG (memory IgG). Den prosentvise av memory IgG+ celler, effector memory CD38high IgG+ celler og plasmatis B celler (CD38high/CD27high) var også redusert.

    – T-celler viste en økning av CD25 nivåer hovedsaklig i CD8+ populasjonen. Ki67 som er en markør for spredning var signifikant redusert i CD4 T-celler og denne tendensen ble også observert for CD8 T-celler. I tilleg ble det vist en økning ac CD5 i CD8 T-celle populasjonen, noe som kan indikere en «anergic state», som betyr at T-cellene mister eller feiler immunresponsen til T-celler spesifikke antigen. Det ble ikke vist noen tegn til endret av CD57+ T-celler eller aktivering av CD38+, HLA-DR+ eller doble positive celler i CD4 eller CD8 subsets, men CD8 T-celler viste et høyere uttrykk av FAS og PD-1 og en svak høyere spontan celledød.

    – NK-celler viste en signifikant nedgang i CD57+ uttrykket. De uttrykte høyere nivåer av CD69 og aktivering av NK cytotoksisk reseptorene (NCR) NKp30, NKp44 og NKp46. Disse endrede fenotypene endret ikke den cytotoksiske funksjonen til NK-cellene. Det ble ikke observert endret cytotoksitet i NK cellene mellom CFS og kontrollene.

    Denne forkergruppen konkluderer med at CFS pasienter viser kvalitative endringer i lymfocyttene men ikke kvantitative endringer. B cellene presenterer fenotyper som er lik for noen autoimmune sykdommer eller virale infeksjoner. De finner det interessant at anergic
    fenotype, som ble observert i T-celler, som kan relateres til nedsatt kontroll av virusinfeksjoner. Endringer i NK fenotyper så ikke ut til å
    endre eller modifisere cytotoksiteten til NK-cellene. Resultatene viser at det er en immunologisk dysfunksjon som bidrar til mekanismene en ser i CFS-pasienter.

    Subset CD og cytokiner m.m finner du på denne siden: http://www.copewithcytokines.de/cope.cgi?key=CD16

    Link: http://meforum.info/viewtopic.php?f=78&t=11395

    😉 med forbehold med kognitiv svikt feil *jadajada ;)*

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