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Aller førs vil jeg bare si at dette var svært skuffende. Hvor ble det av det nye de skulle presentere om dysfunksjon i CD8-cellene? Som jeg skrev om for et par dager siden i denne posten, skulle følgende tas opp på møtet:
De vil presentere sine funn om XMRV, og enda viktigere, de vil presentere nye funn de har gjort om en felles immun-dysfunksjon de har funnet hos alle ME-pasienter: immunsvikt på grunn av CD8-celler (for sammenlignings skyld: HIV er en sykdom der det er immunsvikt på grunn av CD4-celler, mens vi har immunsvikt på grunn av den lave CD8-verdien).
De vil også forklare for pasienter som vil være til stede (vi har først og fremst invitert pasientorganisasjoner) hvordan vi skal leve til det er en behandling for XMRV.
Kan vi håpe at det kommer mer informasjon fra møtet senere?
Referatet som presenteres kommer her:
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 could be 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