cytokineproductie XMRV-geinfekteerde immuuncellen

komt aardig overeen met

cytokineprofiel (een deel van de) ME/CVS-patiŽnten






Uit een posterpresentatie op de tienjaarlijkse retrovirus bijeenkomst (CRM) blijkt dat

de cytokines die door XMRV-geinfekteerde afweercellen in vitro geproduceerd worden

goed stroken met het "cytokineprofiel" dat bij ME/CVS-patiŽnten gevonden wordt (klik hier).


Dit lijkt te bevestigen dat XMRV bij (een deel van de) ME/CVS-patiŽnten een hoofdrol speelt.









Characterization of innate immune responses in Xenotropic Murine Leukemia Retrovirus-Related Virus (XMRV) infected individuals

J. Mikovits 1, V. Lombardi 1, K. Hagen 1, D. Goetz 1, M. Marshall 2, I. Barao-Silvestre 1

  1. Whittemore Peterson Institute, Research, Reno, USA
  2. University of Nevada, Microbiology and Immunology, Reno, USA


Centennial Retrovirus Meeting (CRM)

April 29 - May 4, 2010

Institute of Molecular Genetics, Prague, Czech Republic

Poster Presentations P62



Chronic fatigue syndrome (CFS)

is a debilitating disease

manifested by inflammatory sequelae

including innate immune activation, low natural killer cell numbers and function.


We recently demonstrated

the first direct isolation of

an infectious gammaretrovirus, XMRV,

from the blood of CFS patients.


We have developed

quantitative assays to detect XMRV replication and methods for infection in culture.


Moreover, we found evidence of

XMRV infection in >95% of the 141 CFS patients tested to date.


These data implicate

a role for XMRV infection in the pathogenesis of CFS.


We studied

the interaction of XMRV with the immune system,

first by identifying

cellular targets of XMRV ex vivo by flow cytometry (FCM).


We hypothesized

that NK cells could be a target of infection and

that infection of other PBMC cell types

could lead to dysfunction of NK cells

either directly or

indirectly through the upregulation of inflammatory cytokines and chemokines,

which are also a hallmark of this disease.



isolated leukocytes from XMRV infected individuals

analyzed phenotypic differences from uninfected controls by FCM.


Using purified

primary B, T monocyte macrophage and dendritic cells and

cell line models

we infected with XMRV and

profiled cytokine and chemokine expression by Luminex multiplex assays.


We analyzed

XMRV infection

by quantitative RT-PCR and intracellular FCM.


Infection of PBMC in vitro

results in

a cytokine signature similar to

that signature seen in the plasma of CFS patients.


These data advance our understanding of the pathogenesis of CFS and

may ultimately lead to new therapeutic interventions.





http://www.crm2010.org/images/stories/pdf/CRM2010-Programme-and-Abstract-book.pdf, blz. 57