Viral protein helps Epstein-Barr virus-infected B cells escape human killer T cells

JennyJenny

Well-Known Member
Viral protein helps Epstein-Barr virus-infected B cells escape human killer T cells

This wasn't specific research for ME/CFS so of course I put it under "Other" but I have to say I was never terribly convinced our problem is the EBV as not many of us come up with EBV being active. I am sure it can happen but I don't know if they have any information that we have EBV active in more than the general population or those with other chronic or neuro-immune or other autoimmune illnesses. I think they are researching it for ME/CFS but I just don't see it being our issue.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Viral protein helps Epstein-Barr virus-infected B cells escape human killer T cells

This wasn't specific research for ME/CFS so of course I put it under "Other" but I have to say I was never terribly convinced our problem is the EBV as not many of us come up with EBV being active. I am sure it can happen but I don't know if they have any information that we have EBV active in more than the general population or those with other chronic or neuro-immune or other autoimmune illnesses. I think they are researching it for ME/CFS but I just don't see it being our issue.
Thanks! Fascinating stuff. EBV is able to tamp down the level of the proteins our immune system uses to recognize it and it's found ways to turn off the attack response of T-cells.

It's quite a virus - that for sure. :woot::woot:

Examining the mechanism underlying the LMP2A-mediated evasion, they found several ways in which it interferes with the recognition of EBV-infected cells. First, LMP2A reduced levels of several EBV proteins whose fragments are recognized by CD8+ T cells on the surface of the cell targeted for killing. Second, LMP2A disturbs expression of cellular molecules on infected B cells that interact with NKG2D, a host molecule on the surface of CD8+ T cells that aids their activation, thereby weakening the immune response against EBV-infected cells.

"Taken together," the researchers conclude, "we describe here a functional immunomodulatory effect for the EBV protein LMP2A, and show that LMP2A mediates partial escape of infected B cells from recognition by CD8+ T cells." They also suggest that that similar immune evasion mechanisms to the ones revealed may operate in different types of LMP2A-expressing cancers caused by EBV.
 

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