Monday, 25 January 2016

Antibody response to EBV associated with lesion burden

Humoral response to EBV is associated with cortical atrophy and lesion burden in patients with MS. Zivadinov R, Cerza N, Hagemeier J, Carl E, Badgett D, Ramasamy DP, Weinstock-Guttman B, Ramanathan M.Neurol Neuroimmunol Neuroinflamm. 2016 Jan 7;3(1):e190. doi: 10.1212/NXI.0000000000000190. eCollection 2016 Feb.


OBJECTIVE:Because dysregulated Epstein-Barr virus (EBV)-infected B cells may induce meningeal inflammation, which contributes to cortical pathology in multiple sclerosis (MS), we investigated associations between antibody responses to EBV and development of cortical pathology in MS.
METHODS:We included 539 patients with MS (369 with relapsing-remitting MS, 135 with secondary progressive MS, and 35 with primary progressive MS), 66 patients with clinically isolated syndrome (CIS), 63 patients with other neurologic diseases (OND), and 178 age- and sex-matched healthy controls (HC). All participants were scanned on 3T MRI. Serum samples were analyzed for IgG antibodies against EBV viral capsid antigen (VCA) and EBV nuclear antigen-1 (EBNA-1), and their quartiles were determined on the whole study sample. Differences between the study groups were assessed using analysis of covariance adjusted for multiple comparisons.
RESULTS:More than 30% of patients with MS and CIS presented with the highest quartile of anti-EBV-VCA and -EBNA-1 status compared to ≤10% of HC (p < 0.001). The figures were 9 (14.3%) and 7 (12.3%) for patients with OND. Patients with MS with the highest quartile of anti-EBV-VCA showed significantly increased T2 lesion volume (p = 0.001), T1 lesion number (p = 0.002), and T1 lesion volume (p = 0.04) and decreased gray matter (p = 0.041) and cortical (p = 0.043) volumes compared to patients with MS with lower quartiles. No significant differences of MRI outcomes in patients with CIS, patients with OND, and HC with lower or highest quartiles of anti-EBV-VCA and -EBNA-1 were detected.
CONCLUSIONS:Humoral response to anti-EBV-VCA and -EBNA-1 is associated with more advanced cortical atrophy, accumulation of chronic T1 black holes, and focal white matter lesions in patients with MS.


We can all read the conclusions and this suggests that higher levels of EBV-specific antibodies are associted with more grey and white matter lesions. Is it cause and effectoris this further evidence that EBV is related to the pathology

12 comments:

  1. It would be interesting to doctors to receive a patient with suspected MS give a "look" for anti-EBV antibodies ...

    A guy asked me saying that when he was at the research stage made anti EBV tests were negative. I said there are many tests can give false-negative or positive ...

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  2. And if it is confirmed the percentage above 30% is equal to the genetic risk factors for the disease...

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  3. If I understand people infected with HIV and under HAART therapy are protected against MS. HIV is attacking the lymphocytes and deplete them. Antiviral drugs are attacking retro-virus like EBV. So independently it seems that the later would be useful against MS (but Charcot I failed). The former seems also to be protective against MS (but most DMT based on that are partially efficient and with bad side effects). Here is an hypothesis: these people are protected against MS because of HIV "AND" antiviral. You need the conjunction of both to track down MS. With both a DMT and an antiviral you would attack both the circulating virus and its shelter. Make sense, no? Seems like a pledge for cocktail therapies.

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    1. I already disagree, for me it's just action of anti-virus, not the virus HIV. I know it's "guesses" based on a case "isolated", because I know the person in question, she lives in Southern Brazil, but the person in question found that had MS and later found to have HIV, and she claims that it had improving MS symptoms and progression of the disease itself after she began to deal with HAART ...

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    2. Thank you for reading my comment. I do not understand why you disagree? It seems that your case study is just reinforcing on of my point: HIV is insufficient to fight MS. I added to that that antiviral like HAART alone is insufficient to fight MS as illustrated by the failure of Charcot I. But HIV + HAART are necessary to fight MS.

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    3. "HAART alone is insufficient to fight MS as illustrated by the failure of Charcot I"
      You seems to forget that HAART is a combination therapy (three or more antivirals).
      In Charcot I they tried only a single antiviral.

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    4. I agree with you Anon. And this could be one explanation why Charcot I failed. That HAART is a combination and not a single drug. On this point It would have been great to start with HAART and remove one med at the time. This would have (dis)prove my hypothesis: HAART alone and no HIV (or no DMT) can stop MS. This is why it would be nice to know which DMTs took the patient enrolled in Charcot I.

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    5. "his is why it would be nice to know which DMTs took the patient enrolled in Charcot I"

      It's not a secret; Docs. said it a lot of times on this blog: the antiviral used was Raltegravir .....

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    6. Then to me still holding that is a specific anti-viral effect, and as Anon 11:36am said, HAART is a combination of at least 3 ir more antiretrovirus.
      In this case I know, she reported that when he discovered the AIDS the your MS worsened together, and I thought talking to her "worsening must have been because despite the HIV suppress lymphocytes it also affects the Central Nervous System too."
      That's when she told me that after he started the anti-HIV cocktail to MS had improved...

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    7. To Anon 5:31. Sorry I was unclear, by DMT I mean immuno-suppressor/modulator. Raltegravir is not an immunomodulator but an anti-viral. Surely people treated with Raltegravir were already taking an immunomodulator for their MS. Which one?

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    8. To Cinara. Are there clinical trials using HAART for MS? Why are charcot projects are using only one and not the three drugs?

      Thank you for sharing this interesting case report. Out of curiosity. Do you still give immuno suppresor for MS when you have the HIV?

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    9. one was used because that was funded by a drug company, but the logic of that one relied on anecdote, rather than biology. HERV have already intergrated and so how an anti-integrase inhibitor was going to work. But who needs biology if it works look at the CRAB drugs as an example.

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