Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus

[nerd]

Jog NR and James JA (2021) Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus. Front. Immunol. 11:623944. doi: 10.3389/fimmu.2020.623944

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease. Infections or infectious reactivation are potential triggers for initiation of autoimmunity and for SLE flares. Epstein-Barr virus (EBV) is gamma herpes virus that has been associated with several autoimmune diseases such as SLE, multiple sclerosis, Sjogren’s syndrome, and systemic sclerosis. In this review, we will discuss the recent advances regarding how EBV may contribute to immune dysregulation, and how these mechanisms may relate to SLE disease progression.

Although this isn't about CFS/ME per se, this discussion shows the latest state of research on EBV causality with SLE. I think SLE is the only disease for which most of EBV's pathophysiology is modeled and verified, especially the dynamic that allows autoimmune antibodies to be formed/multiplied. That a molecular antigen mimicry can lead to antibody formation is an important finding because it could be projected on other mimicking viral genes of other viruses. It might be the explanation for all presumed virus-induced diseases for which disease severity or serology correlates with specific viral antibodies, such as EBV IgG and EBV's EA IgG in the case of SLE.

As a side note, this can not be applied 1:1 to other diseases. For MS, the presumed mechanism of EBV is very different in parts (10.1556/eujmi.1.2011.4.2).

 

[pattismith]

Fatigue and widespread pain are often associated to SLE, here a 2021 paper from Germany:


Improvement of lupus-associated fatigue with modafinil: Report of two cases


Peter Korsten, Silvia Piantoni
First Published February 15, 2021 Research Article
https://doi.org/10.1177/0961203321995252

free full article

Abstract

Fatigue is a frequently reported and disabling symptom in patients with systemic lupus erythematosus (SLE).

The management of Lupus-associated fatigue (LAF) is complex and requires the exclusion of disease activity and comorbidities as potentially treatable causes.

Standard of care recommendations includes psychological counselling and regular physical activity. However, many SLE patients still report the persistence of LAF despite these measures.

Therefore, pharmacological management may be required, which has been insufficiently investigated in clinical trials.

Here, we report two patients who improved with pharmacological treatment with modafinil (MODA), a central nervous system stimulant. Both patients had an overall low disease activity (SLEDAI-2K score of 0).

Their FACIT fatigue scores were 15 and 20, respectively (with a maximum score of 52, where 52 indicates the best quality of life).

With MODA treatment, the first patient’s FACIT fatigue score improved from 15 to 42, the second patient’s score from 20 to 37. In the latter patient, it returned to 21 after stopping the drug and increased back again to 37 after re-treatment.

In conclusion, our report demonstrates, for the first time, that MODA treatment is a potential pharmacological treatment option in selected patients with LAF. Clinical trials in SLE are required to confirm our observations.

 

[gbells]

Jog NR and James JA (2021) Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus. Front. Immunol. 11:623944. doi: 10.3389/fimmu.2020.623944



Although this isn't about CFS/ME per se, this discussion shows the latest state of research on EBV causality with SLE. I think SLE is the only disease for which most of EBV's pathophysiology is modeled and verified, especially the dynamic that allows autoimmune antibodies to be formed/multiplied. That a molecular antigen mimicry can lead to antibody formation is an important finding because it could be projected on other mimicking viral genes of other viruses. It might be the explanation for all presumed virus-induced diseases for which disease severity or serology correlates with specific viral antibodies, such as EBV IgG and EBV's EA IgG in the case of SLE.

As a side note, this can not be applied 1:1 to other diseases. For MS, the presumed mechanism of EBV is very different in parts (10.1556/eujmi.1.2011.4.2).

I'm disappointed it didn't occur to to them to talk about coinfections.

 

[nerd]

I'm disappointed it didn't occur to to them to talk about coinfections.

How do you mean?