'Autoimmune disease: A role for new anti-viral therapies?'

[Ema]

Several recent reports suggest a role of retroviral integrase inhibitors as therapy for herpes virus infections either by effects on a herpes recombinase related to the retroviral integrase [14,15], or by effects on another conserved family of herpes virus proteins termed terminases required for genome cleavage and viral packaging [16].

Because of the patient's documented elevated titers of IgG to both EBV and other human herpes viruses, she was offered a trial of Raltegravir (Issentress), a retroviral integrase inhibitor with FDA approval for use in HIV-1 infection [17–19].

Remarkably, in contrast to her complete lack of response to acyclovir 2 years previously she experienced a complete remission of all of her symptoms after less than one week of Raltegravir.

Autoimmun Rev.2011 Dec;11(2):88-97. doi: 10.1016/j.autrev.2011.08.005. Epub 2011 Aug 18.
Autoimmune disease: A role for new anti-viral therapies?
Dreyfus DH1.
Author information

Abstract
Many chronic human diseases may have an underlying autoimmune mechanism. In this review, the author presents a case of autoimmune CIU (chronic idiopathic urticaria) in stable remission after therapy with a retroviral integrase inhibitor, raltegravir (Isentress). Previous reports located using the search terms "autoimmunity" and "anti-viral" and related topics in the pubmed data-base are reviewed suggesting that novel anti-viral agents such as retroviral integrase inhibitors, gene silencing therapies and eventually vaccines may provide new options for anti-viral therapy of autoimmune diseases. Cited epidemiologic and experimental evidence suggests that increased replication of epigenomic viral pathogens such as Epstein-Barr Virus (EBV) in chronic human autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), and multiple sclerosis (MS) may activate endogenous human retroviruses (HERV) as a pathologic mechanism. Memory B cells are the reservoir of infection of EBV and also express endogenous retroviruses, thus depletion of memory b-lymphocytes by monoclonal antibodies (Rituximab) may have therapeutic anti-viral effects in addition to effects on B-lymphocyte presentation of both EBV and HERV superantigens. Other novel anti-viral therapies of chronic autoimmune diseases, such as retroviral integrase inhibitors, could be effective, although not without risk.

 

[Wonkmonk]

Do they say in the full text paper what the "other herpesviruses" with elevated titers were?

 

[used_to_race]

Do they say in the full text paper what the "other herpesviruses" with elevated titers were?

PM me if you want the full paper, I can get it through my company.

 

[Ema]

Do they say in the full text paper what the "other herpesviruses" with elevated titers were?

I can’t remember offhand but I also have the full text. Let me know if you would like to read it.

 

[pattismith]

Cited epidemiologic and experimental evidence suggests that increased replication of epigenomic viral pathogens such as Epstein-Barr Virus (EBV) in chronic human autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), and multiple sclerosis (MS) may activate endogenous human retroviruses (HERV) as a pathologic mechanism.
Memory B cells are the reservoir of infection of EBV and also express endogenous retroviruses, thus depletion of memory b-lymphocytes by monoclonal antibodies (Rituximab) may have therapeutic anti-viral effects in addition to effects on B-lymphocyte presentation of both EBV and HERV superantigens. Other novel anti-viral therapies of chronic autoimmune diseases, such as retroviral integrase inhibitors, could be effective, although not without risk.

I'm not sure if I understand well the link between EBV and HERV, but here a study of this year which is related to HERV antibodies:

Humoral immunity response to HERV-K/W differentiates between amyotrophic lateral sclerosis and other neurological diseases.


Abstract
Human endogenous retroviruses-K/W seem play a role in fostering and exacerbation of some neurological diseases, including amyotrophic lateral sclerosis (ALS).
Given these findings, we investigated the immunity response against HERV-K and HERV-W envelope surface (env-su) glycoprotein antigens in serum and cerebrospinal fluid (CSF) of ALS, multiple sclerosis (MS) and Alzheimer's disease (AD) patients, and in healthy controls (HCs).
Four antigenic peptides derived respectively from HERV-K and HERV-W env surface proteins were studied in twenty-one definite or probable ALS, twenty-six possible or definite relapsing-remitting (RR) MS, eighteen patients with AD and thirty-nine HCs.
An indirect ELISA was set up to detect specific antibodies (Abs) against env surface peptides.
Among the measured levels of Abs against the four different HERV-K peptide fragments, HERV-K env-su 19-37 only was significantly elevated in ALS compared to other groups, both in serum and CSF. Instead, among the Abs levels directed against the four different HERV-W peptide fragments, only HERV-W env-su 93-108 and HERV-W env-su 248-262 were significantly elevated, in serum and CSF of MS, compared to other groups.
In ALS patients, the HERV-K env-su 19-37 antibodies levels were significantly correlated with clinical measures of disease severity, both in serum and CSF.
Increased circulating levels of Abs directed against the HERV-W env-su 93-108 and HERV-W env-su 248-262 peptide fragments could serve as possible biomarkers in patients with MS.
Similarly, increased circulating levels of Abs directed against the HERV-K env-su19-37 peptide fragment could serve as possible early novel biomarker in patients with ALS.