•Transgenic mice were used to make genetically human EBV mAbs against gp350 and gp42
•mAbs potently neutralize EBV infection by blocking receptor-ligand interactions
•mAbs prevent EBV infection following EBV challenge in humanized mice
We know that there is interest in stopping EBV and there is a view of vaccinating against EBV. However this has sent a chill down the spine of some vaccine people because those do-gooding immunologists in their haste to explain hoe EBV causes MS have kind of said that EBV vaccination can cause MS meaning some vaccine people do not want to go near MS vaccination. This because the do-gooders have made the point that antibodies against EBV cross react with the CNS to cause damage.
Now this idea comes responses to a few target on EBV. Now in terms of targetting EBV you can go to block the infection of cells by the virus as done here or you could try and vaccinate against the virus when it is hiding in cells. Now the vaccine will make antibodies against the binding sites and another approach is to make the antibodies and then transfer them to do the blocking. This what is happening here they have made antibodies in mice and reported that this can limit infection….Horryah…Let’s hope it works but there is form in this approach and that was with COVID-19 virus. By the time the companies had made and tested the antibody, the virus had mutated such that the antibodies didn’t work….It is one in the eye for the creationists, as it is perhaps a great example of natural selection and evolution in practice and in action. No need to wait for years for Darwin’s finches in the Galapagos islands to evolve this was happening within weeks and months. EBV however is not a respiratory virus like SARS-CoV-2 so lets hope it evolves slower.
Chhan CB, Lang K, Davis AR, Wan YH, Aldridge NT, Kher G, Scharffenberger SC, Hardy SR, Iureniev R, Giltiay NV, Edwards KR, Radtke S, Kiem HP, Pancera M, McGuire AT. Transgenic mouse-derived human monoclonal antibodies targeting EBV gp350 and gp42 provide basis for therapeutic development. Cell Rep Med. 2026 Feb 17;7(2):102618
Epstein-Barr virus (EBV) causes infectious mononucleosis and contributes to neurodegenerative disorders and malignancies, particularly in immune-compromised hosts. Transplant patients face high risk of post-transplant lymphoproliferative disease, a life-threatening EBV-driven lymphoma. There are no EBV-specific vaccines or treatments; however, neutralizing antibodies against EBV glycoproteins may offer utility as therapeutic agents. EBV entry into B cells involves gp350, which binds complement receptors, and gp42, which engages HLA class II to trigger fusion. Most existing monoclonal antibodies (mAbs) against these antigens are non-human, limiting clinical use. Using a transgenic mouse model, we generate two gp350 and eight gp42 genetically human neutralizing mAbs that block receptor binding. Structural analyses reveal extended sites of vulnerability relevant to vaccine development. Delivery of a gp42 mAb protects humanized mice from EBV challenge, while a gp350 mAb provides partial protection. These mAbs highlight the utility of transgenic mice to produce therapeutic mAbs for preventing EBV-driven disease.
Anyway whilst digging this one up I came across this one (It’s unreviewed and the proof in the pudding will be if anyone repeats the work)
If it is worth saying once it is worth saying twice
Younis S, Rasouli S, Loeffler JW, Sattarnezhad N, Courtney Y, Moutusy SI, Jahanbani S, Pandit M, Tomczak A, Wong HH, Sharpe O, Utz PJ, Meffre E, Kipp LB, Dunn JE, Lanz TV, Steinman L, Robinson WH. EBV reprograms autoreactive anti-CNS B cells as antigen presenting cells in multiple sclerosis. bioRxiv [Preprint]. 2026:2026.02.11.701910. doi: 10.64898/2026.02.11.701910. PMID: 41727017; PMCID: PMC12919047.
Multiple sclerosis (MS) is a chronic autoimmune disease targeting the central nervous system (CNS). MS develops almost exclusively in individuals previously infected with Epstein-Barr virus (EBV) 1, yet the mechanisms linking EBV infection to MS pathogenesis remain incompletely defined (Yarn). Here we characterized EBV-infected B cells in MS and demonstrated that EBV directly infects autoreactive anti-CNS antigen B cells and reprograms them into pro-inflammatory antigen-presenting cells (APCs). EBV⁺ B cells in MS were enriched within the CD27⁺CD21 low memory B-cell subset and exhibited upregulated B cell activation and APC transcriptional programs. Recombinant antibodies derived from MS blood and cerebrospinal fluid (CSF) EBV⁺ B cells bound brain tissue, and several cross-bound both MS-associated autoantigens and Epstein-Barr virus nuclear antigen-1 (EBNA1). (A couple of weeks ago they were telling us they targeted Lupus antigens) In vitro , EBV⁺ B cells functioned as APCs that stimulated T peripheral helper cells, with associated activation of EBV⁻ anti-CNS antigen B cells. Collectively, these findings support a mechanistic framework in which EBV infects and transcriptionally reprograms autoreactive anti-CNS antigen B cells into APCs that drive pathogenic anti-CNS antigen T cell and EBV – B cell responses in MS.
They say “Our data reveal that EBV infects and reprograms diverse antiCNS B cells to become APCs, including autoreactive anti-anoctamin-2 (Ano2) and anti-alpha-B available….so was the idea that it was glialcam a duff idea?, As this is what they originallly said
The make the antibodies and stain mouse brain but hang on the staining is in the grey matter and not the white matter so has MS pathology been wrong all this time?
To be fair They say “Although MS has historically been viewed as a predominantly periventricular whitematter disease, one of its most specific pathological hallmarks is the presence of gray-matter
lesions, particularly subpial cortical lesions. This pathological pattern is consistent with the EBV⁺ B cell–encoded anti-neuronal autoantibodies identified here”
B cells to the total number of sequenced B cells per sample,
and observed a mean EBV+ B cell frequency of ~5 per 10,000 sequenced B cells in MS (range:0 to 20 per 10,000 B cells). In contrast, we detected a significantly higher mean frequency of EBV+ B cells in SLE (~25 per 10,000 B cells, range: 2.3 to 82 per 10,000), while in Healthy controls we detected a significantly lower mean frequency of EBV+ B cells (~1 per 10,000 sequenced B cells, range: 0 to 3 per 10,000 B cells)
Yep they said this already
Younis S, Moutusy SI, Rasouli S, Jahanbani S, Pandit M, Wu X, Acharya S, Sharpe O, Wijeratne TU, Harris ML, Yang EY, Chaichian Y, Parsafar S, Baker MC, Harley JB, Meffre E, Steinman L, Marshak-Rothstein A, James JA, Martinez OM, Utz PJ, Orange DE, Lanz TV, Robinson WH. Epstein-Barr virus reprograms autoreactive B cells as antigen-presenting cells in systemic lupus erythematosus. Sci Transl Med. 2025 Nov 12;17(824):eady0210
So the implication is that EBV is a cause of autoimmunity , not just MS and this means you need to think about the problem differently
Source: multiple-sclerosis-research.org