So, last Friday, we discussed the relationship between EBV (Epstein Barr Virus) and MS (Multiple Sclerosis).  That could be exciting- because should we develop a vacinne, it could eradicate the scourge of MS and its crippling affects.  (Right now there are some 1 million American citizens (plus many more around the world) suffering from MS.)

The problem is exacerbated because EBV is often maintained in our bodies (being latent- meaning being present without effecting any actions; i.e. remaining dormant), until it is activated.  (We will discuss tomorrow how COVID-19 is one such “sleeping beauty kiss”.)

Except, we didn’t know an awful lot about the EBV. Until now. When we finally figured out (actually, it’s not we but Dr. Italo Tempera and his group based based at the Wistar Institute [Philadelphia, PA]  (augmented by other talented team members).

The team (besides Dr. Tempera, includes Drs. SM Morgan, LB Caruso, A Kossenkov, S Boyle, and PM Lieberman of Wistar; Dr. H Tanizawa from the University of Oregon; Dr. M Hulse of Temple, Y Tan of Fox Chase Cancer center; and J Madzo and K Keith of the Coriel Institute of Camden) published its findings in Nature Communications in the article The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity.  (I always find it amazing how complex a scientific paper title can be- making it difficult for most folks to discern what the real crux of the matter is.)

It turns out that Poly [ADP-ribose] polymerase 1 (aka, PARP1) binds the genome of the Epstein Barr virus (thereby stabilizing CTCF binding), among other critical actions for the EBV. This enzyme is so critical to the functionality of the EBV that if it is restricted, the EBV will find it difficult to be its normal gruesome self.

Heretofore, we thought PARP1 was critical in the field of DNA damage, but this new study identifies it poses a critical role in chromatin folding and gene expression.

Moreover, Dr. Tempera identified two cellular proteins (CTFC and PARP1) that help govern the folding of the EBV genome.  [Note that these two proteins also play vital functions in human genome expression.] And, there are already identified drugs that target these proteins. Once we interfere with the genome folding, its viral functionality is diminished.

Now, recognize that EBV does more than just cause MS (assuming others confirm the data we discussed yesterday), it is a ubiquitous virus that affects almost every human on earth. Once the virus causes of B-cells (part of our immune system) to respond (which almost always means they overmultiply), that’s when problems begin.  Which is a really big problem for those of us with compromised immune systems (consider transplant patients, as an example).

This opens the chance for Lynparza (olaparib) to deal with the EBV.  (Lynparza is already part of the arsenal used to treat ovarian cancer. And, this new study means it should also be effective against lymphomas- those that are EBV positive.)While this YouTube video talks about cancer, you can see how the PARP inhibitors can  stop the actions of EBV.  And, hopefully, stop MS manifestations.

It’s already been a whole week since we were permitted to file personal taxes with the IRS.  It won’t be until the 15th of February when recipients of the ACTA and those seeking an EIC (Earned Income Credit) can file.  So, get my book now to find the ways yuo can minimize your tax burden.

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