Apparently, I found Viral Genetics' current patent. And as I had previously speculated, I was correct that the treatment is going to modify B cells. I knew it! Buy me a drink, eh?
Here is a link to the patent online: http://www.faqs.org/patents/app/20100166789
Patent application title: PROTEINS FOR USE IN DIAGNOSING AND TREATING INFECTION AND DISEASE
Inventors: Haig Keledjian (San Marino, CA, US) Michael Agadjanyan (Huntington Beach, CA, US) Martha Karen Newell (Colorado Springs, CO, US) Evan Newell (Menlo Park, CA, US)
Assignees: THE REGENTS OF THE UNIVERSITY OF COLORADO Viral Genetics, Inc.
IPC8 Class: AA61K3900FI
USPC Class: 4241851
Class name: Amino acid sequence disclosed in whole or in part; or conjugate, complex, or fusion protein or fusion polypeptide including the same
Publication date: 07/01/2010
Patent application number: 20100166789
And here are the excerpts on how the invention will be used to treat chronic Lyme disease (patent text slightly modified to correct spelling errors):
 Lyme Disease is a tick-borne disease caused by bacteria belonging to the genus Borrelia. Borrelia burgdorferi is a predominant cause of Lyme disease in the US, whereas Borrelia afzelii and Borrelia garinii are implicated in some European countries. Early manifestations of infection may include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. Long-term the disease involves malfunctions of the joints, heart, and nervous system. Currently the disease is treated with antibiotics. The antibiotics generally used for the treatment of the disease are doxycycline (in adults), amoxicillin (in children), and ceftriaxone. Late, delayed, or inadequate treatment can lead to late manifestations of Lyme disease which can be disabling and difficult to treat.
 A vaccine, called Lymerix, against a North American strain of the spirochetal bacteria was approved by the FDA and later removed from the market. It was based on the outer surface protein A (OspA) of B. burgdorferi. It was discovered that patients with the genetic allele HLA-DR4 were susceptible to T-cell cross-reactivity between epitopes of OspA and lymphocyte function-associated antigen in these patients causing an autoimmune reaction.
 It is believed according to the invention that Borrelia burgdorferi also produces a Toll ligand for TLR2. Replacement of the CLIP on the surface of the B cell by treatment with a thymus derived peptide with high affinity for the MHC fingerprint of a particular individual, would result in activation of the important Tregs that can in turn cause reduction in antigen-non-specific B cells. Thus treatment with thymus derived peptides could reactivate specific Tregs and dampen the pathological inflammation that is required for the chronic inflammatory condition characteristic of Lyme Disease. With the appropriate MHC analysis of the subject, a specific thymus derived peptide can be synthesized to treat that subject. Thus individuals with all different types of MHC fingerprints could effectively be treated for Lyme disease.
 Chronic Lyme disease is sometimes treated with a combination of a macrolide antibiotic such as clarithromycin (biaxin) with hydrochloroquine (plaquenil). It is thought that the hydroxychloroquine raises the pH of intracellular acidic vacuoles in which B. burgdorferi may reside; raising the pH is thought to activate the macrolide antibiotic, allowing it to inhibit protein synthesis by the spirochete.
Read more: http://www.faqs.org/patents/app/20100166789
How will this theoretically stop inflammation present in chronic Lyme disease? What does the above all mean, in English? More details coming soon - for now I wanted to share this.
In the meantime, you might want to review this: http://en.wikipedia.org/wiki/Thymus
Image credit: Thymus by LearnAnatomy from Wikipedia under a CC 3.0 license.
This work by Camp Other is licensed under a Creative Commons
Attribution-NonCommercial-ShareAlike 3.0 Unported License.