If my understanding it correct, it helps our cells, thus wards off lyme.
Does that mean P11 also helps to raise CD57?
Is there a way for us to have more P11?
I'm thinking if we could have more Pll, then we could increase our CD57.
I'm intrigued by many of your posts, to say the least.
I don't confess to know, much less be able to explain, what you do though, but I am trying to understand, as much as I possibly can.
Love, Light, & Health, Jennie
-------------------- My Lyme dx:11/05. My Mom's Lyme dx:5/16. ISO ASAP-Lyme Literate Dr & Neurologist-Prefer IL, IN, KY, MO, OH, TN. Can travel farther. Finances limited. Prefer Drs take Medicare or Payments. Need great list to find best fit. Tyvm. Posts: 701 | From Owensboro, KY | Registered: Sep 2005
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AliG
Frequent Contributor (1K+ posts)
Member # 9734
posted
I've been doing some reading & found that Malaria can reactivate latent EBV & EBV has been found in autopsied MS brains.
EBV + Malaria cause Burkitt's Lymphoma?
CD-57=cancer fighting T-cells.
I'm wondering if Babesia can re-activate EBV as well.
I'm wondering if the combo of Bb, EBV & Babesia can cause the persistently low CD-57 and perhaps the reason CD-57 is low in chronic Lyme cases is because Babs has had a chance to get EBV all riled up.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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AliG
Frequent Contributor (1K+ posts)
Member # 9734
posted
Pubmed search = EBV IgG (I don't know why I searched for that, but these are some things I turned up )
Although malaria and Epstein-Barr (EBV) infection are recognized cofactors in the genesis of endemic Burkitt lymphoma (BL), their relative contribution is not understood. BL, the most common paediatric cancer in equatorial Africa, is a high-grade B cell lymphoma characterized by c-myc translocation.
EBV is a ubiquitous B lymphotropic virus that persists in a latent state after primary infection, and in Africa, most children have sero-converted by 3 y of age.
Malaria infection profoundly affects the B cell compartment, inducing polyclonal activation and hyper-gammaglobulinemia.
We recently identified the cystein-rich inter-domain region 1α (CIDR1α) of the Plasmodium falciparum membrane protein 1 as a polyclonal B cell activator that preferentially activates the memory compartment, where EBV is known to persist.
Here, we have addressed the mechanisms of interaction between CIDR1α and EBV in the context of B cells.
We show that CIDR1α binds to the EBV-positive B cell line Akata and increases the number of cells switching to the viral lytic cycle as measured by green fluorescent protein (GFP) expression driven by a lytic promoter.
The virus production in CIDR1α-exposed cultures was directly proportional to the number of GFP-positive Akata cells (lytic EBV) and to the increased expression of the EBV lytic promoter BZLF1.
Furthermore, CIDR1α stimulated the production of EBV in peripheral blood mononuclear cells derived from healthy donors and children with BL.
Our results suggest that P. falciparum antigens such as CIDR1α can directly induce EBV reactivation during malaria infection that may increase the risk of BL development for children living in malaria-endemic areas.
To our knowledge, this is the first report to show that a microbial protein can drive a latently infected B cell into EBV replication.
Author Summary
Malaria and Epstein-Barr virus (EBV) infections are recognized cofactors in the genesis of endemic Burkitt lymphoma, the most common paediatric cancer in equatorial Africa.
EBV is a ubiquitous virus residing in B lymphocytes that establishes a lifelong persistence in the host after primary infection.
EBV has two lifestyles: latent infection (non-productive), and lytic replication (productive).
Children living in malaria-endemic areas exhibit an elevated viral load, and acute malaria infection increases the levels of circulating EBV.
The mechanisms leading to viral reactivation during Plasmodium falciparum malaria infection are not well understood.
Cystein-rich inter-domain region 1α (CIDR1α) is a domain of a large protein expressed at the surface of P. falciparum-infected red blood cells.
Based on previous findings showing that CIDR1α activates and expands the B cells compartment where EBV persists, we assessed the impact of CIDR1α on viral reactivation.
Here, we identify CIDR1α as the first microbial protein able to drive a latently EBV-infected B cell (no virus production) into lytic replication (virus production).
Our results suggest that P. falciparum-derived proteins can lead to a direct reactivation of EBV during acute malaria infection, increasing the risk of Burkitt lymphoma development for children living in malaria-endemic areas.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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