EPSTEIN-BARR VIRUS in MC and AUTOIMMUNITY!!

[Zizzle]

Study finds interferon, one of the body's proteins, induces persistent viral infection

Scientists at The Scripps Research Institute (TSRI) have made a counterintuitive finding that may lead to new ways to clear persistent infection that is the hallmark of such diseases as AIDS, hepatitis B and hepatitis C.

http://medicalxpress.com/news/2013-04-i ... l.html#jCp

[Zizzle]

More evidence, this time related to how EBV can trigger Lupus.



Bull NYU Hosp Jt Dis. 2006;64(1-2):45-50.

Epstein-Barr virus infection induces lupus autoimmunity.
Harley JB, James JA.
Source
Departments of Medicineand Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.

Abstract

Systemic lupus erythematosus (SLE or lupus) is a systemic autoimmune disease characterized by a constellation of varied clinical presentations, although the nearly universal presence of autoantibodies is a salient unifying feature. Ongoing research efforts focus on understanding the complex combination of genetic and environmental factors that lead to SLE in select individuals. Our previous work has demonstrated that years before diagnosis abnormal autoantibody responses are present in the sera of patients who will subsequently develop lupus and, further, that the initial targets of two of these key responses (anti-Sm B' and anti-60 kD Ro alone) have been identified for some patients. Indeed, our results suggest that the first lupus-specific autoantibodies arise from particular antibodies directed against Epstein-Barr virus Nuclear Antigen-1 (EBNA-1) and that infection with Epstein-Barr virus (EBV) is an environmental risk factor for lupus. The predicted sequence of events is normal immunity, followed by Epstein- Barr virus infection, the generation of anti-EBNA-1 antibodies, then followed by those particular anti-EBNA-1 antibodies that also bind lupus-specific autoantigens (Sm or Ro), followed by the development of more complex autoimmune responses, and, finally, culminating in clinical disease. Studies from others and those underway suggest that lupus patients have unusual immune responses to Epstein-Barr virus. In aggregate, these results are consistent with an immune response against Epstein-Barr virus being important in at least some patients for the initiation of lupus autoimmunity.

[Zizzle]

WOW, an important article about the role of low Vitamin D in a variety of autoimmune diseases. This is especially interesting...

http://ard.bmj.com/content/72/4/473.long

A new and intriguing study links low serum 25(OH)D and elevated immunoreactivity against Epstein–Barr virus (EBV) in 25 individuals who had donated blood prior to the first clinical MS manifestation (clinically isolated syndrome).14 In fact, a novel role for low vitamin D as risk factor and/or modifier of autoimmune response is introduced. It is proposed that deprivation of solar light or low serum 25(OH)D at higher latitudes, facilitates the development of autoimmune diseases by aggravating the CD8 T-cell deficiency, thereby further impairing control of EBV and permitting clonal expansion of autoreactive B cells infected with EBV.

All this clinical and epidemiological evidence seems in agreement with several experimental studies, showing that UV radiation acts as an immunosuppressant by up-regulating Th2 cells, down-regulating Th1 cells, and inducing the production of interleukin-10 and T regulatory cells.27 ,28 UV-B exposure (solar light) could thus decrease the risk of RA onset as well as relapses, through increasing serum vitamin D, which exerts known immunomodulatory effects.29

Conclusions
Evidence supports an increased risk for autoimmune diseases, as well as for infections and cancer, in vitamin D deficiency. In the presence of overt disease, the severity of the process seems related to vitamin D deficiency. The link between the seasonality of 1,25(OH)D3 deficiency and the circannual incidence and severity of at least some autoimmune rheumatic disorders, might be reduced by its therapeutic supplementation.

[CathyMe.]

I don't have time right now to read this entire thread but just got a call from the nurse @ my doctors office and I have tested positive for the EBV that causes mono. This would explain my increased liver enzyme level, my contiued fatigue, the low WBC, and the reason why my doctor questioned me numerous times about having mono when I was younger, which I did not. I will read through all of the posts....I didn't even realize that she had tested me for this virus.

[ldubois7]

I had mono when I was 17. And, yes, you'd remember if you had it, because you stay sick for weeks and feel like you're dying!

My son has it now. :(

[Zizzle]

Wow Cathy! Getting EBV as a grown up is no fun! I didn't realize there was a connection to elevated liver enzymes. I thought it did most if its damage in the spleen and lymph nodes. Did she confirm you have an active infection or just evidence of past infection? I believe they would tell comparing Igm to IgG antibodies.

[CathyMe.]

Her nurse indicated it was active but that was one of the questions I asked...she just said no contact sports for 4 weeks?? I am going to speak to the doctor tomorrow.

[Zizzle]

Yup, no contact sports is to protect the swollen spleen. Sounds like active infection. Hope you get over it sooner than most and have no residual problems. I hate EBV!!

[gluten]

Hi Zizzle, Your comment about low body temperature is very interesting. My temperature is always low. Low body temperature effects certain enzymes. I did have two weeks of mono in college and it was not severe. Fortunately, I was in good physical condition from playing sports. Jon

[Zizzle]

Hi Zizzle, Your comment about low body temperature is very interesting. My temperature is always low. Low body temperature effects certain enzymes. I did have two weeks of mono in college and it was not severe. Fortunately, I was in good physical condition from playing sports. Jon

My mono at age 12 was also not severe, although it lasted several weeks and included multiple positive throat cultures for strep before being diagnosed.

My OB/GYN was certain I have thyroid issues given my low temp, slow pulse and low BP, but my multiple thyroid tests came back in ideal ranges.

[gluten]

Hi Zizzle, Your comment about pulse rate reminded me of college. Since there was an abundance of coeds in the nursing program. They would always want to check my pulse and they thought I was dead beacuse it was so low. But on the serious side, when I had a 24hr holter moniter test my doctor commented that my results showed that my pulse rate dropped to under thirty when sleeping. After researching about phages I found it interesting that they are looking into developing them to replace antibiotics. They would use a virus that would destroy the bacteria. What if, virus's like EBV, HIV, etc. destroy the good bacteria in our G.I. tract and that would promote the overgrowth of the bad bacterias. Since many of the good bacterias hide in bioflims and create certain enzymes that we use to assimulate the foods we eat but the virus's brake through the bioflim and destroy the bacteria. Interesting reading "Phage treatment of human infections" www.ncbi.nlm.nih.gov>Journal List> Bacteriophage. Jon

[Camie]

I had mono as a teenager. I was in the hospital for a week

[Zizzle]

Hmmm, rates of childhood infection with Epstein Barr are declining, especially among white children. Could the absence of EBV predispose some kids to immune conditions? Or, is the fact that they eventually get infected later in childhood/adolescence (more likely as mono) setting them up for autoimmune diseases later?

Antibody prevalence for Epstein-Barr virus has declined in US children from 2003-2004 to 2009-2010, according to recent study findings published in the Journal of Infectious Diseases.

“Another important finding was that antibody prevalence across all age groups was substantially higher in non-Hispanic blacks and Mexican Americans, who had essentially the same high age-specific antibody prevalence,”

"The two important findings of our study are that non-Hispanic white children acquired their first infection with Epstein-Barr virus at an older age than non-Hispanic blacks or Mexican Americans, and the prevalence of EBV infections in U.S. children is declining at a rate of about 1% per year,”

http://www.healio.com/pediatrics/emergi ... 03-to-2010


Here is an excellent (free) peer-reviewed article tying EBV infection to Lupus:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395176/

The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens.

[Zizzle]

Bet you were wondering when I'd dig up this thread again, eh?

Well, my son was just diagnosed with Pityriases Rosea, a skin disease that should last 8 weeks. It produces non-itchy bumps on his chest and back. I diagnosed it myself, but everyone around me was freaked out, so I took him to the pediatrician who confirmed it. I did some searches on PubMed and found a few studies tying this rash to Human Herpes Virus 7 (one of the Roseola viruses).

Interestingly, my daughter had a 5-day fever and viral syndrome before Thanksgiving. My working hypothesis is that her illness was a primary infection with HHV-7 (similar to Roseola-HHV-6, which all kids get as infants). My son probably already had HHV-7, and exposure to her may have reactivated his, or this may be his form of primary infection, given his exceedingly robust immune response (He never gets sick).

http://en.wikipedia.org/wiki/Human_herpesvirus_7

My daughter's illness also caused my autoimmune rash to flare temporarily. I’ve long suspected my rash to be related to my previous Epstein Barr infection (HHV-4). Darn viruses!!

Here is an excellent article about how these viruses live in our bodies. I think it's fascinating.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809354/


Of note is the role that stress plays on allowing viral reactivation as we age.

In most cases, reactivation does not lead to serious disease. It is sufficient for the virus to be shed in the oral cavity, and even HSV appears in the saliva in the absence of sores (48). Then again the level of viral activity most likely correlates with clinical symptoms. Innate and acquired host factors will affect the balance between viral activity and immune surveillance, making some people more susceptible to problematic infections than others.

In this context, it should be mentioned that we tend to attribute guilt by association. If symptoms correlate with the detection of virus, we tend to assume that the virus is responsible. This may lead to a faulty diagnosis and suboptimal treatment. The herpesviruses are likely to be reactivated as a consequence of a variety of conditions, but they are not necessarily involved in the underlying etiology. Due to their almost ubiquitous presence and ease of activation, clinical findings and epidemiology may suggest a causative role, even if the viruses are mere opportunists.

The delicate balance between latency and reactivation is designed by evolution. In a normal host, experiencing the normal interaction with the virus, the process is tuned to a long-term relationship that does not cause undue harm. However, if environmental factors upset this balance, or if the host for whatever reason is immunocompromised, the virus may inadvertently cause disease.

One might speculate that the optimal strategy for counteracting disease is to encourage early life exposure to herpesviruses. For the average person, infant inoculation with EBV and CMV may be beneficial, but the strategy does imply a risk for disease in rare individuals. Moreover, we live to an age where it is expected that the immune system has reduced potential, and occasionally we need to subdue the system in connection with various treatments. Thus, harmful consequences of these viruses are likely to occur at some point in life.

[gluten]

Hi Zizzle, There are at least two amino acids that promote virus's. I have researched the foods that contain one of those amino acids and will post what I found. Jon