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Krooniset bakteeri-infektiot (Luettu 189384 kertaa)
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Re: Krooniset bakteeri-infektiot
Vastaus #315 - 21.04.2017 - 16:08:53
 
EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model.

https://www.ncbi.nlm.nih.gov/pubmed/27836419

Dec 2016

Abstract

Multiple sclerosis (MS) is thought to be initiated by the interaction of genetic and environmental factors, eliciting an autoimmune attack on the central nervous system. Epstein-Barr virus (EBV) is the strongest infectious risk factor, but an explanation for the paradox between high infection prevalence and low MS incidence remains elusive. We discuss new data using marmosets with experimental autoimmune encephalomyelitis (EAE) - a valid primate model of MS. The findings may help to explain how a common infection can contribute to the pathogenesis of MS. We propose that EBV infection induces citrullination of peptides in conjunction with autophagy during antigen processing, endowing B cells with the capacity to cross-present autoantigen to CD8+CD56+ T cells, thereby leading to MS progression.
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Re: Krooniset bakteeri-infektiot
Vastaus #316 - 12.05.2017 - 16:35:34
 
Cancer-causing virus masters cell's replication, immortality
Epstein-Barr virus steers the B-cell to hide in plain sight


https://www.sciencedaily.com/releases/2017/05/170502204538.htm

May 2, 2017
Viruses are notorious for taking over their host's operations and using them to their own advantage. But few human viruses make themselves quite as cozy as the Epstein-Barr virus, which can be found in an estimated nine out of ten humans without causing any ill effects.

That is, until this virus causes mononucleosis in adolescents or various cancers of the lymph nodes, including Hodgkin's and non-Hodgkin's lymphomas, in immune compromised people.

In a paper appearing in the open access journal eLife, a team of researchers from Duke's School of Medicine details just how the Epstein-Barr virus manages to persist so well inside the immune system's B cells, a type of white blood cell that is normally responsible for recognizing and responding to foreign invaders.

"The challenge is that it's a really efficient pathogen," and evades the host's immune system well even when it's recognized as an invader, said Micah Luftig, an associate professor of molecular genetics and microbiology and co-author on the new study.

Luftig's team has found that with a few select chemical signals used early in the course of an infection, Epstein-Barr mimics the beginning of the B cell's normal response to an infectious agent. From within, the virus manages to ramp up the B-cell's reproduction of itself, while at the same time helping the cell resist its own self-destruct signals.

"The virus actually taps into the B cell's normal protection against apoptosis," the programmed cell death that takes B cells out of circulation, Luftig said.

Once the infection is established, Epstein-Barr prefers to hide out in what are known as "memory B cells," relatively slowly reproducing cells that circulate throughout the body. "All of this is about establishing latency," Luftig said, or the ability to hide quietly in plain sight.

Using a new technique developed elsewhere called BH3 profiling that allowed them to test the critical cellular pro- and anti-apoptosis proteins individually, the team was able to see which of these the virus was controlling and then watch the transition from an uninfected cell to the active early infection phase to the latent infection in an immortal cell. The key piece they've uncovered is a viral protein called EBNA3A which manages apoptosis resistance in infected B cells.

The risk for cancers "is largely an issue if you're immune suppressed," Luftig said. But, for example, a recent National Cancer Institute study found that children who receive organ transplants have a 200-times higher chance of getting Non-Hodgkin's Lymphoma, one of the cancers caused by Epstein-Barr.

The team thinks BH3 profiling could prove useful in guiding treatment decisions on Epstein-Barr associated cancers such as these.




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Re: Krooniset bakteeri-infektiot
Vastaus #317 - 26.05.2017 - 18:22:39
 
Evaluation of reactive Epstein-Barr virus (EBV) in Iranian patients with different subtypes of multiple sclerosis (MS)

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-867020130002000...

March/April 2013

ABSTRACT

OBJECTIVES: Epstein-Barr virus has been recently associated with the onset of multiple sclerosis, yet understanding how it elicits autoimmunity remains elusive. We investigated the relation between Epstein-Barr virus reactivation and disease development in different subtypes of multiple sclerosis.

METHODS: In the present research, we have determined the Epstein-Barr virus-DNA load by quantitative real-time polymerase chain reaction and Epstein-Barr virus antibody levels by EIA technique in both multiple sclerosis patients (n = 78) and healthy controls (n = 123).

RESULTS: Our results demonstrated increased titer of both anti-Epstein-Barr virus-IgG and IgM antibodies in patients (91.02% vs 82.11% in controls, p < 0.001 and 14.1% vs 4.06% in controls, p < 0.001, respectively). Overall, Epstein-Barr virus reactivation was found in 68.75% of subtypes of multiple sclerosis, 4.54% of multiple sclerosis primary subtype, and in only 3.25% of healthy control subjects. Moreover, in samples of patients with disease relapse (exacerbation) cell free viral DNA was elevated in contrast to other patients (p < 0.001).

CONCLUSIONS: These findings provide further support for the detrimental effects of Epstein- Barr virus in the reactivation of multiple sclerosis attacks.
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Re: Krooniset bakteeri-infektiot
Vastaus #318 - 02.06.2017 - 13:54:24
 
Time correlation between mononucleosis and initial symptoms of MS

http://nn.neurology.org/content/4/3/e308.full.pdf

ABSTRACT
Objective:
To determine the average age of MS onset vs the age at which Epstein-Barr infection has previously occurred and stratify this analysis by sex and the blood level of Epstein-Barr nuclear antigen 1 (EBNA1) antibody.

Methods:
Using infectious mononucleosis (IM) as a temporal marker in data from the Swedish epidemiologic investigation of MS, 259 adult IM/MS cases were identified and then augmented to account for “missing” childhood data so that the average age of MS onset could be determined for cases binned by age of IM (as stratified by sex and EBNA1 titer level).

Results:
Mean age of IM vs mean age of MS reveals a positive time correlation for all IM ages (from 5to 30 years), with IM-to-MS delay decreasing with increased age. When bifurcated by sex or EBNA1 blood titer levels, males and high-titer subpopulations show even stronger positive time correlation, while females and low-titer populations show negative time correlation in early childhood (long IM/MS delay). The correlation becomes positive in females beyond puberty.

Conclusions:
IM/MS time correlation implies causality if IM is time random. Alternative confounding models seem implausible, in light of constraints imposed by time-invariant delay observed here. Childhood infection with Epstein-Barr virus (EBV) in females and/or those genetically prone to low EBNA1 blood titers will develop MS slowly. Males and/or high EBNA1-prone develop MS more rapidly following IM infection at all ages. For all, postpubescent EBV infection is critical for the initiation and rapid development of MS.

Neurol Neuroimmunol Neuroinflamm 2017;4:e308; doi:10.1212/
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Re: Krooniset bakteeri-infektiot
Vastaus #319 - 16.06.2017 - 20:35:24
 
Suomessa, Jyväskylän yliopistossa, on kehitetty testi borrelioosin ja lisäinfektioiden testaamiseen EU:n tuella. Testi on ollut käytössä Saksassa Arminlabsissa toukokuun alusta. Yhdellä testillä voi selvitä onko borrelioosi, clamydia pneumonia jne. Maailmalla on tulossa monia samankaltaisia testejä, esimerkiksi sen tutkimiseen sairastaako viruksen tai bakteerin aiheuttamaa infektiota.Eli tämä on aika kehittynyttä teknologiaa. Olen kuullut että Suomessa ainakaan infektiolääkärit eivät hyväksy testin tuloksia. Itselläni on taas aika tutkituttaa infektiotilanne, ja  tämä on yksi vaihtoehto. Kokonaiskuvan saamiseen tämä on halvin, yhden tai kahden infektion tutkimiseen kallis (n. 500€)

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Our technology is intended to tests for both early and late Lyme Disease and other tick-borne diseases. Our tests facilitate healthcare providers to test up to 20 tick-borne disease microbes against multiple antibody types that aids in pinpointing not only the causative agent for a patient’s illness but also the stage of illness, thus our tests are a multiplex and multi-functional diagnostic kits. Furthermore, the kits are equipped very specific antigens to enable detection at a higher sensitivity than ever before. Lastly, Te?teds digital healthcare solution is intended to deliver processed results to clinicians in order to expedite convenience and ease. Our vision is to establish our products as the standard for diagnosing tick-borne diseases so that patients no longer need to compromise with their quality of life and living standards. We truly believe if the patient can be tested the patient can be treated.

http://tezted.com/#focus
https://www.arminlabs.com/en/news/tickplex
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Re: Krooniset bakteeri-infektiot
Vastaus #320 - 12.07.2017 - 17:31:02
 
Hidden herpes virus may play key role in MS, other brain disorders

https://www.sciencedaily.com/releases/2017/07/170710122959.htm

July 10, 2017

The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain's ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.

"While latent HHV-6 -- which can be found in cells throughout the brain -- has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases," said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. "These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin."

It is estimated that more than 80 percent of people have been exposed to HHV6 at some point during their early childhood. HHV-6 is the most common human herpesvirus and infections that occur during childhood often go unnoticed but the virus can cause roseola, which is characterized by a fever and rash in infants. A much smaller number -- one percent of people -have congenital HHV6 where a single copy of the virus is acquired through either the father's sperm or mother's egg and is passed on to the developing child.

While the immune system fights off the most active forms of the infection, the virus never truly leaves our bodies and can reactivate later in life. The herpesvirus 6 accomplishes this form of latency by integrating itself into our genetic code and thus hiding in cells and evading the immune system.

One of the first studies to show an association between latent HHV-6 infection and demyelinating disorders was conducted in 2003 by URMC researchers David Mock, M.D., who is a co-author of the current study, Andrew Goodman, M.D. and others. They noted that HHV6 genetic code could be found in the brain cells of individuals with severe forms of multiple sclerosis.

Viruses have long been suspected to contribute to multiple sclerosis, a disorder in which the body's own immune system attacks and destroys myelin -- the fatty tissue that insulates the connections between nerve cells. However, while the 2003 study indicated that the herpes virus played some role in multiple sclerosis, it has subsequently become clear that the virus is unlikely to trigger the disease.

The Rochester researchers in the current paper took a new approach and asked instead whether the virus could have an impact on a critical support cell found in the brain called oligodendrocyte progenitor cells (OPCs). These cells play an important role in maintaining the brain's supply of myelin. When myelin is lost to disease, age, or injury, OPCs are activated, migrate to where they are needed, and mature into myelin-producing cells which repair the damage.

The researchers examined the impact of the latent HHV-6 on the activity of human OPCs, which was possible through the work of Chris Proschel, a co-author of the manuscript with expertise in the generation of human OPCs. One of the ways the virus stays hidden in cells is by expressing a protein called U94 that helps it keep its place in the human DNA and remain undetected from the immune system. By studying human cells and transplanting human OPCs into animal models, the team discovered that when U94 was expressed in OPCs, the cells stopped migrating to where they were needed.

What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?

"More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases," said Mayer-Proschel. "But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases."
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Re: Krooniset bakteeri-infektiot
Vastaus #321 - 29.07.2017 - 19:34:01
 
Quantitative Detection of Epstein-Barr Virus DNA in Cerebrospinal Fluid and Blood Samples of Patients with Relapsing-Remitting Multiple Sclerosis

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0094497

April 10, 2014

Abstract

The presence of Epstein-Barr Virus (EBV) DNA in cerebrospinal fluid (CSF) and peripheral blood (PB) samples collected from 55 patients with clinical and radiologically-active relapsing-remitting MS (RRMS) and 51 subjects with other neurological diseases was determined using standardized commercially available kits for viral nucleic acid extraction and quantitative EBV DNA detection. Both cell-free and cell-associated CSF and PB fractions were analyzed, to distinguish latent from lytic EBV infection. EBV DNA was detected in 5.5% and 18.2% of cell-free and cell-associated CSF fractions of patients with RRMS as compared to 7.8% and 7.8% of controls; plasma and peripheral blood mononuclear cells (PBMC) positivity rates were 7.3% and 47.3% versus 5.8% and 31.4%, respectively. No significant difference in median EBV viral loads of positive samples was found between RRMS and control patients in all tested samples. Absence of statistically significant differences in EBV positivity rates between RRMS and control patients, despite the use of highly sensitive standardized methods, points to the lack of association between EBV and MS disease activity.
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Tämä tutkimus ei siis löytänyt yhteyttä EBV-viruksen ja MS:n välillä. Toiset tutkimukset ovat löytäneet yhteyden, joten potilaat vaan joutuvat odottamaan jonkinlaista selvyyttä.
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Re: Krooniset bakteeri-infektiot
Vastaus #322 - 05.08.2017 - 16:36:33
 
Programmed death 1 is highly expressed on CD8+CD57+ T cells in patients with stable multiple sclerosis and inhibits their cytotoxic response to EBV.

Cencioni MT1, Magliozzi R1,2, Nicholas R1,3, Ali R1,3, Malik O1,3, Reynolds R1, Borsellino G4, Battistini L4, Muraro P1,3.

https://www.ncbi.nlm.nih.gov/pubmed/28767147


Abstract

Growing evidence points to a deregulated response to Epstein-Barr virus (EBV) in the CNS of patients with Multiple Sclerosis (pwMS) as a possible cause of disease. In this study, we have investigated the response of a subpopulation of effector CD8+ T cells to EBV in 36 healthy donors and in 35 pwMS in active and inactive disease. We have measured the expression of markers of degranulation, the release of cytokines, cytotoxicity and the regulation of effector functions by inhibitory receptors, such as programmed death-1 (PD-1) and human inhibitor receptor Ig-like transcript 2 (ILT2). We demonstrate that polyfunctional cytotoxic CD8+CD57+ T cells are able to kill EBV-infected cells in healthy donors. In contrast, an anergic exhaustion-like phenotype of CD8+CD57+ T cells with high expression of PD-1 was observed in inactive pwMS compared with active pwMS or healthy donors. Detection of CD8+CD57+ T cells in meningeal inflammatory infiltrates from post-mortem MS tissue confirmed the association of this cell phenotype with the disease pathological process. The overall results suggest that ineffective immune control of EBV in pwMS during remission may be one factor preceding and enabling the reactivation of the virus in the CNS and may cause exacerbation of the disease.
This article is protected by copyright. All rights reserved.
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Itselläni CD8+ testattiin keväällä pyynnöstäni Tallinnassa ja heinäkuussa testautin CD57+ arvot uudelleen, tällä kertaa myös Tallinnassa. Kuten oletin, testien mukaan CD8 on selvästi minimitason alapuolella. CD57 on testattu säännöllisesti Saksassa liittyen krooniseen borrelioosiin, ja se on ollut olematon kunnes viime vuonna ponnisti minimiin ja on pysynyt siellä. Aikoinaan MS-diagoosin yhteydessä tutkittiin paljon eri viruksia, muttei EBV:tä. Eikä otettu borrelioosi verikokeita, eikä borrelioosi DNA:ta selkäydinnesteestä. Itse asiassa borrelioosin diagnoosi on kliininen (koska verikokeet eivät ole täysin luotettavia), mutta minua ei tutkinut infektiolääkäri, joka olisi poissulkenut borrelioosin. Kliininen diagnoosi tapahtui vasta myöhemmin, kun lähdin asiaa itse selvittämään.
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