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Krooniset bakteeri-infektiot (Luettu 191533 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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Re: Krooniset bakteeri-infektiot
Vastaus #323 - 22.09.2017 - 15:54:20
 
Epstein-Barr virus, cytomegalovirus, and multiple sclerosis susceptibility

http://www.neurology.org/content/early/2017/08/30/WNL.0000000000004412


Abstract

Objective: To determine whether Epstein-Barr virus (EBV) or cytomegalovirus (CMV) seropositivity is associated with multiple sclerosis (MS) in blacks and Hispanics and to what extent measures of the hygiene hypothesis or breastfeeding could explain these findings. EBV and CMV have been associated with MS risk in whites, and the timing and frequency of both viruses vary by factors implicated in the hygiene hypothesis.

Methods: Incident cases of MS or its precursor, clinically isolated syndrome (CIS), and matched controls (blacks, 111 cases/128 controls; Hispanics, 173/187; whites, 235/256) were recruited from the membership of Kaiser Permanente Southern California. Logistic regression models accounted for HLA-DRB1*1501 status, smoking, socioeconomic status, age, sex, genetic ancestry, and country of birth.

Results: Epstein-Barr nuclear antigen-1 (EBNA-1) seropositivity was independently associated with an increased odds of MS/CIS in all 3 racial/ethnic groups (p < 0.001 for blacks and whites, p = 0.02 for Hispanics). In contrast, CMV seropositivity was associated with a lower risk of MS/CIS in Hispanics (p = 0.004) but not in blacks (p = 0.95) or whites (p = 0.96). Being born in a low/middle-income country was associated with a lower risk of MS in Hispanics (p = 0.02) but not after accounting for EBNA-1 seropositivity. Accounting for breastfeeding did not diminish the association between CMV and MS in Hispanics.

Conclusions: The consistency of EBNA-1 seropositivity with MS across racial/ethnic groups and between studies points to a strong biological link between EBV infection and MS risk. The association between past CMV infection and MS risk supports the broader hygiene hypothesis, but the inconsistency of this association across racial/ethnic groups implies noncausal associations.
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Re: Krooniset bakteeri-infektiot
Vastaus #324 - 08.10.2017 - 13:38:15
 
Multiple sclerosis: an example of pathogenic viral interaction?

https://virologyj.biomedcentral.com/articles/10.1186/s12985-017-0719-3

Abstract

A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen. Such virally induced T-cell responses might secondarily also lead to local autoimmune phenomena. Finally, research recommendations are formulated for substantiating the hypothesis on several levels: epidemiologically, genetically, and viral expression in the brain.
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Conclusion

A link is postulated between HHV-6A and EBV in the aetio-pathogenesis of MS.

In summary, the tenet is that infection with the neurotropic HHV-6A leads to transformation of latently EBV-infected B-cells in the CNS. Both viruses will elicit a T-cell response, either specific towards HHV-6A and EBV, or non-specific as a response to the HERV-K18-encoded superantigen. Such viral induced T-cell responses might secondarily also lead to autoimmune phenomena. Evidence for mechanisms for induction of autoimmunity by viral infections has recently been reviewed [56].
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Re: Krooniset bakteeri-infektiot
Vastaus #325 - 08.10.2017 - 13:44:43
 
How seemingly acute viral infections can persist

https://www.sciencedaily.com/releases/2017/10/171006085921.htm

October 6, 2017
Infections caused by viruses, such as respiratory syncytial virus, or RSV, measles, parainfluenza and Ebola, are typically considered acute. These viruses cause disease quickly and live within a host for a limited time. But in some cases the effects of the infection, and presence of the virus itself, can persist. RSV, for example, can lead to chronic respiratory problems, measles can lead to encephalitis and the Ebola virus can be transmitted by patients thought to be cured of the disease.

New findings from the University of Pennsylvania suggest a mechanism that may explain how viruses can linger. Products of viral infection called defective viral genomes, DVGs for short, which have been known to be involved in triggering an immune response, can also kick off a molecular pathway that keeps infected cells alive, the researchers discovered. The study used a novel technique to examine the presence of DVGs on a cell-by-cell basis to show that DVG-enriched cells had strategies to survive in the face of an immune-system attack.

"One of the things the field has known for a long time is that DVGs promote persistent infections in tissue culture," said Carolina B. López, an associate professor of microbiology and immunology in Penn's School of Veterinary Medicine. "But the question was, How do you reconcile that with the fact that they're also very immunostimulatory? How can they help clear virus at the same time as they promote persistence? Our work helps explain this apparent paradox."

López was senior author on the work, teaming with co-lead authors and lab members Jie Xu and Yan Sun. Fellow coauthors included Gordon Ruthel and Daniel Beiting of Penn Vet, Yize Li and Susan R. Weiss of Penn's Perelman School of Medicine and Arjun Raj of the School of Engineering and Applied Science. Their study was published in Nature Communications.

DVGs have been a major focus of López's lab for years. These partial viral genomes are produced in infected cells when a virus begins to replicate rapidly, leading to defective versions of itself that contain large deletions. Once thought not to have any biological function, DVGs are increasingly believed to be important components of viral infections.

In 2013, López and colleagues reported that DVGs were critical in stimulating an immune response to respiratory viruses in mice; when DVGs were depleted from a virus, mice had more severe infections. In 2015 they reported that DVGs are also critical for stimulating an immune response to the human virus RSV, also demonstrating for the first time that the presence of DVGs in human respiratory samples from infected patients correlates with enhanced antiviral immune responses.

In the current work, López's team used a sophisticated technique that allowed them to differentiate full-length genomes from the partial genomes of DVGs at the single-cell level. They studied cells in culture infected with the Sendai virus, or with RSV, a virus that often affects infants and can lead to chronic respiratory problems,

Labeling the full-length genomes in red and the partial DVGs in green, the researchers found differences from cell to cell. Some cells had hardly any DVGs, while others were highly enriched with DVGs, with only a small number of full-length genomes.

"We saw this in many different cell lines and even in infected lungs in mice," López said. "We hadn't appreciated before that there is a lot of heterogeneity in what is going on with these DVGs."

To dig deeper into how the DVGs were influencing the course of infection, the researchers infected cells either with a version of the Sendai virus that lacked DVGs or one enriched in DVGs. The cells infected with the virus high in DVGs survived more than twice as long as those infected with virus lacking DVGs. Adding purified DVGs boosted the cells' survival time, indicating a direct role for the DVGs in promoting cell survival.

The results were similar in parallel experiments with RSV, suggesting that the pro-survival role of DVGs held across viral types.

The researchers next were curious to know what molecular pathways might enable the DVG-rich cells to avoid apoptosis. An analysis of highly-expressed genes in DVG-enriched cells compared to the cells with full-length viral genomes revealed that a host of pro-survival genes were activated in the DVG-rich cells. Notably, these genes encoded signaling proteins of the TNF pathway, known to both boost immunity and cell survival, and IFN, known to play a role in antiviral immunity.

A final set of experiments elucidated the mechanism by which a subset of DVG-enriched cells persisted during viral infection. López and colleagues found that signaling through the proteins MAVS and TNF receptor 2 protects infected cells from apoptosis that is otherwise triggered by TNF?.

"We found this dual role for TNF during these infections," López said. "If TNF binds to a cell that doesn't have the MAVS pathway engaged but is infected, the cell is killed, but, if the cell does have this pathway engaged, then it is protected. MAVS is engaged during the antiviral response, and only cells that have a lot of DVGs activate this pathway. These data show that our cells are wired to survive if they are engaged in an antiviral response, explaining the paradoxical functions of DVGs. It seems that in order to persist, the virus is taking advantage of these host pathways that are there to promote the survival of cells working to eliminate the virus."

The results, though limited to in vitro studies in the current report, point to a way that DVGs could enable "acute" viral infections to linger.

López hopes to build on these findings to be sure they hold in vivo. She's also curious to learn more about the dual roles of TNF, which may help explain why the use of TNF-targeted therapies hasn't always turned out as expected.

"I want to see if there's a way we can harness this pathway to minimize and avoid the persistence of these viruses, which is really relevant if we think about the chronic diseases associated with some of these respiratory viruses," López said.

In addition, she would like to explore how generalizable this pathway is and if it could, perhaps, help explain the problems with viral persistence seen in such infections with the Ebola and Zika viruses.
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