Modulatory effects on dendritic cells by human herpesvirus 6

Gustafsson, Rasmus; Svensson, Mattias; Fogdell‐Hahn, Anna

doi:10.3389/fmicb.2015.00388

Cited by 6 publications

(5 citation statements)

References 60 publications

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“…Given that HHV‐6A can infect oligodendrocytes, it is possible that it directs the immune system against this host cell by incorporation of host cell proteins and lipids in its membrane [32] and thus specifically directs the immune system against the oligodendrocytes. However, upon inoculation with HHV‐6A the most potent activator of T‐cells (i.e., dendritic cells) lose their capacity to activate T‐cell proliferation [33,34] suggesting that the hypothesis of host cell protein incorporation and molecular mimicry, which requires that the virus constitutes an adjuvant effect, is somewhat problematic. Fortunately, the virus is not able to completely avoid immune detection and serological responses are indeed mounted against HHV‐6A, as seen in the present study as well as previous studies.…”

Section: Discussionmentioning

confidence: 99%

Epstein–Barr virus infection after adolescence and human herpesvirus 6A as risk factors for multiple sclerosis

Biström

Jons

Engdahl

et al. 2020

Euro J of Neurology

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Background and purposeInfections with human herpesvirus 6A (HHV‐6A) and Epstein–Barr virus (EBV) have been linked to multiple sclerosis (MS) development. For EBV, late infection has been proposed as a risk factor, but serological support is lacking. The objective of this study was to investigate how age affects the EBV and HHV‐6A associated risks of developing MS.MethodsIn this nested case–control study, Swedish biobanks were accessed to find pre‐symptomatically collected blood samples from 670 individuals who later developed relapsing MS and 670 matched controls. A bead‐based multiplex assay was used to determine serological response against EBV and HHV‐6A. Conditional logistic regression was used to calculate odds ratios and 95% confidence intervals.ResultsSeropositivity against EBV exhibited a pattern where associations switched from a decreased risk of developing MS in the group below 20 years of age to an increased risk amongst individuals aged 20–29 and 30–39 years (p for trend 0.020). The age of transition was estimated to be 18.8 years. In contrast, HHV‐6A was associated with increased MS risk in all age groups (total cohort odds ratio 2.1, 95% confidence interval 1.6–2.7).ConclusionsThis study suggests EBV infection after adolescence and age independent HHV‐6A infection as risk factors for MS.

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Section: Discussionmentioning

confidence: 99%

Epstein–Barr virus infection after adolescence and human herpesvirus 6A as risk factors for multiple sclerosis

Biström

Jons

Engdahl

et al. 2020

Euro J of Neurology

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“…Both the molecular mimicry and the host cell incorporation model relies on the idea that HHV-6 virion can trigger the T cell stimulatory capacity of APC. However, we and others have shown that inoculation of DC with both HHV-6A and HHV-6B instead hamper the capacity of DC to activate T cells, both in absence and presence of viral replication, and for both allogenic and autologous T cells ( 74 – 79 ). Hence, HHV-6 induced pathogenesis in MS does not seem to occur through neither of these models.…”

Section: Hhv-6 In Msmentioning

confidence: 72%

Human Herpesvirus 6A Is a Risk Factor for Multiple Sclerosis

Lundström

Gustafsson

2022

Front. Immunol.

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The role for human herpesvirus (HHV)-6A or HHV-6B in multiple sclerosis (MS) pathogenesis has been controversial. Possibly because the damage of the virus infection may occur before onset of clinical symptoms and because it has been difficult to detect active infection and separate serological responses to HHV-6A or 6B. Recent studies report that in MS patients the serological response against HHV-6A is increased whereas it is decreased against HHV-6B. This effect seems to be even more pronounced in MS patients prior to diagnosis and supports previous studies postulating a predomination for HHV-6A in MS disease and suggests that the infection is important at early stages of the disease. Furthermore, HHV-6A infection interacts with other factors suspected of modulating MS susceptibility and progression such as infection with Epstein-Barr virus (EBV) and Cytomegalovirus (CMV), tobacco smoking, HLA alleles, UV irradiation and vitamin D levels. The multifactorial nature of MS and pathophysiological role for HHV-6A in inflammation and autoimmunity are discussed.

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“…However, DC can also be targets for viral infections, and with their antigen capturing capacity may be exposed to large amounts of virions. HHV-6A and 6B are very successful viruses that most people have been exposed to, as seen with a high seroprevalence in the human population [ 9 ] and have developed various specific viral immune-escape mechanisms that can hamper the ability of DC to activate T cells [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

Human Herpesvirus 6A Induces Dendritic Cell Death and HMGB1 Release without Virus Replication

Gustafsson

2021

Pathogens

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Human herpesvirus 6A (HHV-6A) is a common virus that has important immunomodulatory effects. Dendritic cells (DC) are key players in innate and adaptive immunity and are implicated in the pathogenesis of many human diseases, including infections. (1) Background: Previous studies have demonstrated suppressive effects of HHV-6A on key DC functions. (2) Methods: human monocyte derived dendritic cells were inoculated with HHV-6A and viral replication, cell viability, and release of high mobility group box 1 (HMGB1) protein from DC and of the cytokines IL-2, IL-4, IL-6, IL-10, TNF and IFN-γ after co-culture with allogenic CD4+ T cells were assessed. (3) Results: Nonproductive infection of HHV-6A in DC leads to titer-dependent cell death and the release of HMGB1 protein, and a Th2 polarization. (4) Conclusion: These immune responses aimed to clear the infection may also imply risks for inflammatory pathologies associated with HHV-6A such as multiple sclerosis.

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Modulatory effects on dendritic cells by human herpesvirus 6

Cited by 6 publications

References 60 publications

Epstein–Barr virus infection after adolescence and human herpesvirus 6A as risk factors for multiple sclerosis

Epstein–Barr virus infection after adolescence and human herpesvirus 6A as risk factors for multiple sclerosis

Human Herpesvirus 6A Is a Risk Factor for Multiple Sclerosis

Human Herpesvirus 6A Induces Dendritic Cell Death and HMGB1 Release without Virus Replication

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