Natural Killer Cell Responses during Human γ-Herpesvirus Infections

Münz, Christian

doi:10.3390/vaccines9060655

Cited by 7 publications

(7 citation statements)

References 125 publications

(163 reference statements)

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“…As further evidence of the disarray in NK results in CFS/ME, Rivas et al in 2018 [7] reported a lower expression of NKG2C, an activating receptor that recognizes Human Leucocyte Antigen E (HLA-E), in contrast to an earlier study where no differences were observed and with the differences attributed to frozen PMBC used in one study and whole blood in the other [47]. Importantly, altered expression of activating and inhibitory NK cell receptors are evident in chronic cytomegalovirus (CMV) infections and in coinfections with other viruses, notably Epstein-Barr virus (EBV) [48]. In patients with severe ME/CFS, defects in protein kinase gene expression in NK cells has been reported [49].…”

Section: Natural Killer Cell Analyses In Me/cfsmentioning

confidence: 83%

What Causes ME/CFS: The Role of the Dysfunctional Immune System and Viral Infections

Bansal¹

2022

J Immuno Allerg

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) remains an enigmatic highly disabling and complex long-term condition with a wide range of aetiologies and symptoms. A viral onset is commonly mentioned by patients and several bodily systems are ultimately disturbed. The parallel with long-covid is clear. However, immune dysregulation with impaired NK cell dysfunction and tendency to novel autoimmunity have been frequently reported. These may contribute to reactivation of previous acquired viruses/retrovirusesaccompanied by impaired endocrine regulation and mitochondrial energy generation. The unpredictable nature of seemingly unconnected and diverse symptoms that are poorly responsive to several allopathic and alternative therapies then contributes to an escalation of the illness with secondary dysfunction of multiple other systems. Treatment of established ME/CFS is therefore difficult and requires multi-specialty input addressing each of the areas affected by the illness.

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Section: Natural Killer Cell Analyses In Me/cfsmentioning

confidence: 83%

What Causes ME/CFS: The Role of the Dysfunctional Immune System and Viral Infections

Bansal¹

2022

J Immuno Allerg

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“…Similar to EBV, KSV infects primarily cells of the B lymphocyte lineage, where it can establish latency. It also shares with EBV an oncogenic potential, leading, in particular, to primary effusion lymphoma [165][166][167]. A role for γδ T cells in HHV-8 infections has been reported in one study [168], where patients selected for shedding HHV-8 in saliva (n = 7) were compared to seronegative controls.…”

Section: γδ and Ksv/hhv-8mentioning

confidence: 98%

“…CMV infection results in a dramatic change of the expression of NKG2A/C HLA-E-binding receptors on NK cells. NKG2A is an inhibitory receptor expressed on early differentiated NK cells, whereas NKG2C is activatory and expressed on terminally differentiated memory-like NK cells [167]. During CMV infection NKG2C + NK cells expand while NKG2A + NK cells are lost in transplant patients, but also in healthy CMV + children [218][219][220].…”

Section: Hiv-hhv Co-infectionsmentioning

confidence: 99%

The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections

Martini

Champagne

2021

Viruses

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γδ T cells are activated in viral, bacterial and parasitic infections. Among viruses that promote γδ T cell mobilisation in humans, herpes viruses (HHVs) occupy a particular place since they infect the majority of the human population and persist indefinitely in the organism in a latent state. Thus, other infections should, in most instances, be considered co-infections, and the reactivation of HHV is a serious confounding factor in attributing γδ T cell alterations to a particular pathogen in human diseases. We review here the literature data on γδ T cell mobilisation in HHV infections and co-infections, and discuss the possible contribution of HHVs to γδ alterations observed in various infectious settings. As multiple infections seemingly mobilise overlapping γδ subsets, we also address the concept of possible cross-protection.

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“…NK cells probably play a role during gammaherpesvirus infection (Münz, 2021). Accordingly, to counteract this arm of the immune response, human gammaherpesviruses have developed various strategies to evade NK cell-mediated immune responses, mostly by suppressing the signaling of activating receptors and triggering the signaling of inhibitory receptors (Münz, 2021). Multiple observations support the theory that NK cells contribute to the cellular immune response following human gammaherpesvirus infections.…”

Section: The Nk Cell-mediated Response During Ebv and Mhv68 Infectionmentioning

confidence: 99%

The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection

Rex

Zargari

Stempel

et al. 2023

Front. Cell. Infect. Microbiol.

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Immediately after entry into host cells, viruses are sensed by the innate immune system, leading to the activation of innate antiviral effector mechanisms including the type I interferon (IFN) response and natural killer (NK) cells. This innate immune response helps to shape an effective adaptive T cell immune response mediated by cytotoxic T cells and CD4+ T helper cells and is also critical for the maintenance of protective T cells during chronic infection. The human gammaherpesvirus Epstein-Barr virus (EBV) is a highly prevalent lymphotropic oncovirus that establishes chronic lifelong infections in the vast majority of the adult population. Although acute EBV infection is controlled in an immunocompetent host, chronic EBV infection can lead to severe complications in immunosuppressed patients. Given that EBV is strictly host-specific, its murine homolog murid herpesvirus 4 or MHV68 is a widely used model to obtain in vivo insights into the interaction between gammaherpesviruses and their host. Despite the fact that EBV and MHV68 have developed strategies to evade the innate and adaptive immune response, innate antiviral effector mechanisms still play a vital role in not only controlling the acute infection but also shaping an efficient long-lasting adaptive immune response. Here, we summarize the current knowledge about the innate immune response mediated by the type I IFN system and NK cells, and the adaptive T cell-mediated response during EBV and MHV68 infection. Investigating the fine-tuned interplay between the innate immune and T cell response will provide valuable insights which may be exploited to design better therapeutic strategies to vanquish chronic herpesviral infection.

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Natural Killer Cell Responses during Human γ-Herpesvirus Infections

Cited by 7 publications

References 125 publications

What Causes ME/CFS: The Role of the Dysfunctional Immune System and Viral Infections

What Causes ME/CFS: The Role of the Dysfunctional Immune System and Viral Infections

The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections

The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection

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