Manipulation of the Innate Immune Response by Varicella Zoster Virus

Gerada, Chelsea; Campbell, Tessa Mollie; Kennedy, Jarrod John; McSharry, Brian P.; Steain, Megan; Slobedman, Barry; Abendroth, Allison

doi:10.3389/fimmu.2020.00001

Cited by 341 publications

(423 citation statements)

References 173 publications

(241 reference statements)

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“…The viral infection could also further promote inhibition of inflammatory signaling pathways causing immunosuppression [ 57 ]. Recently, Bouwman and colleagues reported that JAK/STAT signaling system could be a valuable indicator of a strong immune response to SARS-CoV-2 infections [ 58 ]. Interestingly, another report stated that the inhibition of the JAK/STAT pathway could reduce the hyperinflammatory conditions but not the viral clearance [ 59 ].…”

Section: Role Of Jak/stat Signaling Pathway In the Immune Systemmentioning

confidence: 99%

JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy

Satarker

Tom²,

Shaji³

et al. 2020

Postgraduate Medicine

121

117

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As the incidence of COVID-19 increases with time, more and more efforts are made to pave a way out for the therapeutic strategies to deal with the disease progression. Inflammation being a significant influencer has implicated us to re-look into its signaling cascades drawing attention towards the JAK/STAT pathway. Considered as a major signaling mediator of cytokines and chemokines, the JAK/STAT pathway has significantly contributed to the worsening of COVID-19. JAK phosphorylation mediated by cytokine receptor activation leads to phosphorylation of STATs that translocate into the nucleus to translate for inflammatory mediators. The SARS-CoV-2 infection triggers the inflammation via the JAK/STAT pathway mainly through its structural and non-structural proteins leading towards the development of cytokine storms. This produces various inflammatory markers in the host that determine the disease severity. Therefore, inhibiting JAK/STAT signaling with JAK/STAT inhibitors like Ruxolitinib, Baricitinib, Tofacitinib could hamper the inflammatory cascade and reduce inflammation. Even though they are implicated with multiple adverse effects, the regulatory authorities have supported its use, and numerous clinical trials are in progress to prove their safety and efficacy. On the contrary, the exact mechanism of JAK/STAT inhibition at molecular levels remains to be speculative for which further investigations are required.

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Section: Role Of Jak/stat Signaling Pathway In the Immune Systemmentioning

confidence: 99%

JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy

Satarker

Tom²,

Shaji³

et al. 2020

Postgraduate Medicine

121

117

View full text Add to dashboard Cite

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“…Although NETosis is a very powerful mechanism fighting for the infection, the ability of NETs to damage tissues is well-documented in infection and sterile disease. NETs directly kill epithelial and endothelial cells [11,38], and excessive NETosis damages the epithelium in pulmonary fungal infection [12] and the endothelium in transfusion-related acute lung injury [39].…”

Section: Ag Proteins and Their Role In Netosismentioning

confidence: 99%

Proteins associated with neutrophil degranulation are upregulated in nasopharyngeal swabs from SARS-CoV-2 patients

et al. 2020

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COVID-19 or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) appeared throughout the World and currently affected more than 9 million people and caused the death of around 470,000 patients. The novel strain of the coronavirus disease is transmittable at a devastating rate with a high rate of severe hospitalization even more so for the elderly population. Naso-oro-pharyngeal swab samples as the first step towards detecting suspected infection of SARS-CoV-2 provides a non-invasive method for PCR testing at a high confidence rate. Furthermore, proteomics analysis of PCR positive and negative nasooropharyngeal samples provides information on the molecular level which highlights disease pathology. Samples from 15 PCR positive cases and 15 PCR negative cases were analyzed with nanoLC-MS/MS to identify the differentially expressed proteins. Proteomic analyses identified 207 proteins across the sample set and 17 of them were statistically significant. Protein-protein interaction analyses emphasized pathways like Neutrophil degranulation, Innate Immune System, Antimicrobial Peptides. Neutrophil Elastase (ELANE), Azurocidin (AZU1), Myeloperoxidase (MPO), Myeloblastin (PRTN3), Cathepsin G (CTSG) and Transcobalamine-1 (TCN1) were found to be significantly altered in naso-oropharyngeal samples of SARS-CoV-2 patients. The identified proteins are linked to alteration in the innate immune system specifically via neutrophil degranulation and NETosis.

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“…In sharp contrast, VZV-infected iDCs do not undergo apoptosis, suggesting that VZV benefits from viable directly infected iDCs for virus dissemination and persistence [70,110]. In this regard, VZV selectively downregulates Fas on the surface of infected iDCs and mDCs, very likely to inhibit apoptosis of these cells [111].…”

Section: Herpesviruses Modulate Cell Survival Of Idcsmentioning

confidence: 99%

How Human Herpesviruses Subvert Dendritic Cell Biology and Function

Popella¹,

Steinkasserer²

2021

Innate Immunity in Health and Disease

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In the last decades, a multitude of distinct herpesvirus-mediated immune evasion mechanisms targeting dendritic cell (DC) biology were uncovered. Within this chapter, we summarize the current knowledge how herpesviruses, especially the α-herpesviruses HSV-1, HSV-2, varicella-zoster virus (VZV), and the β-herpesvirus HCMV, shape and exploit the function of myeloid DCs in order to hamper the induction of potent antiviral immune responses. In particular, the main topics covering herpesvirus-mediated immune evasion will involve: (i) the modulation of immature DC (iDC) phenotype, (ii) modulation of iDC apoptosis, (iii) the inhibition of DC maturation, (iv) degradation of the immune-modulatory molecule CD83 in mature DCs (mDCs), (v) interference with the negative regulator of β2 integrin activity, cytohesin-1 interaction partner (CYTIP), (vi) resulting in modulation of adhesion and migration of mDCs, (vii) autophagic degradation of lamins to support productive HSV-1 replication in iDCs, (viii) the release of uninfectious L-particles with immune-modulatory potential from HSV-1-infected mDCs, and (ix) the implications of DC subversion regarding T lymphocyte activation.

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Manipulation of the Innate Immune Response by Varicella Zoster Virus

Cited by 341 publications

References 173 publications

JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy

JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy

Proteins associated with neutrophil degranulation are upregulated in nasopharyngeal swabs from SARS-CoV-2 patients

How Human Herpesviruses Subvert Dendritic Cell Biology and Function

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