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

Martini, Fanny; Champagne, Éric

doi:10.3390/v13122372

Cited by 5 publications

(5 citation statements)

References 309 publications

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“… 23 Some studies have demonstrated that a high incidence of herpesvirus reactivation is associated with patients admitted to the intensive care unit for severe COVID‐19. 24 , 25 Thus, according to de evidence, it is not preposterous to hypothesize that the SARS‐CoV‐2 virus might be a biological trigger agent for this autoimmune condition. 21 However, long‐term studies will shed light on this hypothesis to determine the possible etiopathogenic role of SARS‐CoV‐2 as a trigger agent for achalasia.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, Facco et al have identified an oligoclonal lymphocytic infiltrate within the LES of achalasia patients with the ability to recognize human HSV‐1 antigens associated with increased proliferation and Th1‐type cytokines release 23 . Some studies have demonstrated that a high incidence of herpesvirus reactivation is associated with patients admitted to the intensive care unit for severe COVID‐19 24,25 . Thus, according to de evidence, it is not preposterous to hypothesize that the SARS‐CoV‐2 virus might be a biological trigger agent for this autoimmune condition 21 .…”

Section: Discussionmentioning

confidence: 99%

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Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Neurogastroenterology Motil

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Background Achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and induces the disease in a genetically susceptible host. The association between achalasia and coronaviruses has not been reported. Aims To evaluate the presence of the SARS‐CoV‐2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter muscle (LESm) of achalasia patients who posteriorly had SARS‐CoV‐2 (achalasia‐COVID‐19) infection before laparoscopic Heller myotomy (LHM) and compare the findings with type II achalasia patients and transplant donors (controls) without COVID‐19. Methods The LESm of 7 achalasia‐COVID‐19 patients (diagnosed by PCR), ten achalasia patients, and ten controls without COVID‐19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and effector CD4 T cell and regulatory subsets were determined by immunohistochemistry. Key Results Coronavirus was detected in 6/7 patients‐COVID‐19. The SARS‐CoV‐2 was undetectable in the LESm of the achalasia patients and controls. ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post‐COVID‐19. The percentage of Th22/Th17/Th1/pDCreg was higher in achalasia and achalasia‐COVID‐19 pre‐HLM vs. controls. The Th2/Treg/Breg cell percentages were higher only in achalasia vs. controls. Conclusion & Inferences SARS‐CoV2 and its receptor expression in the LESm of achalasia patients who posteriorly had COVID‐19 but not in the controls suggests that it could affect the myenteric plexus. Unlike achalasia, patients‐COVID‐19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Neurogastroenterology Motil

View full text Add to dashboard Cite

show abstract

“…24 Some studies have demonstrated that a high incidence of herpesvirus reactivation is associated in patients admitted to the intensive care unit for severe COVID-19. 25,26 Thus, according to de evidence, it is not preposterous to hypothesize that the SARS-CoV-2 virus might be a biological trigger agent for this autoimmune condition. 22 However, long-term studies will shed light on this hypothesis to determine the possible etiopathogenic role of SARS-CoV-2 as a trigger agent for achalasia.…”

Section: Discussionmentioning

confidence: 99%

Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Preprint

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Introduction: Previous studies have suggested that achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and, in a genetically susceptible host, induces the disease. The association between achalasia and coronaviruses has not been reported in the literature. Objective: To evaluate the presence of the SARS-CoV-2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter (LES) muscle of patients with achalasia who had SARS-CoV-2 infection before laparoscopic Heller myotomy (LHM) and compare the findings with patients with type II achalasia and transplant donors (controls) without COVID-19. Material and Methods: The LES muscle of 7 patients with achalasia who had SARS-CoV-2 infection before LHM (diagnosed by PCR), ten patients with achalasia, and ten transplant donors (controls) without COVID-19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and CD4 T cell and regulatory subsets were determined by immunohistochemistry. Results: All patients had type II achalasia. Coronavirus was detected in 6/7 patients who had COVID-19. The SARS-CoV-2 was undetectable in the LES muscle of the achalasia patients and transplant donors (controls). The ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post-COVID-19. The percentage of Th22, Th17, Th1, and pDCreg was higher in achalasia and achalasia-COVID-19 pre-HLM vs. transplant donors. The Th2, Treg, and Breg cell percentages were higher only in achalasia vs. transplant donors. Conclusion: The presence of the SARS-CoV2 and its receptor in the LES muscle of patients with type II achalasia who had COVID-19 pre-LHM but not in the controls suggests that it could affect the myenteric plexus. Unlike patients with achalasia, patients who had COVID-19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.

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“…42 Children with uncomplicated malaria showed an increased expression of CD16 + on Vδ1 + T cells, although there was a possibility of co-infection with cytomegalovirus, which is known to induce CD16 + -expressing Vδ1 + T cells. 43 Therefore, further studies are needed to investigate role of coexisting infection in Vδ1 + T-cell response.…”

Section: Response Of Human γδ T Cells To Plasmodium Parasitesmentioning

confidence: 99%

γδ T‐cell–mediated immune responses to malaria

Bayarsaikhan

Ibraheem

Inoue

2023

Microbiology and Immunology

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Malaria is one of the deadliest infectious diseases. Licensed vaccine have demonstrated just over 30% efficacy, and therefore, developing new vaccine candidates and understanding immune responses to Plasmodium have become necessary. γδ T cells have been suggested to be associated with immune responses to malaria due to the observation of their expansion in patients with malaria and experimental models of malaria. γδ T cells act as both “innate‐like” and “adaptive‐like” cells during immune response to malaria. Studies have found that γδ T cells can recognize Plasmodium phosphoantigen, present the antigen, and initiate adaptive immune response during blood‐stage Plasmodium infection. Recent reports also suggested the phagocytic and cytotoxic potential of γδ T cells. Furthermore, γδ T cells can provide protection upon immunization with whole parasite. In addition, γδ T cells during the liver‐stage infection were able to prevent experimental cerebral malaria. Despite these new findings, questions related to γδ T‐cell response during Plasmodium infection remain to be answered. However, investigating these cells in humans remains difficult in many ways; in this regard, rodent models of malarial infection enable us to study these cells in more detail. Insights from experimental malaria models give rise to new cues for development of malarial vaccine and adjunctive therapy for severe malaria. Here, we review our current knowledge of γδ T‐cell immune function in human and experimental mouse malarial infection models; especially, we focus on the mechanisms underlying γδ T cells that are associated with protective immunity during malarial infection.

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

Cited by 5 publications

References 309 publications

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?

γδ T‐cell–mediated immune responses to malaria

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