scholarly journals A case of recurrent herpes simplex 2 encephalitis, VZV reactivations, and dominant partial interferon-gamma-receptor-1 deficiency supports relevance of IFNgamma for antiviral defense in humans

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Julia Körholz ◽  
Nicole Richter ◽  
Jochen Schäfer ◽  
Catharina Schuetz ◽  
Joachim Roesler
Keyword(s):  
Herpes Simplex ◽  
Interferon Gamma ◽  
Viral Infections ◽  
Viral Disease ◽  
Antiviral Defense ◽  
Case Presentation ◽  
Gamma Receptor ◽  
Recurrent Herpes ◽  
Increased Susceptibility

Abstract Background Unlike infections with mycobacteria, reports of unusual viral infections in interferon-gamma-receptor (IFNγR) deficient patients are scarce. Therefore, discussion about increased susceptibility to viral infections in these patients is ongoing. Case presentation We describe a 51-year-old male with dominant partial interferon-gamma-receptor-1 (IFNγR1)-deficiency and recurrent Herpes simplex 2 meningoencephalitis as well as other viral reactivations since childhood. Conclusions This case further confirms an enhanced risk for viral disease in IFNγR-deficient patients and a role of interferon gamma for human antiviral defense.

scholarly journals Innate Immunity in Children and the Role of ACE2 Expression in SARS-CoV-2 Infection

2021 ◽  
Vol 13 (3) ◽  
pp. 363-382
Author(s):  
Mario Dioguardi ◽  
Angela Pia Cazzolla ◽  
Claudia Arena ◽  
Diego Sovereto ◽  
Giorgia Apollonia Caloro ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Viral Infections ◽  
Respiratory Infections ◽  
Viral Disease ◽  
Receptor Expression ◽  
Virus Infections ◽  
Search Terms ◽  
Bibliographic Search ◽  
Meta Analyses

COVID-19 (Coronavirus Disease 2019) is an emerging viral disease caused by the coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which leads to severe respiratory infections in humans. The first reports came in December 2019 from the city of Wuhan in the province of Hubei in China. It was immediately clear that children developed a milder disease than adults. The reasons for the milder course of the disease were attributed to several factors: innate immunity, difference in ACE2 (angiotensin-converting enzyme II) receptor expression, and previous infections with other common coronaviruses (CovH). This literature review aims to summarize aspects of innate immunity by focusing on the role of ACE2 expression and viral infections in children in modulating the antibody response to SARS-CoV-2 infection. This review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Articles deemed potentially eligible were considered, including those dealing with COVID-19 in children and providing more up-to-date and significant data in terms of epidemiology, prognosis, course, and symptoms, focusing on the etiopathogenesis of SARS-CoV-2 disease in children. The bibliographic search was conducted using the search engines PubMed and Scopus. The following search terms were entered in PubMed and Scopus: COVID-19 AND ACE2 AND Children; COVID-19 AND Immunity innate AND children. The search identified 857 records, and 18 studies were applicable based on inclusion and exclusion criteria that addressed the issues of COVID-19 concerning the role of ACE2 expression in children. The scientific literature agrees that children develop milder COVID-19 disease than adults. Milder symptomatology could be attributed to innate immunity or previous CovH virus infections, while it is not yet fully understood how the differential expression of ACE2 in children could contribute to milder disease.

scholarly journals Functional IRF3 deficiency in a patient with herpes simplex encephalitis

2015 ◽  
Vol 212 (9) ◽  
pp. 1371-1379 ◽  
Author(s):  
Line Lykke Andersen ◽  
Nanna Mørk ◽  
Line S. Reinert ◽  
Emil Kofod-Olsen ◽  
Ryo Narita ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Autosomal Dominant ◽  
Viral Infections ◽  
Herpes Simplex Encephalitis ◽  
Type I ◽  
Toll Like Receptor ◽  
Loss Of Function ◽  
Impaired Ability ◽  
Increased Susceptibility ◽  
Hsv 1

Herpes simplex encephalitis (HSE) in children has previously been linked to defects in type I interferon (IFN) production downstream of Toll-like receptor 3. Here, we describe a novel genetic etiology of HSE by identifying a heterozygous loss-of-function mutation in the IFN regulatory factor 3 (IRF3) gene, leading to autosomal dominant (AD) IRF3 deficiency by haploinsufficiency, in an adolescent female patient with HSE. IRF3 is activated by most pattern recognition receptors recognizing viral infections and plays an essential role in induction of type I IFN. The identified IRF3 R285Q amino acid substitution results in impaired IFN responses to HSV-1 infection and particularly impairs signaling through the TLR3–TRIF pathway. In addition, the R285Q mutant of IRF3 fails to become phosphorylated at S386 and undergo dimerization, and thus has impaired ability to activate transcription. Finally, transduction with WT IRF3 rescues the ability of patient fibroblasts to express IFN in response to HSV-1 infection. The identification of IRF3 deficiency in HSE provides the first description of a defect in an IFN-regulating transcription factor conferring increased susceptibility to a viral infection in the CNS in humans.

scholarly journals Immunological Aspects of Acute and Recurrent Herpes Simplex Keratitis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jacek Rolinski ◽  
Iwona Hus
Keyword(s):  
Herpes Simplex ◽  
Current Knowledge ◽  
Ocular Infection ◽  
Corneal Scarring ◽  
Recurrent Herpes ◽  
Chronic Inflammatory Reaction ◽  
Herpes Simplex Keratitis ◽  
Methods Of Treatment ◽  
Therapeutical Options

Herpes simplex keratitis (HSK) belongs to the major causes of visual morbidity worldwide and available methods of treatment remain unsatisfactory. Primary infection occurs usually early in life and is often asymptomatic. Chronic visual impairment and visual loss are caused by corneal scaring, thinning, and vascularization connected with recurrent HSV infections. The pathogenesis of herpetic keratitis is complex and is still not fully understood. According to the current knowledge, corneal scarring and vascularization are the result of chronic inflammatory reaction against HSV antigens. In this review we discuss the role of innate and adaptive immunities in acute and recurrent HSV ocular infection and present the potential future targets for novel therapeutical options based on immune interventions.

scholarly journals The Role of Tissue Resident Memory CD4 T Cells in Herpes Simplex Viral and HIV Infection

2020 ◽  
Author(s):  
Thomas Ray O'Neil ◽  
Kevin Hu ◽  
Naomi Truong ◽  
Sana Arshad ◽  
Barbara Shacklett ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex ◽  
Cd4 T Cells ◽  
Sexual Transmission ◽  
Trigeminal Ganglia ◽  
Hiv Replication ◽  
Recurrent Herpes ◽  
Resident Memory T Cells ◽  
Memory Cd4 T Cells

Tissue resident memory T cells (TRM) were first described in 2009. While initially the major focus was on CD8 TRM, there has been recently an increased interest in defining the phenotype and the role of CD4 TRM in diseases. Circulating CD4 T cells seed tissue CD4 TRM, but there also appears to be an equilibrium between CD4 TRM and blood CD4 T cells. CD4 TRM are more mobile than CD8 TRM, usually localized deeper within the dermis/lamina propria and yet may exhibit synergy with CD8 TRM in disease control. This has been demonstrated in herpes simplex infections in mice. In human recurrent herpes infections, both CD4 and CD8 TRM persisting between lesions may control asymptomatic shedding through interferon gamma secretion, although this has been more clearly shown for CD8 T cells. The exact role of the CD4/CD8 TRM axis in the trigeminal ganglia and/or cornea in controlling recurrent herpetic keratitis is unknown. In HIV, CD4 TRM have now been shown to be a major target for productive and latent infection in cervix. In HSV and HIV co-infections, CD4 TRM persisting in the dermis support HIV replication. Further understanding of the role of CD4 TRM and their induction by vaccines may help control sexual transmission by both viruses.

scholarly journals ROLE OF INFECTION IN THE ORIGIN, COURSE, RESULTS OF TREATMENT OF TOXIC GOITER

2020 ◽  
Vol 23 (2) ◽  
pp. 195-200
Author(s):  
I. V. Tereshchenko
Keyword(s):  
Herpes Simplex ◽  
Viral Infections ◽  
Autoimmune Process ◽  
Results Of Treatment ◽  
Acute Infections ◽  
Epstein Barr ◽  
Combined Infection ◽  
Simplex Virus ◽  
Toxic Goiter

To date, the question of the causes of toxic goiter has not been resolved. Purpose: to analyze the role of infection in the occurrence, course, treatment outcome of toxic goiter. Observed in the dynamics of 64 patients with toxic goiter. In 36% of cases, thyrotoxicosis manifested itself after acute infections. Foci of chronic bacterial infection were detected in 59 (92.2%) patients. Serological indices of persistence of herpes simplex virus, Epstein- Barr, cytomegalovirus (HSV, EBV, CMV) were high in all patients with suspected viral persistence (n = 20). In 1/3 of the observations a combined infection was established. The infection was cured in 34 patients. The infection was not cured in 30 patients. The observations showed that acute and chronic bacterial and viral infections can provoke the onset of toxic goiter, worsen its course, reduce the effectiveness of therapy, affecting the main link in the pathogenesis of the disease - the activity of the autoimmune process in the thyroid gland. Infection exacerbations stimulate the production of AT-rTTG, leading to relapses thyrotoxicosis. Conclusion: although infection is not the main etiological factor of toxic goiter, its role in the manifestation, course of toxic goiter, the effectiveness of therapy, and the distant prognosis is undeniable. Starting treatment for toxic goiter, in including planning surgical treatment or radioiodine therapy, it is necessary to identify and sanitize foci of infection, to check the possible persistence of common viruses of herpes simplex, Epstein-Barr, cytomegalovirus. This will improve the prognosis, reduce the high risks of thyrotoxicosis relapses.

scholarly journals Dysfunctional Senescent Herpes Simplex Virus Specific CD57+CD8+ T cells are Associated with Recurrent Symptomatic Herpes in Humans

2022 ◽  
Author(s):  
Lbachir BenMohamed ◽  
Arif A. Khan ◽  
Ruchi Srivastava ◽  
Hawa Vahed
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cd8 T Cells ◽  
High Frequency ◽  
Recurrent Herpes ◽  
Natural Protection ◽  
Simplex Virus ◽  
And Function

Herpes simplex virus (HSV)-specific CD8+ T cells protect mice from herpes infection and disease. However, the phenotype and function of HSV-specific CD8+ T cells that play a key role in the "natural" protection seen in HSV-1-seropositive healthy asymptomatic (ASYMP) individuals (who have never had clinical herpes disease) remain to be determined. We previously reported that symptomatic (SYMP) patients (who have frequent bouts of recurrent herpes disease) had more less-differentiated and dysfunctional HSV-specific CD8+ T cells. In contrast, healthy ASYMP individuals maintained a significantly higher proportion of differentiated polyfunctional CD8+ T cells. Here we report that, HSV-specific CD8+ T cells from SYMP patients, but not from ASYMP individuals, have phenotypic and functional characteristics of cellular senescence, including: (i) high frequency of senescent (CD57+) and exhausted (PD-1+) CD8+ T cells; (ii) late terminally differentiated (KLRG1+), non-proliferating CD8+ T cells; (iii) HSV-specific CD8+ T cells were declined overtime and were not maintained homeostatistically (CD127+CD8+ T cells); (iv) loss of co-stimulatory molecule (CD28)on HSV-specific CD8+ T cells; (v) decreased production of effector molecules (granzyme B and perforin) by HSV-specific CD8+ T cells. Our findings provide insights into the role of senescence in HSV-specific CD8+ T cells in susceptibility to recurrent herpes and have implications for T-cell-based immunotherapeutic strategies against recurrent herpes in humans.

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