Probing Reconstituted Human Immune Systems in Mice With Oncogenic γ-Herpesvirus Infections

Münz, Christian

doi:10.3389/fimmu.2020.581419

Cited by 3 publications

(3 citation statements)

References 82 publications

(131 reference statements)

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“…During the evaluation of vaccines against most pathogens, challenge experiments in animal models are considered the gold standard for the final assessment of vaccine efficacy ( 137 – 141 ). However, due to the restricted host tropism of EBV, a human herpesvirus, there is a limited range of susceptible candidate animal models ( 142 – 144 ) ( Figure 3 ).…”

Section: Evaluation Systems For Vaccinesmentioning

confidence: 99%

The Status and Prospects of Epstein–Barr Virus Prophylactic Vaccine Development

et al. 2021

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Epstein–Barr virus (EBV) is a human herpesvirus that is common among the global population, causing an enormous disease burden. EBV can directly cause infectious mononucleosis and is also associated with various malignancies and autoimmune diseases. In order to prevent primary infection and subsequent chronic disease, efforts have been made to develop a prophylactic vaccine against EBV in recent years, but there is still no vaccine in clinical use. The outbreak of the COVID-19 pandemic and the global cooperation in vaccine development against SARS-CoV-2 provide insights for next-generation antiviral vaccine design and opportunities for developing an effective prophylactic EBV vaccine. With improvements in antigen selection, vaccine platforms, formulation and evaluation systems, novel vaccines against EBV are expected to elicit dual protection against infection of both B lymphocytes and epithelial cells. This would provide sustainable immunity against EBV-associated malignancies, finally enabling the control of worldwide EBV infection and management of EBV-associated diseases.

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Section: Evaluation Systems For Vaccinesmentioning

confidence: 99%

The Status and Prospects of Epstein–Barr Virus Prophylactic Vaccine Development

et al. 2021

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“…On the other hand, since it has developed a variety of mechanisms to evade the host immune system [ 15 , 30 ], HHV8 may lead to the proliferation of infected cells, up to cancer development [ 19 ]. The kinetics of virus‐associated disease progression depends on the balance of power between host immune defenses and the virus [ 26 ]. HHV8 is considered an oncogenic virus mainly in a favorable context, such as immunosuppression.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory KIR2DL2 receptor and HHV-8 in classic or endemic Kaposi sarcoma

et al. 2022

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KIR2DL2, an inhibitory Killer cell Immunoglobulin-like Receptor (KIR), has been shown to predispose to the development of several herpesvirus-associated diseases by inhibiting the efficiency of Natural Killer (NK) cells against virus-infected cells. The aim of this observational study was to assess the prevalence of KIR2DL2 and Human Herpes Virus 8 (HHV8) in patients affected with classical and endemic Kaposi sarcoma (KS), as well as in controls. Blood samples collected from 17 Caucasian, HIV-negative, immunocompetent patients affected with classical KS (c-KS), 12 African, HIV-negative patients with endemic KS (e-KS), 83 healthy subjects and 26 psoriatic patients were processed for genotypization by PCR for two KIR alleles, such as KIR2DL2 and KIR2DL3 and analyzed for HHV-8 presence. The totality of both c-KS and e-KS patients presented HHV-8 infection, whereas HHV8 was found in 26.9% of psoriatic subjects and 19.3% of healthy subjects. KIR2DL2 was found in the 76.5% of c-KS subjects, while the receptor was found in 41.7% of the e-KS group, 34.6% of psoriatic patients and 43.4% of healthy controls (p < 0.0001). A significantly higher prevalence of KIR2DL2 in c-KS patients than in all the other subjects was also confirmed comparing age-matched groups. Based on these results, the inhibitory KIR2DL2 genotype appears to be a possible cofactor which increases the risk of developing c-KS in HHV8-positive, immunocompetent subjects, while it seems less relevant in e-KS pathogenesis.

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“…We have intentionally omitted discussion of KSHV manipulation of cytokine expression and signaling from this work as it is complex, and we have recently reviewed the topic comprehensively elsewhere (Alomari and Totonchy, 2020). Moreover, we have omitted discussion of humanized mouse models for KSHV infection as they have also been reviewed very recently (Münz, 2020).…”

Section: Introductionmentioning

confidence: 99%

Molecular Virology of KSHV in the Lymphocyte Compartment—Insights From Patient Samples and De Novo Infection Models

Aalam

Totonchy

2020

Front. Cell. Infect. Microbiol.

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The incidence of Kaposi’s sarcoma-associated herpesvirus (KSHV)-associated Kaposi Sarcoma has declined precipitously in the present era of effective HIV treatment. However, KSHV-associated lymphoproliferative disorders although rare, have not seen a similar decline. Lymphoma is now a leading cause of death in people living with HIV (PLWH), indicating that the immune reconstitution provided by antiretroviral therapy is not sufficient to fully correct the lymphomagenic immune dysregulation perpetrated by HIV infection. As such, novel insights into the mechanisms of KSHV-mediated pathogenesis in the immune compartment are urgently needed in order to develop novel therapeutics aimed at prevention and treatment of KSHV-associated lymphoproliferations. In this review, we will discuss our current understanding of KSHV molecular virology in the lymphocyte compartment, concentrating on studies which explore mechanisms unique to infection in B lymphocytes.

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Probing Reconstituted Human Immune Systems in Mice With Oncogenic γ-Herpesvirus Infections

Cited by 3 publications

References 82 publications

The Status and Prospects of Epstein–Barr Virus Prophylactic Vaccine Development

The Status and Prospects of Epstein–Barr Virus Prophylactic Vaccine Development

Inhibitory KIR2DL2 receptor and HHV-8 in classic or endemic Kaposi sarcoma

Molecular Virology of KSHV in the Lymphocyte Compartment—Insights From Patient Samples and De Novo Infection Models

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