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Autoimmunity and Immune Pathological Aspects of Virus Disease
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
H. Wege, R. Dörries, P. Massa, R. Watanabe
Clinical diseases caused by LCM virus are only rarely observed in humans. The infection is transmitted from mice or hamsters and may lead to typical lymphocytic choriomeningitis, to acute meningoencephalomyelitis, or to influenza-like syndromes. The majority of patients develop a benign course without further sequelae. It is not known if the disease in humans involves immune pathological mechanisms.2,89 LCM virions are composed of four structural proteins and contain a negative-stranded RNA genome made of two segments. Virus strains differ widely in their ability to induce acute and chronic diseases based on persistent infections of lymphocytes, hormone-producing cells, and neural cells. Analysis of reassortant viruses has recently helped to map different pathogenic properties of the genome.7,8,90
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Aseptic Meningitis Acute lymphocytic choriomeningitis. A clinical condition characterized by signs of meningeal irritation and sterile cerebrospinal fluid. Described by Arvid Johan Wallgren (1889–1973) of Stockholm in 1924. The causative virus was identified by Charles Armstrong (1886–1967) and Ralph Dougall Lillie (b 1896) in 1934. Several viruses including lymphocytic choreomeningitis virus, ECHO virus and coxsackie virus were later identified as causes.
Arenaviruses and Neurovirology
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
In 1934, reports (Armstrong and Lillie 1934; Armstrong and Wooley 1935) began to appear of a previously undescribed virus causing neurological disease in man. The original isolation was discovered during passage, in monkeys, of an agent from brain tissue of an individual who died in St. Louis, Missouri, during an encephalitis epidemic in 1933. In monkeys and subsequently in mice, the pathology found was a lymphocytic meningitis, most prominent in the choroid plexus structure in the ventricles of the brain where cerebrospinal fluid is produced, consisting of modified ependymal cells. Because of the histopathologic appearance, the agent was called lymphocytic choriomeningitis virus. Although fatal cases of infection were well represented in the initial cases, the most common disease state recognized due to LCM was a benign, self-limited meningitis.
Original antigen sin and COVID-19: implications for seasonal vaccination
Published in Expert Opinion on Biological Therapy, 2022
Original antigenic sin has also been reported with human immunodeficiency virus (HIV) [54]. Haynes and colleagues observed primer-induced antibody suppression using an HIV peptide envelope immunogen in BALB/c mice consistent with original antigenic sin [55]. Interestingly, reversing the sequence of antigen exposure completely overcame HIV primer-induced antibody suppression. The immunologic mechanism has remained opaque, but it is thought that original antigenic sin may be due to faulty cytotoxic T lymphocytes that impair clearance of viruses and may enhance the immune escape of mutant viruses evolving within an individual host [56,57]. Klenerman and colleagues found that mice primed with lymphocytic choriomeningitis virus (LCMV) respond to a subsequent infection by a novel variant with a cytotoxic T cell response directed against the initial epitope rather than against the new variant epitope [58].
Next-generation immunotherapy for solid tumors: combination immunotherapy with crosstalk blockade of TGFβ and PD-1/PD-L1
Published in Expert Opinion on Investigational Drugs, 2022
Hue Tu Quach, Zhaohua Hou, Rebecca Y. Bellis, Jasmeen K. Saini, Alfredo Amador-Molina, Prasad S. Adusumilli, Yuquan Xiong
Additionally, PD-1/PD-L1 ligation is also involved in TGFβ production. Up-regulated PD-1 signaling upon PD-L1 ligation or TCR engagement promote naïve T-cell polarization to regulatory phenotypes and function, resulting in TGFβ-level augmentation [97] (Figure 2). A ‘PD-1-FoxO1-PD-1’ positive feedback loop in CTL during lymphocytic choriomeningitis virus (LCMV) infection was described [24]. First, FoxO1 directly binds to Pdcd1 promotor and promotes the expression of PD-1 in exhausted CD8 + T Cells, indicating FoxO1 role in PD-1 induction for the terminal differentiation of exhausted CTL. Furthermore, impaired mTOR activation results in enhanced FoxO1 activity and blockade of PD-1 in vivo increases mTOR activation. Since PD-L1 triggers PD-1 signaling AKT, mTOR, and S6 activation, it can be concluded that PD-1 maintains FoxO1 activation and facilitates its interaction with the PD-1 promoter by suppression of mTOR/S6 and following FoxO1 phosphorylation. In this model, the level of PD-1 increases even though the nuclear translocation of NFATc1 and NF-kB, which are downstream of TCR-CD28 stimulation, would be proximally inhibited by PD-1/PD-L1.
Live-attenuated lymphocytic choriomeningitis virus-based vaccines for active immunotherapy of HPV16-positive cancer
Published in OncoImmunology, 2020
Sarah Schmidt, Weldy V. Bonilla, Andrea Reiter, Felix Stemeseder, Theresa Kleissner, Daniel Oeler, Ursula Berka, Ahmed El-Gazzar, Bettina Kiefmann, Sophie C. Schulha, Josipa Raguz, Mohamed Habbeddine, Marilies Scheinost, Xiaoping Qing, Henning Lauterbach, Igor Matushansky, Daniel D. Pinschewer, Klaus K. Orlinger
To date, active immunization has not induced consistent efficacy as cancer immunotherapy in clinical Phase III trials.16-18 The goal of immunotherapy by cancer vaccines is to achieve large numbers of CTLs infiltrating and targeting tumor tissues and to establish memory cells for lasting tumor control. From this perspective, replicating viral vaccines, which can deliver tumor-associated antigens in the context of viral infection, are well suited to fulfill this task. Previously, we have demonstrated the potential of this strategy by generating a stably attenuated, replicating lymphocytic choriomeningitis virus (LCMV)-based vector.19 LCMV, the prototype member of the arenavirus family, was chosen primarily for its ability to elicit potent effector CTL responses, life-long CTL immunity and because LCMV-based vectors have demonstrated the capacity to induce tumor regression in a CD8+ T cell-dependent manner.19,20 In addition, LCMV has low seroprevalence in humans21,22 and the glycosylation of its surface protein renders the host neutralizing Ab response inefficient, which allows for re-administrations of the vector.19,23 The replication-competent, stably attenuated LCMV vector can deliver tumor-associated antigens to professional antigen-presenting cells to induce potent CTL responses and triggers the release of alarmin IL-33 from lymphoid stroma cells resulting in a superior effector CTL response than that induced by replication-deficient LCMV vectors.19