The Immune Response to Viral Infections

Nash, Anthony; Dutia, Bernadette M.

doi:10.1002/9780470688618.taw0220

Cited by 3 publications

(3 citation statements)

References 151 publications

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“…Moreover, HSV, Cytomegalovirus (CMV), Epstein Barr virus (EBV), and HIV are able to disrupt the crucial step of antigen presentation. Some viruses, especially those who belong in the Herpesviridae family, become latent, and can reactivate later in response to stress or immunosuppression [ Table 2 ; ( 73 )].…”

Section: Pathogenesis Of Severe De Novo Viral Infementioning

confidence: 99%

Update in Viral Infections in the Intensive Care Unit

et al. 2021

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The advent of highly sensitive molecular diagnostic techniques has improved our ability to detect viral pathogens leading to severe and often fatal infections that require admission to the Intensive Care Unit (ICU). Viral infections in the ICU have pleomorphic clinical presentations including pneumonia, acute respiratory distress syndrome, respiratory failure, central or peripheral nervous system manifestations, and viral-induced shock. Besides de novo infections, certain viruses fall into latency and can be reactivated in both immunosuppressed and immunocompetent critically ill patients. Depending on the viral strain, transmission occurs either directly through contact with infectious materials and large droplets, or indirectly through suspended air particles (airborne transmission of droplet nuclei). Many viruses can efficiently spread within hospital environment leading to in-hospital outbreaks, sometimes with high rates of mortality and morbidity, thus infection control measures are of paramount importance. Despite the advances in detecting viral pathogens, limited progress has been made in antiviral treatments, contributing to unexpectedly high rates of unfavorable outcomes. Herein, we review the most updated data on epidemiology, common clinical features, diagnosis, pathogenesis, treatment and prevention of severe community- and hospital-acquired viral infections in the ICU settings.

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Section: Pathogenesis Of Severe De Novo Viral Infementioning

confidence: 99%

Update in Viral Infections in the Intensive Care Unit

et al. 2021

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“…As part of the innate immune response within the infection microenvironment, type I interferon (IFN), and tumor necrosis factor (TNF) initiate anti‐viral responses by triggering the production of anti‐viral proteins (Ivashkiv & Donlin, 2014; Thompson, Kaminski, Kurt‐Jones, & Fitzgerald, 2011). Simultaneous activation of the adaptive immune response through T H and T C cells, and subsequent secretion of interleukin (IL)‐12 and IL‐4‐dependent signaling provides effective Th1/Th2 balance against invading pathogens (Nash & Dutia, 2010). However, the dysregulated immune response has been reported in several viral infections such as influenza, Ebola, hantavirus, and severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) which leads to severe symptoms such as anaphylactic shock, trauma, local tissue damage, and multi‐organ failure (Jain, Khaiboullina, & Baranwal, 2020; Martynova et al, 2021; Tang et al, 2020; Tisoncik et al, 2012; Younan et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Antiinflammatory phytochemicals against virus‐induced hyperinflammatory responses: Scope, rationale, application, and limitations

Baranwal

Gupta

Dey

et al. 2021

Phytotherapy Research

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Uncontrolled inflammatory responses or cytokine storm associated with viral infections results in deleterious consequences such as vascular leakage, severe hemorrhage, shock, immune paralysis, multi‐organ failure, and even death. With the emerging new viral infections and lack of effective prophylactic vaccines, evidence‐based complementary strategies that limit viral infection‐mediated hyperinflammatory responses could be a promising approach to limit host tissue injury. The present review emphasizes the potentials of antiinflammatory phytochemicals in limiting hyperinflammatory injury caused by viral infections. The predominant phytochemicals along with their mechanism in limiting hyperimmune and pro‐inflammatory responses under viral infection have been reviewed comprehensively. How certain phytochemicals can be effective in limiting hyper‐inflammatory response indirectly by favorably modulating gut microbiota and maintaining a functional intestinal barrier has also been presented. Finally, we have discussed improved systemic bioavailability of phytochemicals, efficient delivery strategies, and safety measures for effective antiinflammatory phytotherapies, in addition to emphasizing the requirement of tightly controlled clinical studies to establish the antiinflammatory efficacy of the phytochemicals. Collectively, the review provides a scooping overview on the potentials of bioactive phytochemicals to mitigate pro‐inflammatory injury associated with viral infections.

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“…The first one assumed intratumoral LV injections every two days and the end of the experiment on the 6th day from the start of the study. Since adaptive antiviral response takes about one week to develop ( 29 ), at this timepoint, an immune response after the use of LVs may be observed, but the elimination of transduced cells should not occur yet. In the second scheme, the interval between the first and second administrations of LVs was extended to 6 days, in order to check whether repeated administration of the vectors after the development of the adaptive immune response induced by the first injection would also be effective in reducing the concentration of IL-10 in the TME, which was measured on the 10th day after the first LV application.…”

Section: Discussionmentioning

confidence: 99%

Treatment with lentiviral vectors encoding shRNA against interleukin 10 modulates the immunosuppressive activity of murine colon carcinoma‑associated myeloid‑derived suppressor cells

et al. 2021

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Myeloid-derived suppressor cells (MDSCs) are potent suppressors of antitumor immunity and their accumulation is often associated with poor prognosis. The aim of the present study was to determine the mechanisms of action of lentiviral vectors encoding short hairpin (sh)RNA against interleukin-10 (IL-10), with particular emphasis on their influence on the activity of tumor-derived MDSCs. Lentiviral vectors encoding shRNA against IL-10 (shIL-10 LVs) were utilized to silence the expression of IL-10 either in MDSCs that were generated ex vivo from bone marrow cells cultured in the presence of supernatant from MC38 colon carcinoma cells, or in situ in the MC38 murine colon carcinoma environment. Although monocytic MDSCs (M-MDSCs) transduced with shIL-10 LVs exhibited increased suppressor activity, transduction of polymorphonuclear MDSCs (PMN-MDSCs) appeared to reduce their ability to inhibit T lymphocyte functions. Analysis of EGFP expression in MC38 tumors revealed that intratumorally inoculated shIL-10 LVs transduced tumor-infiltrating myeloid cells with the highest efficiency and, led to a decreased IL-10 level in the tumor microenvironment. However, the effect was accompanied by increased influx of PMN-MDSCs into tumors observed both on the 6th and on the 10th day after shIL-10 LV injections. Nevertheless, it was noted that suppressor activity of myeloid cells isolated from tumors was dependent on the efficiency of tumor-derived PMN-MDSC transduction with shIL-10 LVs. The increased percentage of transduced PMN-MDSCs on the 10th day was associated with diminished immunosuppressive activity of tumor-derived myeloid cells and an elevated ratio of cytotoxic T lymphocytes to M-MDSCs. The obtained data indicated that treatment with shIL-10 LVs may result in modulation of the immunosuppressive activity of MC38 colon carcinoma-derived MDSCs.

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The Immune Response to Viral Infections

Cited by 3 publications

References 151 publications

Update in Viral Infections in the Intensive Care Unit

Update in Viral Infections in the Intensive Care Unit

Antiinflammatory phytochemicals against virus‐induced hyperinflammatory responses: Scope, rationale, application, and limitations

Treatment with lentiviral vectors encoding shRNA against interleukin 10 modulates the immunosuppressive activity of murine colon carcinoma‑associated myeloid‑derived suppressor cells

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