Different curdlan sulfates were synthesized by modification of curdlan with sulfur trioxide-pyridine complex, and the one with the highest sulfur content (9.23 ± 0.16) %, CS3, was used to study the immunomodulating effect on murine RAW264.7 macrophages and bone marrow derived dendritic cells (BMDCs). The results showed that the treatment of macrophages with CS3 could not only increase the nitric oxide (NO) release and the cytokines TNF-α, IL-6 and IL-1β production significantly, but also enhance the inducible NOS (iNOS) expression, NF-κBp65 nuclear translocation, Erk1/2 and SAPK/JNK phosphorylation. The combination of CS3 with GM-CSF upregulated immature BMDCs to express major histocompatibility complex II (MHCII) and CD11c surface markers, CD40, CD80 and CD86 costimulatory molecules, as well as the cytokines of IL-12p70 and IL-6. The surface plasmon resonance (SPR) analysis found that CS3 exhibited binding affinity against dectin-1. These results suggested that curdlan sulfate can possibly be developed as a new immunotherapy agent and anti-viral vaccine adjuvant.

Frontiers in Immunology

A viral vaccine design harnessing prior BCG immunization confers protection against Ebola virus

Article

Author: Wirchnianski, Ariel S ; Porcelli, Steven A ; Marzi, Andrea ; Ng, Tony W ; Jacobs, William R ; Saavedra-Ávila, Noemí A ; Furuyama, Wakako ; Johndrow, Christopher T ; Chandran, Kartik

Previous studies have demonstrated the efficacy and feasibility of an anti-viral vaccine strategy that takes advantage of pre-existing CD4+ helper T (Th) cells induced by Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccination. This strategy uses immunization with recombinant fusion proteins comprised of a cell surface expressed viral antigen, such as a viral envelope glycoprotein, engineered to contain well-defined BCG Th cell epitopes, thus rapidly recruiting Th cells induced by prior BCG vaccination to provide intrastructural help to virus-specific B cells. In the current study, we show that Th cells induced by BCG were localized predominantly outside of germinal centers and promoted antibody class switching to isotypes characterized by strong Fc receptor interactions and effector functions. Furthermore, BCG vaccination also upregulated FcγR expression to potentially maximize antibody-dependent effector activities. Using a mouse model of Ebola virus (EBOV) infection, this vaccine strategy provided sustained antibody levels with strong IgG2c bias and protection against lethal challenge. This general approach can be easily adapted to other viruses, and may be a rapid and effective method of immunization against emerging pandemics in populations that routinely receive BCG vaccination.

Infection and Drug Resistance

Immunity Cell Responses to RSV and the Role of Antiviral Inhibitors: A Systematic Review

Review

Author: Abebe, Lulu ; Churiso, Gemechu ; Bulbula, Denebo ; Husen, Gose

Antigen-presenting cells recognize respiratory syncytial virus antigens, and produce cytokines and chemokines that act on immune cells. Dendritic cells play the main role in inflammatory cytokine responses. Similarly, alveolar macrophages produce IFN-β, IFN-α, TNF-α, IL-6, CXCL10, and CCL3, while alternatively activated macrophages differentiate at the late phase, and require IL-13 or IL-4 cytokines. Furthermore, activated NKT cells secrete IL-13 and IL-4 that cause lung epithelial, endothelial and fibroblasts to secrete eotaxin that enhances the recruitment of eosinophil to the lung. CD8⁺ and CD4⁺T cells infection by the virus decreases the IFN-γ and IL-2 production. Despite this, both are involved in terminating virus replication. CD8⁺T cells produce a larger amount of IFN-γ than CD4⁺T cells, and CD8⁺T cells activated under type 2 conditions produce IL-4, down regulating CD8 expression, granzyme and IFN-γ production. Antiviral inhibitors inhibit biological functions of viral proteins. Some of them directly target the virus replication machinery and are effective at later stages of infection; while others inhibit F protein dependent fusion and syncytium formation. TMC353121 reduces inflammatory cytokines, TNF-α, IL-6, and IL-1β and chemokines, KC, IP-10, MCP and MIP1-α. EDP-938 inhibits viral nucleoprotein (N), while GRP-156784 blocks the activity of respiratory syncytial virus ribonucleic acid (RNA) polymerase. PC786 inhibits non-structural protein 1 (NS-1) gene, RANTES transcripts, virus-induced CCL5, IL-6, and mucin increase. In general, it is an immune reaction that is blamed for the disease severity and pathogenesis in respiratory syncytial virus infection. Anti-viral inhibitors not only inhibit viral entry and replication, but also may reduce inflammatory cytokines and chemokines. Many respiratory syncytial virus inhibitors are proposed; however, only palivizumab and ribavirin are approved for prophylaxis and treatment, respectively. Hence, this review is focused on immunity cell responses to respiratory syncytial virus and the role of antiviral inhibitors.

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Indication	Highest Phase	Country/Location	Organization	Date
COVID-19	Preclinical	GB	Bio Immunitas Ltd.	26 Jun 2024

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