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Commentaries

A safe and efficient BCG vectored vaccine to prevent the disease caused by the human Respiratory Syncytial Virus

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Pages 2092-2097 | Received 02 May 2017, Accepted 19 May 2017, Published online: 24 Jul 2017

Figures & data

Figure 1. Immune response induced by hRSV in absence or presence of the recombinant rBCG-N-hRSV vaccine. hRSV induce an aberrant immune response due to the erratic T cell polarization, producing a high pro-inflammatory and allergic-like response (A). On the other hand, the rBCG-N-hRSV induces an effective immune response that could control the infection through the polarization of CD4+ and CD8+ T cells and neutralizing antibodies decreasing the recruitment of immune cells such as neutrophils, eosinophils and the mucus secretion (B).

Figure 1. Immune response induced by hRSV in absence or presence of the recombinant rBCG-N-hRSV vaccine. hRSV induce an aberrant immune response due to the erratic T cell polarization, producing a high pro-inflammatory and allergic-like response (A). On the other hand, the rBCG-N-hRSV induces an effective immune response that could control the infection through the polarization of CD4+ and CD8+ T cells and neutralizing antibodies decreasing the recruitment of immune cells such as neutrophils, eosinophils and the mucus secretion (B).

Figure 2. Proposed mechanism of the rBCG-N-hRSV vaccine that controls the hRSV-infection. Subsequent to the rBCG-N-hRSV infection and the viral infection, the events goes as follows. (1) Immunological synapsis between the APC (Dendritic cells) and T cells. (2) TH-1 response polarization and secretion of IFN-γ by CD4+ and CD8+ T cells. (3) Activation of B cells by the T cells. (4) Antibodies secretion by plasma cells with the proper neutralizing isotype. (5) Cytotoxic activity of the CD8+ T cell and depletion of infected-cells. (6) A TH-17 profile induction suggests a possible way of control for the exacerbated TH-1 response. (7) Possible IL-27 secretion and proliferation of CD4+ T cells and induction of IFN-γ secretion. (8) IL-27 secretion could inhibit the TH-17 response. (9) Relation between the TH-17+ Treg that might decrease the hRSV-pathology.

Figure 2. Proposed mechanism of the rBCG-N-hRSV vaccine that controls the hRSV-infection. Subsequent to the rBCG-N-hRSV infection and the viral infection, the events goes as follows. (1) Immunological synapsis between the APC (Dendritic cells) and T cells. (2) TH-1 response polarization and secretion of IFN-γ by CD4+ and CD8+ T cells. (3) Activation of B cells by the T cells. (4) Antibodies secretion by plasma cells with the proper neutralizing isotype. (5) Cytotoxic activity of the CD8+ T cell and depletion of infected-cells. (6) A TH-17 profile induction suggests a possible way of control for the exacerbated TH-1 response. (7) Possible IL-27 secretion and proliferation of CD4+ T cells and induction of IFN-γ secretion. (8) IL-27 secretion could inhibit the TH-17 response. (9) Relation between the TH-17+ Treg that might decrease the hRSV-pathology.

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