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  1. Nov 24, 2020 · The pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility.

  2. Apr 22, 2024 · The Dengue virus 3’ UTR stimulates translation through both cap-dependent and cap-independent mechanisms. Furthermore, the 3’ stem-loop structure complements this process by enhancing polysome formation.

  3. Dec 15, 2021 · Potential antiviral mechanism and molecular targets of the bioactive compounds inhibiting viral entry and replication of dengue virus. Infection of virus involves various stages: In the initial steps, DENV binds to cell receptors including mannose-binding receptor (MR) and DC-SIGN (dendritic cell-specific ICAM3 grabbing nonintegrin) receptor ...

    • 10.1155/2021/4224816
    • 2021
    • Biomed Res Int. 2021; 2021: 4224816.
  4. May 1, 2024 · Bleeding following dengue virus infection occurs due to multiple mechanisms including platelet activation by NS1, serotonin, and PAF, accompanied by a wide range of other coagulation abnormalities.

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  6. Nov 19, 2023 · The Life Cycle of Dengue Virus. (Dengue virus enters the host by receptor-mediated endocytosis, which subsequently results in the fusion of vesicular and viral membranes. This fusion allows the secretion of genomic RNA into the cytoplasm, which plays a role as mRNA for replication and translation.

  7. Jan 15, 2023 · FcR-dependent ADE is the most common mechanism for a wide range of virus infection such as HIV, influenza A, dengue and Ebola. Cells which have FcR such as monocytes, B cells, neutrophils and macrophages are easily attached by the virus-antibody complexes because the Fc region of the antibody will bind on the cell surface with FcR which leads ...

  8. Dengue virus gains entry into the host organism through the skin following an infected mosquito bite. Humoral, cellular, and innate host immune responses are implicated in the progression of the illness and the more severe clinical signs occur following the rapid clearance of the virus from the host organism.

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