Immune Response against Yellow Fever Virus

The immune response against yellow fever virus involves a sophisticated interaction between the **innate immune system** (e.g., production of type I and type II interferons, activation of monocytes and dendritic cells) and the **adaptive immune system** (robust responses from CD4+ and CD8+ T lymphocytes and long-lasting neutralizing antibodies from B cells)[1][2][3][5]. Vaccination with the live-attenuated YF-17D virus provides strong, durable immunity through activation of both antibody and T cell responses, with neutralizing IgG antibodies remaining detectable for decades. Early responses include IFN-γ and activation of CLEC5A+ monocytes, and later phases are marked by memory T and B cell development. Drugs directly targeting the virus, such as BDAA, can inhibit viral replication and alter the immune response by exposing viral RNA to innate sensors[4]. **Note:** This entry does not describe a single molecular target but encompasses an entire host response. Canonical molecular immune targets relevant for intervention or study might include "Type I interferon receptor", "C-type lectin domain containing 5A (CLEC5A)", or "Yellow fever virus envelope protein," but "Immune response against Yellow Fever Virus" is not a discrete target and should be re-specified if granular molecular-level data is required[1][2][3][4][5].

Other names

Yellow fever immune responseYellow fever virus immunityImmune reaction to yellow fever

Yellow fever vaccine induces both humoral (antibody-mediated) and cellular (T cell-mediated) immune responses, providing protective immunity that can last for decades by stimulating production of neutralizing antibodies and memory T cells[1][2][3][5]. BDAA disrupts the yellow fever virus replication organelles, directly inhibiting viral replication and enhancing cytokine responses by exposing viral RNA to intracellular sensors (RIG-I, MDA5)[4].