Prior immunization of hamsters with three heterologous flaviviruses (Japanese encephalitis virus [JEV] SA14-2-8 vaccine, wild-type St. Louis encephalitis virus [SLEV], and Yellow fever virus [YFV] 17D vaccine) reduces the severity of subsequent West Nile virus (WNV) infection. Groups of adult hamsters were immunized with each of the heterologous flaviviruses; approximately 30 days later, the animals were injected intraperitoneally with a virulent New York strain of WNV. Subsequent levels of viremia, antibody response, and deaths were compared with those in nonimmune (control) hamsters. Immunity to JEV and SLEV was protective against clinical encephalitis and death after challenge with WNV. The antibody response in the sequentially infected hamsters also illustrates the difficulty in making a serologic diagnosis of WNV infection in animals (or humans) with preexisting Flavivirus immunity.
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http://dx.doi.org/10.3201/eid0803.010238 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
November 2024
Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, CDMX 07360, México.
Zika virus (ZIKV) infection has been associated with damage to neural stem cells in microcephaly in newborns. The virus possesses specific tropism for glioma stem cells mediated by the ZIKV E protein. This infection causes endoplasmic reticulum stress and activation of the unfolded protein response (UPR).
View Article and Find Full Text PDFFront Microbiol
November 2024
School of Basic Medical Sciences, Health Science Center, Ningbo University, Ningbo, China.
Nat Commun
November 2024
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Am J Trop Med Hyg
January 2025
Infection and Immunity Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Malaysia.
Flavivirus infection, especially dengue virus infection caused by DENV, is known to be a significant health concern globally owing to the high incidence and mortality rate. The expanding and increasing disease burden calls for the need to develop an effective treatment and prevent the event of fatal complications, including dengue hemorrhagic fever/dengue shock syndrome. The DENV-induced immune response has been described as paradoxical because it has a protective role in viral clearance but, at the same time, causes more severe infection through viral-specific immunity.
View Article and Find Full Text PDFPLoS Pathog
October 2024
Department of Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, United States of America.
Dengue virus (DENV) is the causative agent of dengue, a mosquito-borne disease that represents a significant and growing public health burden around the world. A unique pathophysiological feature of dengue is immune-mediated enhancement, wherein preexisting immunity elicited by a primary infection can enhance the severity of a subsequent infection by a heterologous DENV serotype. A leading mechanistic explanation for this phenomenon is antibody dependent enhancement (ADE), where sub-neutralizing concentrations of DENV-specific IgG antibodies facilitate entry of DENV into FcγR expressing cells such as monocytes, macrophages, and dendritic cells.
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