Last data update: May 06, 2024. (Total: 46732 publications since 2009)
Records 1-2 (of 2 Records) |
Query Trace: Huang CYH[original query] |
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West nile virus vaccination protects against usutu virus disease in mice
Salgado R , Hawks SA , Frere F , Vázquez A , Huang CYH , Duggal NK . Viruses 2021 13 (12) West Nile virus (WNV) and Usutu virus (USUV) are mosquito‐borne flaviviruses that can cause neuroinvasive disease in humans. WNV and USUV circulate in both Africa and Europe and are closely related. Due to antigenic similarity, WNV‐specific antibodies and USUV‐specific antibodies have the potential to bind heterologous viruses; however, it is unclear whether this interaction may offer protection against infection. To investigate how prior WNV exposure would influ-ence USUV infection, we used an attenuated WNV vaccine that contains the surface proteins of WNV in the backbone of a dengue virus 2 vaccine strain and protects against WNV disease. We hypothesized that vaccination with this attenuated WNV vaccine would protect against USUV in-fection. Neutralizing responses against WNV and USUV were measured in vitro using sera following vaccination. Sera from vaccinated CD‐1 and Ifnar1−/− mice cross‐neutralized with WNV and USUV. All mice were then subsequently challenged with an African or European USUV strain. In CD‐1 mice, there was no difference in USUV titers between vaccinated and mock‐vaccinated mice. However, in the Ifnar1−/− model, vaccinated mice had significantly higher survival rates and significantly lower USUV viremia compared to mock‐vaccinated mice. Our results indicate that exposure to an attenuated form of WNV protects against severe USUV disease in mice and elicits a neutralizing response to both WNV and USUV. Future studies will investigate the immune mechanisms responsible for the protection against USUV infection induced by WNV vaccination, providing critical insight that will be essential for USUV and WNV vaccine development. © 2021 by the authors. Licensee MDPI, Basel, Switzerland. |
Molecular determinants of dengue virus 2 envelope protein important for virus entry in Fc?RIIA-mediated antibody-dependent enhancement of infection.
Chotiwan N , Roehrig JT , Schlesinger JJ , Blair CD , Huang CYH . Virology 2014 456-457 (1) 238-246 Antibody-dependent enhancement (ADE) of infection may cause severe illness in patients suffering a secondary infection by a heterologous dengue virus (DENV) serotype. During ADE of infection, cross-reactive non- or poorly-neutralizing antibodies form infectious virus-Ab complexes with the newly infecting serotype and enhance virus infection by binding to the Fc receptors (FcR) on FcR-bearing cells. In this study, we determined that molecular determinants of DENV2 envelope protein critical for virus entry during non-ADE infection are also required for ADE infection mediated by FcRIIA, and binding of virus-Ab complexes with FcRIIA alone is not sufficient for ADE of infection. The FcRIIA mainly plays an auxiliary role in concentrating the virus-Ab complex to the cell surface, and other primary cellular receptors are required for virus entry. Understanding the viral entry pathway in ADE of DENV infection will greatly facilitate rational designs of anti-viral therapeutics against severe dengue disease associated with ADE. |
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