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Rhabdo-immunodeficiency virus, a murine model of acute HIV-1 infection.

Elife. 2019 Oct 23;8
Rachel A Liberatore 1 , Emily J Mastrocola 1 , Elena Cassella 2 , Fabian Schmidt 2 , Jessie R Willen 1 , Dennis Voronin 2 , Trinity M Zang 1 , Theodora Hatziioannou 2 , Paul D Bieniasz 1
Rachel A Liberatore 1 , Emily J Mastrocola 1 , Elena Cassella 2 , Fabian Schmidt 2 , Jessie R Willen 1 , Dennis Voronin 2 , Trinity M Zang 1 , Theodora Hatziioannou 2 , Paul D Bieniasz 1
+ et al

[No authors listed]

Author information
  • 1 Howard Hughes Medical Institute, The Rockefeller University, New York, United States.
  • 2 Laboratory of Retrovirology, The Rockefeller University, New York, United States.

摘要


Numerous challenges have impeded HIV-1 vaccine development. Among these is the lack of a convenient small animal model in which to study antibody elicitation and efficacy. We describe a chimeric Rhabdo-Immunodeficiency virus (RhIV) murine model that recapitulates key features of HIV-1 entry, tropism and antibody sensitivity. RhIVs are based on vesicular stomatitis viruses (VSV), but viral entry is mediated by HIV-1 Env proteins from diverse HIV-1 strains. RhIV infection of transgenic mice expressing human CD4 and CCR5, exclusively on mouse CD4+ cells, at levels mimicking those on human CD4+ T-cells, resulted in acute, resolving viremia and CD4+ T-cell depletion. RhIV infection elicited protective immunity, and antibodies to HIV-1 Env that were primarily non-neutralizing and had modest protective efficacy following passive transfer. The RhIV model enables the convenient in vivo study of HIV-1 Env-receptor interactions, antiviral activity of antibodies and humoral responses against HIV-1 Env, in a genetically manipulatable host.

KEYWORDS: CCR5, CD4, HIV-1, antibody, envelope, infectious disease, microbiology, mouse, neutralization