Arezki Chekaoui
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Arezki Chekaoui has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Andrew D. Luber
Virion Therapeutics, Newark, Delaware, USA
1 shared publication - Dakota Newman
The Wistar Institute, Philadelphia, Pennsylvania, USA
1 shared publication - Hildegund C. J. Ertl
The Wistar Institute, Philadelphia, Pennsylvania, USA
1 shared publication - Mikhail Novikov
The Wistar Institute, Philadelphia, Pennsylvania, USA
1 shared publication - Mohadeseh Hasanpourghadi
The Wistar Institute, Philadelphia, PA 19104, USA
1 shared publication - Robert Ambrose
The Wistar Institute, Philadelphia, Pennsylvania, USA
1 shared publication
Latest Publications
- Open Access
- 8 November 2024
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 9 (21)
A therapeutic HBV vaccine containing a checkpoint modifier enhances CD8+ T cell and antiviral responses
In patients who progress from acute hepatitis B virus (HBV) infection to a chronic HBV (CHB) infection, CD8 + T cells fail to eliminate the virus and become impaired. A functional cure of CHB likely requires CD8 + T cell responses different from those induced by the infection. Here we report preclinical immunogenicity and efficacy of an HBV therapeutic vaccine that includes herpes simplex virus (HSV) glycoprotein D (gD), a checkpoint modifier of early T cell activation, that augments CD8 + T cell responses. The vaccine is based on a chimpanzee adenovirus serotype 6 (AdC6) vector, called AdC6-gDHBV2, which targets conserved and highly immunogenic regions of the viral polymerase and core antigens fused to HSV gD. The vaccine was tested with and without gD in mice for immunogenicity, and in an AAV8-1.3HBV vector model of antiviral efficacy. The vaccine encoding the HBV antigens within gD stimulates potent and broad CD8 + T cell responses. In a surrogate model of HBV infection, a single intramuscular injection achieved pronounced and sustained declines of circulating HBV DNA copies and HBV surface antigen; both inversely correlated with HBV-specific CD8 + T cell frequencies in spleen and liver.
- 8 November 2024
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 9 (21)
Open AccessA therapeutic HBV vaccine containing a checkpoint modifier enhances CD8+ T cell and antiviral responses
In patients who progress from acute hepatitis B virus (HBV) infection to a chronic HBV (CHB) infection, CD8 + T cells fail to eliminate the virus and become impaired. A functional cure of CHB likely requires CD8 + T cell responses different from those induced by the infection. Here we report preclinical immunogenicity and efficacy of an HBV therapeutic vaccine that includes herpes simplex virus (HSV) glycoprotein D (gD), a checkpoint modifier of early T cell activation, that augments CD8 + T cell responses. The vaccine is based on a chimpanzee adenovirus serotype 6 (AdC6) vector, called AdC6-gDHBV2, which targets conserved and highly immunogenic regions of the viral polymerase and core antigens fused to HSV gD. The vaccine was tested with and without gD in mice for immunogenicity, and in an AAV8-1.3HBV vector model of antiviral efficacy. The vaccine encoding the HBV antigens within gD stimulates potent and broad CD8 + T cell responses. In a surrogate model of HBV infection, a single intramuscular injection achieved pronounced and sustained declines of circulating HBV DNA copies and HBV surface antigen; both inversely correlated with HBV-specific CD8 + T cell frequencies in spleen and liver.