Transgene expression kinetics and replication potential of recombinant adenovirus serotype 4 in a mouse model and its use as a herpes simplex virus vaccine
Entry updated:
A mouse study built recombinant adenovirus serotype 4 (Ad4) vectors, including one carrying HSV-2 glycoprotein D (Ad4-gD2), to test expression in mice and protection against HSV-2. Mice given Ad4-gD2 intranasally made HSV-2-neutralizing antibodies and, after intravaginal HSV-2 challenge, had reduced disease scores, increased survival and reduced shedding. The work was done in mice only, and the authors describe the mouse model as semi-permissive to Ad4 infection.
The vaccine was given to mice before challenge, so the design is preventive rather than therapeutic, and the HSV target is HSV-2. The authors report that repeat inoculation with a luciferase-expressing Ad4 gave reduced expression in BALB/c mice but robust expression in humanized mice, and they suggest an immune response to the vector in wild-type mice. They also infer from reduced Ad4 DNA production in cidofovir-treated mice that the virus replicated at a low level in the lungs.
These are animal results; the source text available to the desk did not include group sizes, antibody titers or the size of the changes in disease, survival and shedding.
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- The authors built recombinant adenovirus serotype 4 (Ad4) vectors expressing luciferase, GFP or HSV-2 glycoprotein D (Ad4-gD2) to study transgene expression, vector replication and HSV-2 protection in mice.
- Intranasal vaccination of mice with Ad4-gD2 produced HSV-2-neutralizing antibodies in serum.
- After intravaginal HSV-2 challenge, vaccinated mice had reduced disease scores, increased survival and reduced shedding.
- The authors conclude the BALB/c mouse is semi-permissive to Ad4 mucosal infection, with transgene expression sufficient for studying Ad4-based vaccine candidates.
- Repeat inoculation with Ad4-Luc gave reduced luciferase expression in BALB/c mice but robust expression in humanized mice, which the authors interpret as an immune response to the vector in wild-type mice.
- Reduced Ad4 DNA production in cidofovir-treated mice led the authors to infer that Ad4 replicated at a low level in the lungs.