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Defective parvoviruses acquired via the transplacental route protect mice against lethal adenovirus infection
Infection and Immunity
|July 1, 1982
Abstract:
Adeno-associated virus type 1 (AAV-1) interfered with the replication of its murine adenovirus (MAV) helper in primary mouse kidney cells and in 1-day-old ICR mice. Mice carrying AAV-1 acquired via the transplacental route were protected against lethal infection with MAV. The replication of AAV-1 in these mice could be triggered by multiple challenges with MAV, and antibodies to AAV-1 were subsequently detected.
Insights
Adeno-associated virus type 1 (AAV-1) inhibits murine adenovirus (MAV) replication. Transplacentally acquired AAV-1 protected mice from lethal MAV infection, with MAV challenge triggering AAV-1 replication and antibody production.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Adeno-associated virus type 1 (AAV-1) is a parvovirus.
- Murine adenovirus (MAV) is a species of Mastadenavirus.
- Viral interference is a phenomenon where one virus inhibits the replication of another.
Purpose of the Study:
- To investigate the interaction between AAV-1 and MAV.
- To determine if AAV-1 can protect against MAV infection.
- To examine the immune response to AAV-1 following MAV challenge.
Main Methods:
- Primary mouse kidney cell cultures were used to study viral replication.
- 1-day-old ICR mice were infected with AAV-1 and/or MAV.
- Transplacental AAV-1 acquisition was established.
- Mice were challenged with MAV to assess protection.
- Viral replication and antibody production were measured.
Main Results:
- AAV-1 interfered with MAV replication in vitro and in vivo.
- Mice with transplacentally acquired AAV-1 were protected from lethal MAV infection.
- Repeated MAV challenges in AAV-1-carrying mice triggered AAV-1 replication.
- Antibodies to AAV-1 were detected after MAV challenge.
Conclusions:
- AAV-1 exhibits inhibitory effects on MAV replication.
- Transplacental transfer of AAV-1 provides protection against MAV.
- MAV infection can act as a trigger for latent AAV-1 replication and subsequent immune response.