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Acid phosphatase activity in mouse brain infected with Venezuelan equine encephalomyelitis virus
Abstract:
The mode of development of Venezuelan equine encephalomyelitis virus and the activity of acid phosphatase in the central nervous system of newborn mice were investigated. Precursor particles appeared to be formed in masses of viroplasm, migrating to the membrane of the Golgi cisterns and vacuoles or to the plasma membrane and being transformed into mature viral particles by budding. Mature viral particles were also found in the lumen of the blood vessels and around the myelin sheath of axons. Increased number of Golgi complexes and depletion of polysomes were the main ultrastructural alterations of the nerve cells. Acid phosphatase activity was found to be increased in the Golgi cisterns, vacuoles, and lysosomes of nerve cells. The presence of acid phosphatase activity in the rough endoplasmic reticulum and perinuclear cisterns suggests increased production of the enzyme in the nerve cells infected with Venezuelan equine encephalomyelitis virus.
Insights
Venezuelan equine encephalomyelitis virus (VEEV) replicates via budding, altering nerve cell structures. Increased acid phosphatase in infected nerve cells suggests enhanced enzyme production during VEEV development.
Area of Science:
- Neurovirology
- Cell Biology
- Enzyme Activity
Background:
- Venezuelan equine encephalomyelitis virus (VEEV) is a significant neurotropic pathogen.
- Understanding VEEV's replication cycle and its impact on host cell is crucial for developing antiviral strategies.
Purpose of the Study:
- To investigate the replication mechanism of VEEV in the central nervous system (CNS) of newborn mice.
- To analyze the activity of acid phosphatase in the CNS during VEEV infection.
Main Methods:
- Transmission electron microscopy was used to observe viral ultrastructure and cellular changes.
- Histochemical staining was employed to assess acid phosphatase activity in infected nerve cells.
Main Results:
- VEEV precursor particles budded from Golgi cisterns and plasma membranes, forming mature virions.
- Ultrastructural alterations included increased Golgi complexes and depleted polysomes in nerve cells.
- Elevated acid phosphatase activity was detected in Golgi cisterns, vacuoles, lysosomes, endoplasmic reticulum, and perinuclear cisterns.
Conclusions:
- VEEV replicates through a budding process, affecting neuronal ultrastructure.
- Increased acid phosphatase activity in various cellular compartments suggests enhanced enzyme synthesis in VEEV-infected nerve cells.