Acute adrenal infection by HSV-1: role of apoptosis in viral replication

Replication of herpes simplex virus type 1 (HSV-1) in the adrenal gland of mice was observed 12 h after intravenous inoculation, peaked at 48 h (7 x 1 0(7) PFU/tissue), and was maintained until death. Virus spread to the bilat eral intermediolateral column of the thoracic spinal cord. Infected cells a ppeared in the fascicular zone of the adrenal cortex 12 h after infection, and cell death was evident in lesions found in the adrenal cortex. Lesions involved the medulla 48 h after inoculation. In cortical lesions, cell nucl ei were fragmented or shrunken with little damage to the cytoplasm. DNA fra gmentation appeared 12h after inoculation and increased mainly in cortical lesions, which were characterized by apoptosis induced by HSV-1 infection. In the adrenal medulla, cells were fused and formed multinucleated giant ce lls but rarely displayed cell death. Macrophages, which serve as a frontal barrier to viral infection in the adrenal gland, especially the cortex, wer e fewer in number than those found in the liver or spleen. It is likely tha t HSV-1 easily infects the adrenal gland, resulting in suppression of local immunity, and that adrenal cell apoptosis serves as a primitive type of im munity to limit viral replication.