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 10(7) PFU/tissue), and was maintained until death. Virus spread to the bilateral intermediolateral column of the thoracic spinal cord. Infected cells appeared 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 nuclei were fragmented or shrunken with little damage to the cytoplasm. DNA fragmentation appeared 12 h 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 cells but rarely displayed cell death. Macrophages, which serve as a frontal barrier to viral infection in the adrenal gland, especially the cortex, were fewer in number than those found in the liver or spleen. It is likely that HSV-1 easily infects the adrenal gland, resulting in suppression of local immunity, and that adrenal cell apoptosis serves as a primitive type of immunity to limit viral replication.
Aita
K
K
Department of Pathology, Teikyo University School of Medicine, Tokyo, Japan. aitajoe@mac.com
Irie
H
H
Koyama
A H
AH
Fukuda
A
A
Yoshida
T
T
Shiga
J
J
D000208:Acute Disease; D000311:Adrenal Glands / Q000473:pathology / Q000648:ultrastructure / Q000821:virology*; D000818:Animals; D017209:Apoptosis; D053938:DNA Fragmentation; D006561:Herpes Simplex / Q000473:pathology / Q000821:virology; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000502:physiology*; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D014779:Virus Replication