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THE PATHOGENESIS AND PATHWAY INTO THE CENTRAL NERVOUS SYSTEM AFTER INTRAOCULAR INFECTION OF HERPES SIMPLEX VIRUS TYPE I IN RABBITS
Author(s) -
NARANG H. K.,
CODD A. A.
Publication year - 1978
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1978.tb00554.x
Subject(s) - herpes simplex virus , optic chiasma , optic nerve , pathogenesis , biology , chiasma , virus , myelin , central nervous system , pathology , anatomy , virology , medicine , immunology , neuroscience , chromosome , biochemistry , gene
Herpes simplex virus (HSV) type I was injected into the right eye of 18‐day‐old New Zealand albino rabbits and the animals were killed on the fourth and eighth days after inoculation. Longitudinal section of the optic nerves and chiasma showed that both myelinated axons and neuroglial cells crossed at the chiasma. Semi‐serial (1 μm) and ultrathin sections showed the presence of HSV in both astrocytes and oligodendrocytes, although no particles were seen in the myelinated axons; the infected cells were confined to the medial side of the right optic nerve. HSV travels centropetally along the optic pathway and slowly spreads laterally by cell‐to‐cell infection. The virus does not appear to kill the astrocytes and oligodendrocytes, and also does not directly damage the myelin sheath.