Localization of herpes simplex virus type 1 in sebaceous glands of mice.

The distribution of HSV-1 during the development of zosteriform skin lesions in SCID mice was analyzed by immunofluorescence and electron microscopy. The virus initially appeared within certain keratinocytes, sometimes surrounded by keratinocytes whose surfaces were also positive for the antigens, in the lower epidermal layers including the hair follicles, and then extended upward to the entire epidermis and downward to the sebaceous glands 1-2 days later, when no macroscopic skin lesion was seen. The affected epidermal cells subsequently degenerated and lost their viral antigens within a day, when the zosteriform lesion then became evident. This was followed by a degeneration of the dermis. The sebaceous glands eventually degenerated in 10 days, but some glands in the necrotic skin areas preferentially retained HSV-1. The horizontal spread of the virus in the epidermis beyond the first invaded dermatome occurred much later. In mice passively immunized with specific immune serum, viral antigens were observed even 20 days after the infection in sebaceous glands in necrotized areas. Therefore, HSV-1 appears to spread first via the extracellular fluid among the keratinocytes after being shed from nerve endings, and then produces a successive degeneration of the affected keratinocytes which may prevent any further extension of horizontal viral spread. The pilosebaceous apparatus is possibly acting as a site not only for the replication of HSV-1 with a delayed cytopathic effect, but also as an area that is temporarily sheltered from host defense mechanisms.