Kosei Moriyama

Hepatitis GB virus C genome in the serum of aplastic anaemia patients receiving frequent blood transfusions

GB virus C (GBV‐C) RNA was detected in five of 18 patients with aplastic anaemia who had received blood transfusions, whereas it was not detected in eight patients who had not received any transfusions. Antibody against hepatitis C virus (anti‐HCV) was detected in nine patients in the transfusion group, compared with one of eight who had not received any transfusions. Therefore, the route of transmission of both GBV‐C and HCV in these patients appeared to have been multiple blood transfusion. Since all of the GBV‐C RNA‐positive patients harboured anti‐HCV, GBV‐C seems to frequently superinfect with HCV. Neither GBV‐C nor HCV is likely to have been a causative agent of the anaemia in the cases examined.

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

SummaryThe 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.

Latent Infection of SCID Mice with Herpes Simplex Virus 1 and Lethal Cutaneous Lesions in Pregnancy

Some SCID mice survived primary infection with herpes simplex virus 1 without the development of peripheral lesions but established coculture‐positive ganglionic latency when a low dose of a wild‐type strain was inoculated intracutaneously. The latency was also evidenced by the development of the fatal zosteriform skin lesions and the isolation of the virus during pregnancy. We consider that the viral entry into neurons without successive replication, rather than the arrest of the lytic infection within the cells, is an important mechanism in the establishment of latency.