SUMMARYNude mice have been shown to be as resistant to intraperitoneal infection with herpes simplex virus type 1 (HSV) as their heterozygous littermates. Here we document that both activation of natural killer (NK) cells and interferon induction were normal in nu/nu mice after injection of HSV. Injection of silica caused increased mortality by HSV in C57BL/6 mice. Silica, in addition, led to a significant reduction of NK cell activity but had no effect on the interferon response. Treatment of C57BL/6 mice with anti-asialo GM1 (an antiserum with a predominant effect on NK cells) caused complete abolition of the NK cell response, but had no effect on interferon induction or virus-induced mortality. In further studies a monoclonal anti-thy-1.2 antibody was utilized which possessed high activity in rivo in depleting T cell responses in mice. Injection of anti-thy-1.2 decreased NK cell activation but was without effect on the interferon response. Unexpectedly, in view of the data in nu/nu mice, this antibody increased HSV-induced mortality in C57BL/6 mice. Similar data were obtained when anti-thy-l.2 was injected into nu/nu mice. Our results are compatible with the hypothesis that T cell precursors sensitive to anti-thy-1.2 present in homozygous nude mice play a role in resistance against HSV. Furthermore, the data in the euthymic mice may indicate a role of T cells in the primary resistance of mice against HSV.

Pathologic-histologic and immunocytologic as well as serologic findings from a total number of 50 recently dead or euthanatized moribund harbor seals (Phoca vitulina) are described. In 14 of 31 histologically examined brains of affected seals alterations corresponding to canine distemper encephalitis (CDE) were found. Immunofluorescence-serologic tests using polyclonal as well as monoclonal antibodies against canine distemper virus (CDV) resulted in positive findings in organ sections of 24 dead seals. An agent was isolated from organs of dead seals and subjected to several passages in vero cell cultures as well as in primary seal lung-cell cultures. The agent was able to be identified as canine distemper-like virus with both antibodies.CDV neutralising serum-antibodies were detected in 13 out of 19 serum specimens. Further interdisciplinary investigations are required to determine whether the virus induced alterationsstill to be interpretated only in a purely qualitative senseshould be considered as the manifestation of contributing ecological factors, or as the primary cause of the still present deaths of harbor seals.

Investigations on deaths of harbour seals in the Wadden Sea around Sylt in 1988: Significance of the marked lungworminfestation with hypersensitivity reactionIt is reported on the clinical, pathologic-anatomical, histological and parasitological observations on 8 harbour seals necropsied. A massive parasitic infestation with a general hypersensitivity reaction was seen, the possible significance of which as to the current deaths of harbour seals is discussed. EinleitungDie Ursachen des seit dem 12. April 1988 erstmals in Danemark (AGGERS, 1988) und im AnschluB daran auch im deutschen (HEIDEMANN, 1988) sowie niederlandischen (REIJN-DERS, 1988) Wattenmeer geschilderten Sterbens von Seehunden (Phoca vitulina) sind noch ungeklart. Unter den moglichen Primarursachen werden derzeit verschiedene virale Infektionen diskutiert. OSTERHAUS (1988) wies einen neuen Serotyp des Picornavirus beim Seehund nach, den er fur die aufgetretenen letalen akuten Pneumonien als verantwortlich bezeichnet. MAYR (1988) hingegen gelang der Nachweis eines enteralen Coronavirus mittels Rinder-ELISA, er wertet dies jedoch als einen nosologisch unbedeutenden Befund. Eine zusammenfassende Literaturdarstellung iiber Erkrankungen und mogliche Todesursachen bei Robben hat KOBERC (1985) gegeben. U.S. Copyright Clearance Center C o d e Sraremmt: 093 1 -1793/88/3506-0467$02.50/0

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