Archives of Virology

Recently three strains of herpes simplex virus type 1 (HSV-1), which did not react with MicroTrak Herpes (Syva Co.), were isolated by us from a patient with recurrent herpetic keratitis. In this study we characterized these strains of HSV-1 and found them to be HSV-1 gC− mutants which are very rare isolates from humans. The properties of the HSV-1 strains regarding plaque morphology on Vero cells and chick embryo fibroblasts and viral DNA analysis were the same as those of the usual HSV-1 strains. An immunofluorescence study using anti-gC-1 monoclonal antibody and SDS-PAGE analysis of radiolabeled viral glycoproteins showed that these strains are deficient in gC-1. They were virulent for mice and sensitive to acyclovir and bromovinyldeoxyuridine. Furthermore the infectivity of the strains was inactivated by complement though the phenomenon was not observed in the usual HSV-1 strains. This finding suggests that protection from damages by complement is an important function of gC. In keratitis the effects of complement are thought to be minimal because of the scanty blood supply and this may be the reason why these strains were isolated from the cornea.

Both adult and baby hamsters infected intranasally with human adenovirus type 5 exhibited virologic, serologic, and histologic evidence of infection. When 8-day old hamsters were infected with 4×106 pfu, concentrations of virus up to 2×106 pfu/animal were detected in the lung, peaking on day 2. The minimum infectious dose was 1×103 pfu/animal. This model may be useful in studies of conventional and recombinant adenoviral vaccines for humans.

The action of reducing, oxidizing and thiol-alkylating agents on early steps of Junin virus (JV) multiplication in Vero cells was investigated. The presence of reducing agents during virus adsorption as well as incubation of viral particles with these compounds before infection enhanced JV infectivity. On the contrary, the thiol-alkylating agent 5, 5′ dithiobis (2-nitrobenzoic acid) and the oxidizing compound potassium periodate showed an inhibitory effect, suggesting that sulfhydryl groups and certain sugar moieties of viral glycoproteins play an important role in the first steps of JV infection. Also enzymatic treatment of cell monolayers and addition of concanavalin A to cultures prior to infection suggest that cellular glycoproteins are involved in virus attachment.

Treatment of chick embryo cells with 1-adamantanamine prevented the synthesis of fowl plague virus-directed RNA and the development of the virusinduced depression of cellular protein synthesis. The event sensitive to the compound preceded an early event sensitive to cycloheximide. Interferon production induced by ultraviolt-irradiated virus was depressed by the compound. These data suggest that 1-adamantanamine prevents the release of viral nucleic acid within the cell.