Strains ANG and ANG path of herpes simplex virus type 1 (HSV1) produced fusion from without (FFWO) of cells in culture. FFWO required 45min to become complete. In contrast, fusion from within (FFWI) was not detected until 3–4 h after infection, depending on the cell type. FFWO was temperature dependent: at 0° no fusion could be observed, but increase of temperature increased the degree of fusion. The pH optimum for FFWO was 7.8–8.5. The FFWO activity of the virus was found to be slightly more heat stable at 46° than was infectivity. FFWO was produced in Vero, CV-1 and BSCl cells, but not in BHK clone 13 or in primary or secondary rabbit kidney cells. FFWO was linked to the presence of virus particles and perhaps to other sedimentable, infected-cell material but not to soluble factors. Actinomycin D, cycloheximide, and UV irradiation did not block this activity, indicating no direct activity of the HSV1 genome for FFWO.

SUMMARYInfection of NMRI mice with increasing doses of six different strains of herpes simplex virus type 1 (HSV-1) induced increasing levels of neutralizing antibodies. In contrast, three strains of HSV-2, irrespective of the dose, induced only marginal antibody responses. Only strain HG 52 (HSV-2) at high doses of infection stimulated antibody formation. The virus content of some organs in 6-to 8-week-old mice appeared to be lower after HSV-2 than after HSV-1 infection. Application of immunemodulating drugs [silica or poly(I).poly(C) coupled via L-lysine to CM-cellulose] resulted in little augmentation of antibody formation if compared to HSV-1 infection. Secondary infections with HSV-1 or HSV-2 after a primary dose of HSV-1 were followed by a marked booster response. In contrast, a primary infection with HSV-2 suppressed secondary responses of HSV-I and HSV-2, thus indicating fundamental differences between the antibody-stimulating potency of HSV-1 and HSV-2 strains.

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9-beta-D-Arabinofuranosyladenine 5'-triphosphate (ara-ATP) is an inhibitor both of DNA polymerase-alpha and -beta from noninfected rabbit kidney cells and of the DNA-dependent DNA polymerase induced by herpes simplex virus Type 1 (strain IES). The studies were performed with partially purified enzymes, and each of the different polymerase preparations contained only one DNA-dependent DNA polymerase species. These enzymes were inhibited in a competitive manner. The HSV-induced DNA-dependent DNA polymerase was 39-fold more sensitive to ara-ATP than was cellular DNA polymerase-beta and 116-fold more sensitive than cellular DNA polymerase-alpha. The affinity of the HSV-induced enzyme for ara-ATP was only slightly influenced by the use of different template/initiators in the enzyme assays. In intact cell systems DNA synthesis was affected by 9-beta-D-arabinofuranosyladenine (ara-A) as indicated by the reduced incorporation of deoxythymidine. In herpesvirus-(strain Lennette)-infected cells, however, ara-A shows no influence on the incorporation on deoxythymidine into cellular DNA, but it substantially reduces the incorporation into viral DNA. Ara-A itself is incorporated into both cellular and herpesviral (strain Lennette, D-316 and IES) DNA during DNA synthesis.

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SUMMARYThe La antigen is known to associate, at least transiently, with a series of small nuclear and cytoplasmic ribonucleoprotein particles (snRNPs and scRNPs), e.g. U1 and U6 snRNPs. In CV-1 cells a monoclonal antibody (MAb), directed against the La protein (LalB5), immunostained intranuclear speckles. These speckles were found to co-localize with speckles that were stained by MAbs directed against either all U snRNPs or only against U1 snRNPs. Two h after infection of CV-1 cells with herpes simplex virus type 1 (HSV-1) (strain HFEM) the staining of nuclear speckles with the anti-La MAb disappeared and the La protein was found quantitatively in the cytoplasm. In contrast nuclear speckles remained stained with the MAbs against the U snRNPs. Similar results were obtained using HSV-1 strains Lenette or 17 syn ÷ or temperature-sensitive (ts) mutants defective either in DNA synthesis (tsS) or in the immediate early protein (Mr 175 K) (tsK). Later in infection the La protein returned to the nucleus. Six h after infection most of the nuclear La protein was found to localize within patchy regions. These areas seem to be related to heterogeneous nuclear RNA transcription and/or processing sites, but not to DNA replication sites.