Studies on a temperature-sensitive step essential to herpesvirus DNA replication

Stevens, Jack G.; Jackson, Nola L.

doi:10.1016/0042-6822(67)90041-4

Cited by 13 publications

(3 citation statements)

References 8 publications

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“…It would be of interest to know more about the effect of temperature for both functions. A temperature-dependent step for the growth of a bovine herpesvirus has been reported (17,18). It was thought that the critical step was a block in DNA replication, but we note that DNA replication may be somewhat dependent on RNA and protein synthesis (4).…”

Section: Discussionmentioning

confidence: 85%

Timing of Some of the Molecular Events Required for Cell Fusion Induced by Herpes Simplex Virus Type 1

Kousoulas

Person

Holland

1978

J Virol

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The timing of some of the molecular events that are required for cell fusion was investigated. Cell fusion was produced by a mutant of herpes simplex virus type 1 that causes extensive cell fusion during infection. The timing of molecular events required for fusion was established by the use of blocking agents. Phosphonoacetic acid blocks viral DNA synthesis; actinomycin D blocks RNA synthesis; cycloheximide blocks protein synthesis; 2-deoxyglucose blocks glycosylation of glycoproteins; high temperature, NH4Cl, and adamantanone block unknown steps required for cell fusion. For cells infected at a low multiplicity of infection, phosphonoacetic acid decreased the rate but not the final amount of fusion, but at a multiplicity of infection of 10 it had no effect on the rate of cell fusion. RNA synthesis was required for fusion until 4 h after infection, protein synthesis until 5.5 h after infection, and glycosylation until 7 h after infection. The temperature-dependent step occurred before 6 h after infection, whereas NH4Cl and adamantanone acted at steps that occurred until 8 h after infection. Cycloheximide, temperature, NH4Cl, and adamantanone acted reversibly; actinomycin D and 2-deoxyglucose acted irreversibly. The same order of action of the inhibitors was also determined by using pairs of inhibitors sequentially. These experiments also indicated that the fusion factor was not an a-polypeptide. Virus growth and cell fusion were both found to be highly dependent on temperature in the range of 30 to 40°C. Wild-type infections are apparently characterized by the presence of a fusion factor and a fusion inhibitor. The fusion-blocking agents were added to wild-type-infected cells under a variety of conditions in an attempt to selectively block the production of the fusion inhibitor molecule and thereby cause extensive cell fusion. However, fusion was not observed in any of these experiments.

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Section: Discussionmentioning

confidence: 85%

Timing of Some of the Molecular Events Required for Cell Fusion Induced by Herpes Simplex Virus Type 1

Kousoulas

Person

Holland

1978

J Virol

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“…-A temperature-dependent step for the growth of a bovine herpesvirus has been reported (17,18). It was thought that the critical step was a block in DNA replication, but we note that DNA replication may be somewhat dependent on RNA and protein synthesis (4).…”

mentioning

confidence: 86%

Studies on virus-induced cell fusion. Progress report, August 1, 1977--June 30, 1978

Person¹

1978

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Appendix 3-A study of neutral glycolipids of mock-infected, syn mutant D infected and wild type infected cells Appendix 4-A fluorescence enhancement assay of cell fusion. A publication resulting f(*m. Collaborative work with Prof. Pollard is also /-CO *b*'Ir included (Appendix 5)\: Another manuscript,"The Genetic Evidence for the Existence of 'I\•,0 Viral Genes that Affect Cell Fusion in HSV-1 Infected Cells",

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“…DNA-synthesis: DNA synthesis was followed in infected and non-infected bottle cultures by pulse labelling at 3, 6,9,12,16,24,36 and 48 hours post infection for 120 minutes with Hs-thymidine (specific activity 2 pC/ml. ).…”

mentioning

confidence: 99%

Porcine Parvovirus Infection in vitro: A Study Model for the Replication of Parvoviruses

Bachmann

Danner

1976

Zentralblatt für Veterinärmedizin Reihe B

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It was shown by us that replication of a porcine parvovirus (PPV) in vitro occurs at temperatures of 28 "C, 33 "C and 37 OC without significant differences in maximum titers of infectious virus and hemagglutinin (HA). Virus and H A production, however, were delayed with falling temperatures.At 40 "C virus replication was suppressed, resulting probably in an incomplete infection cycle. Temperature sensitive (ts) mutants were not involved (2).Since the normal body temperature of pigs ranges from 38 O C to 40 O C , studies on the replication of PPV in cell cultures under different conditions could provide useful information for the understanding of the pathogenesis of PPV infections in vivo ( 3 ) . The aim of these investigations was a study of some mechanisms that are involved in the development of virus-induced morphological changes and cellular functions in connection with the production of viral antigens and infectious virus in vitro in a time-course experiment. Materials and MethodsVirus: Porcine parvovirus strain G IO/I, which was originally isolated from a primary swine kidney cell culture (1; 9) and subsequently passaged in the SK cell line was used. Passage numbers 14-17 were employed.Cell cultures: The established pig kidney cell line SK (6) was found to be most sensitive for PPV. The cell line was grown in Hanks MEM with 10 o / o calf serum and 880 mg. NaHCO,/liter. For virus studies the serum content was reduced to 2 o/o and NaHCO, increased to 1,320 mg./liter. Falcon plastic bottles, 16 mm. tube cultures and coverslip cultures were used for all studies. ~ -_ Dedicated to Prof. Dr. Dr. h. c. E. TRAUB on the occasion of his 70th birthday.

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Studies on a temperature-sensitive step essential to herpesvirus DNA replication

Cited by 13 publications

References 8 publications

Timing of Some of the Molecular Events Required for Cell Fusion Induced by Herpes Simplex Virus Type 1

Timing of Some of the Molecular Events Required for Cell Fusion Induced by Herpes Simplex Virus Type 1

Studies on virus-induced cell fusion. Progress report, August 1, 1977--June 30, 1978

Porcine Parvovirus Infection in vitro: A Study Model for the Replication of Parvoviruses

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