Block to influenza virus replication in cells preirradiated with ultraviolet light
Journal Article
·
· Virology; (United States)
Ultraviolet (uv) irradiation of CEF cells immediately before infection with influenza A (fowl plague) virus inhibited virus growth; no inhibition of the growth of a parainfluenza virus (Newcastle disease virus) could be detected in irradiated cells. The kinetics of inhibition after various doses of uv irradiation were multihit, with an extrapolation number of two. When irradiated cells were allowed to photoreactivate by exposure to visible light for 16 hr their capacity to support influenza virus replication was largely restored; this process was sensitive to caffeine, suggesting that it required DNA repair. In CEF cells exposed to 360 ergs/mm/sup 2/ of uv radiation the rate of synthesis of host cellular RNA was reduced by more than 90%, and that of host cellular protein by 40 to 50%, as judged by incorporation of precursor molecules into an acid-insoluble form. When such irradiated cells were infected with influenza virus all the genome RNA segments were transcribed, but the overall concentration of virus-specific poly(A)-containing cRNA was reduced about 50-fold. Within this population of cRNA molecules, the RNAs coding for late proteins (HA, NA, and M) were reduced in amount relative to the other segments. The rates of synthesis of the M and HA proteins were specifically reduced in uv-irradiated cells, but the rates of synthesis of the P, NP, and NS proteins were only slightly reduced compared to normal cells. Immunofluorescent studies showed that, in uv-irradiated cells, NP migrated into the nucleus early after infection and later migrated out into the cytoplasm, as in normal cells. In contrast to normal cells, no specific immunofluorescence associated with M protein could be observed in uv-irradiated cells. It is concluded that uv-induced damage to host cellular DNA alters the pattern of RNA transcription in CEF cells infected with influenza virus, and that this results in a block to late protein synthesis which stops virus production.
- Research Organization:
- Univ. of Cambridge, Eng.
- OSTI ID:
- 5264237
- Journal Information:
- Virology; (United States), Journal Name: Virology; (United States) Vol. 83:1; ISSN VIRLA
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
560121* -- Radiation Effects on Cells-- External Source-- (-1987)
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL CELLS
BIOLOGICAL EFFECTS
BIOLOGICAL RADIATION EFFECTS
BIOLOGICAL RECOVERY
BIOLOGICAL REPAIR
BIOSYNTHESIS
CELL PROLIFERATION
DNA
ELECTROMAGNETIC RADIATION
FLUORESCENCE
LUMINESCENCE
MICROORGANISMS
NUCLEIC ACIDS
ORGANIC COMPOUNDS
PARASITES
PHOTOREACTIVATION
PROTEINS
RADIATION EFFECTS
RADIATIONS
RECOVERY
REPAIR
RNA
SYNTHESIS
ULTRAVIOLET RADIATION
VIRUSES
VISIBLE RADIATION
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL CELLS
BIOLOGICAL EFFECTS
BIOLOGICAL RADIATION EFFECTS
BIOLOGICAL RECOVERY
BIOLOGICAL REPAIR
BIOSYNTHESIS
CELL PROLIFERATION
DNA
ELECTROMAGNETIC RADIATION
FLUORESCENCE
LUMINESCENCE
MICROORGANISMS
NUCLEIC ACIDS
ORGANIC COMPOUNDS
PARASITES
PHOTOREACTIVATION
PROTEINS
RADIATION EFFECTS
RADIATIONS
RECOVERY
REPAIR
RNA
SYNTHESIS
ULTRAVIOLET RADIATION
VIRUSES
VISIBLE RADIATION