UV irradiation analysis of complementation between, and replication of, RNA-negative temperature-sensitivie mutants of Newcastle disease virus

Journal Article · Mon Mar 01 04:00:00 EST 1982 · J. Virol.; (United States)

OSTI ID:5612495

Peeples, M E; Bratt, M A

Random uv irradiation-induced lesions destroy the infectivity of Newcastle disease virus (NDV) by blocking downstream transcription from the single viral promoter. The nucleocapsid-associated polypeptides most likely to be involved in RNA synthesis are located at the extreme ends of the genome: NP and P are promoter proximal genes, and L is the most distal gene. We attempted to order the two temperature-sensitive (ts) RNA-negative (RNA-) mutant groups of NDV by determining the uv target sizes for the complementing abilities of mutants A1 and E1. After uv irradiation, E1 was unable to complement A1, a result compatible with the A mutation lying in the L gene. In contrast, after uv irradiation A1 was able to complement E1 for both virus production and viral protein synthesis, with a target size most consistent with the E mutation lying in the P gene. UV-irradiated virus was unable to replicate as indicated by its absence in the yields of multiply infected cells, either as infectious virus or as particles with complementing activity. After irradiation, ts mutant B1..delta..P, with a non-ts mutation affecting the electrophoretic mobility of the P protein, complemented E1 in a manner similar to A1, but it did not amplify the expression of ..delta..P in infected cells. This too is consistent with irradiated virus being unable to replicate despite the presence of the components needed for replication of E1. At high uv doses, A1 was able to complement E1 in a different, uv-resistant manner, probably by direct donation of input polypeptides. Multiplicity reactivation has previously been observed at high-multiplicity infection by uv-irradiated paramyxoviruses. In this case, virions which are noninfectious because they lack a protein component may be activated by a protein from irradiated virions.

• Research Organization: Univ. of Massachusetts Medical School, Worcester
• OSTI ID: 5612495
• Journal Information: J. Virol.; (United States), Journal Name: J. Virol.; (United States) Vol. 41:3; ISSN JOVIA
• Country of Publication: United States
• Language: English

Related Subjects

560131* -- Radiation Effects on Microorganisms-- Basic Studies-- (-1987)
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
BIOLOGICAL EFFECTS
BIOLOGICAL RADIATION EFFECTS
DISEASES
ELECTROMAGNETIC RADIATION
GENETIC EFFECTS
GENETIC RADIATION EFFECTS
INACTIVATION
INFECTIOUS DISEASES
INFECTIVITY
INHIBITION
MICROORGANISMS
MUTANTS
MUTATIONS
NEWCASTLE DISEASE
PARASITES
RADIATION EFFECTS
RADIATIONS
TEMPERATURE DEPENDENCE
TRANSCRIPTION
ULTRAVIOLET RADIATION
VIRAL DISEASES
VIRUSES