Attenuation of virus production at high multiplicities of infection in Aureococcus anophagefferens

Abstract Infection dynamics (saturation kinetics, infection efficiency, adsorption and burst size) for the Aureococcus anophagefferens -Brown Tide virus ( AaV ) system were investigated using susceptible and resistant strains. Adsorption assays revealed that virus affinity to the cell surface is a k...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2014-10, Vol.466, p.71-81
Main Authors: Brown, Christopher M, Bidle, Kay D
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
ADSORPTION
AFFINITY
BACTERIA
BACTERIOPHAGES
Bloom
Burst size
CELL PROLIFERATION
Chlorophyll - metabolism
Chloroplasts - metabolism
EDTA
EFFICIENCY
ENZYMES
HOST
Host-Pathogen Interactions
Infection
Infectious Disease
INFECTIVITY
LYSIS
MOI
Nucleotide
NUCLEOTIDES
Nucleotides - biosynthesis
Phycodnaviridae - physiology
PHYTOPLANKTON
PRODUCTIVITY
SALINITY
SIGNALS
STRAINS
Stramenopiles - immunology
Stramenopiles - virology
SYNTHESIS
TOXICITY
Virus
Virus Replication
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Summary:Abstract Infection dynamics (saturation kinetics, infection efficiency, adsorption and burst size) for the Aureococcus anophagefferens -Brown Tide virus ( AaV ) system were investigated using susceptible and resistant strains. Adsorption assays revealed that virus affinity to the cell surface is a key determinant of infectivity. Saturation of infection occurred at a multiplicity of infection (MOI) of 8 viruses per host and resulted in ~90–95% of infected cells, with burst sizes ranging from 164 to 191. Insight from the AaV genome implicates recycling of host nucleotides rather than de novo synthesis as a constraint on viral replication. Viral yields and mean burst sizes were significantly diminished with increasing MOI. This phenomenon, which was reminiscent of phage-induced ‘lysis from without’, appeared to be caused by viral contact and was unrelated to bacteria, signaling/toxic compounds, or defective interfering viruses. We posit that high-MOI effects attenuate viral proliferation in natural systems providing a negative feedback on virus-induced bloom collapse.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2014.07.023