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Interaction of encephalomyocarditis virus with ultraviolet-irradiated host cells
Abstract:
Ultraviolet light (UV) impaired the capacity of L cells to support growth of encephalomyocarditis virus. The loss of capacity was partially restored by high multiplicity of infection (MOI). This phenomenon was not due to an increased probability of an infectious virus particle reaching a site of replication undamaged by UV, since UV-inactivated virus at high MOI induced restoration of the capacity to support multiplication of nonirradiated virus adsorbed at low MOI. Multiplicity reactivation of UV-irradiated virus did not play a role in this phenomenon since restoration of capacity took place without multiplication of the UV-irradiated restoring virus. The evidence indicates that restoration of capacity was not due to viral interactions involving genetic exchange. The ability to restore capacity was a property more radioresistant than infectivity, suggesting that the former is a function only of part of the viral genome.
Insights
Ultraviolet light (UV) damages L cells' ability to grow encephalomyocarditis virus. High virus doses partially restore this capacity, indicating a UV-resistant viral component is involved.
Area of Science:
- Virology
- Cell Biology
- Photobiology
Background:
- Ultraviolet (UV) irradiation is known to damage cellular and viral components.
- Understanding how cells recover their capacity to support viral replication after UV damage is crucial.
Purpose of the Study:
- To investigate the mechanism by which high multiplicity of infection (MOI) restores the capacity of UV-impaired L cells to support encephalomyocarditis virus (EMCV) growth.
- To determine if viral genetic exchange or multiplicity reactivation plays a role in this restoration process.
Main Methods:
- Exposing L cells to UV light and subsequently infecting them with EMCV at varying MOIs.
- Utilizing UV-inactivated EMCV at high MOI to assess its effect on the replication of non-irradiated virus adsorbed at low MOI.
- Analyzing the role of multiplicity reactivation and genetic exchange in the observed restoration phenomenon.
Main Results:
- UV irradiation significantly impaired L cells' ability to support EMCV replication.
- High MOI, including UV-inactivated virus, partially restored the cells' capacity to support viral growth.
- The restoration mechanism did not involve multiplicity reactivation or genetic exchange.
- The capacity-restoring property of the virus was more radioresistant than its infectivity.
Conclusions:
- The restoration of L cell capacity to support EMCV growth after UV damage is mediated by a UV-resistant viral component.
- This component likely represents a fraction of the viral genome, as its function is more radioresistant than infectivity.
- The findings suggest a novel mechanism of cellular recovery influenced by viral factors, independent of traditional viral reactivation pathways.