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Establishment and characterization of a persistent infection of MDBK cells with herpes simplex virus
Abstract:
A persistent, dynamic-state infection of a variant of herpes simplex virus type 1 strain MP [HSV-1 (MP)] in MDBK cells was established without supportive measures and maintained for over three years by routine passaging of the cells at 7-9 day intervals. The infection was characterized by a cyclic pattern of monolayer damage and reconstitution, correlated with virus production, which was most evident when the interval between subcultures was intentionally prolonged and the cells were left undisturbed. Occasional periods of cell crisis, with increased virus replication and extensive cytopathology, occurred. Passaging of the cells at higher density avoided eventual loss of the culture during the most severe crises. Presence of specific antibodies did not alter the course of infection. Interferon was constantly found during periods of cell crisis; it appeared on the second day after subculture, reached a maximum in correspondance of the first peak of cytopathology, and disappeared well before the onset of the second wave of cytopathology. Addition of exogenous interferon cured the cells of infection. Defective interfering particles could not be found. Virus isolated during persistence differed from parental virus regarding plaque morphology, temperature sensitivity of growth, and electrophoretic pattern of infected cells glycoproteins. A discussion on the possible mechanisms of persistence is provided.
Insights
A persistent herpes simplex virus type 1 (HSV-1) infection in MDBK cells showed cyclic damage and recovery. Exogenous interferon treatment successfully eliminated the persistent HSV-1 infection.
Area of Science:
- Virology
- Cell Biology
Background:
- Herpes simplex virus type 1 (HSV-1) can establish persistent infections.
- Understanding the dynamics of persistent viral infections is crucial for developing effective treatments.
Purpose of the Study:
- To establish and characterize a persistent infection of HSV-1 (MP) in MDBK cells.
- To investigate the role of cellular responses and potential therapeutic interventions in persistent HSV-1 infections.
Main Methods:
- Establishing a persistent HSV-1 (MP) infection in MDBK cells through routine passaging.
- Monitoring viral production, cytopathology, and cellular responses over extended periods.
- Assessing the effect of exogenous interferon on the persistent infection.
Main Results:
- A dynamic-state persistent infection was maintained for over three years with cyclic monolayer damage and reconstitution.
- Cell crisis periods with increased viral replication and cytopathology were observed, manageable by higher cell density passaging.
- Interferon was detected during cell crisis, and exogenous interferon addition successfully cured the infection.
- Isolated persistent HSV-1 strains exhibited altered characteristics compared to the parental virus.
Conclusions:
- Persistent HSV-1 infection in MDBK cells exhibits a dynamic, cyclic nature.
- Interferon plays a significant role in the host response to persistent HSV-1 infection and can be therapeutically effective.