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Replication kinetics and cytopathic effect of hepatitis A virus
T Cromeans1, H A Fields, M D Sobsey
1University of North Carolina, School of Public Health, Chapel Hill 27514.
The Journal of General Virology
|August 1, 1989
Summary
Hepatitis A virus replication and cell damage depend on cell line passage and virus selection methods. Optimizing these factors influences virus production and infectivity in cell cultures.
Area of Science:
- Virology
- Cell Biology
Background:
- Hepatitis A virus (HAV) infection is a significant public health concern.
- Understanding HAV replication dynamics is crucial for developing effective control strategies.
Purpose of the Study:
- To investigate the influence of cell line passage level and virus selection methods on Hepatitis A virus (HAV) replication and cytopathic effect (c.p.e.).
- To characterize the replication kinetics and yield of HAV strain HM-175 in different cell lines.
Main Methods:
- Hepatitis A virus (HAV) strain HM-175 was cultured and passaged in BS-C-1 and FRhK-4 cell lines.
- Virus replication kinetics were analyzed under single-step growth curve conditions.
- Cytopathic effect (c.p.e.) was assessed in FRhK-4 cells, with variants selected through passage or radioimmunofocus assay.
- The effect of 3 mM-guanidine on viral yield and c.p.e. was evaluated.
- HAV strain MD-1, isolated from groundwater, was studied for its c.p.e. in FRhK-4 cells after passage through persistently infected A-549 cells.
Main Results:
- HAV replication and c.p.e. were significantly influenced by cell line passage level and virus selection methods.
- Maximum virus production varied from 24-28 hours to 10 days post-infection.
- While rapid replication of HM-715 (pHM-175) occurred in BS-C-1 cells, pronounced c.p.e. was observed in FRhK-4 cells.
- Higher virus yields were obtained in FRhK-4 cells compared to BS-C-1 cells.
- 3 mM-guanidine reduced the c.p.e. and infectious yield of pHM-175 in FRhK-4 cells.
- HAV strain MD-1 induced c.p.e. in FRhK-4 cells following passage through infected A-549 cells.
Conclusions:
- Cell line and virus characteristics critically determine HAV replication efficiency and cytopathogenicity.
- FRhK-4 cells are more susceptible to HAV-induced c.p.e. than BS-C-1 cells.
- Guanidine treatment can modulate HAV infectivity and cell damage.
- Environmental HAV isolates can adapt to cause cytopathic effects in cell culture models.