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Studies on human KC cell syncytia formation induced by Mason-Pfizer monkey virus
Abstract:
Human KC cell monolayer inoculated with concentraten Mason-Pfizer monkey virus (MPMV) showed syncytia formation within an hour. The cell fusion was blocked by the treatment of the MPMV with neutralizing antiserum. Treatment of the MPVM with beta-propiolactone resulted in the loss of infectivity although KC cell fusion ability of the virus still remained. KC cells inoculated with unconcentrated MPMV showed no cell fusion even after several transfers, although a chronic MPMV infection was established. The virus-producing KC cells were refractory to fusion by MPMV. Human embryonic lung cells (HEL) were infected by serially diluted MPMV harvested from virus-producing culture, transferred twice, then cultivated together with KC cells for syncytia formation to examine the end point dilution titer of the virus. HEL infected by 10(-4)-diluted MPMV still induced syncytia formation by cocultivation with KC cells.
Insights
Mason-Pfizer monkey virus (MPMV) can cause cell fusion in human KC cells, which can be blocked by antiserum. Concentrated MPMV induces syncytia, while unconcentrated virus establishes chronic infection without fusion.
Area of Science:
- Virology
- Cell Biology
Background:
- Mason-Pfizer monkey virus (MPMV) is a simian retrovirus known to infect various cell types.
- Syncytia formation, or cell fusion, is a hallmark of infection by certain viruses, indicating cytopathic effects.
Purpose of the Study:
- To investigate the syncytia-inducing capabilities of Mason-Pfizer monkey virus (MPMV) in human KC cells.
- To characterize the infectivity and cell fusion potential of MPMV under different conditions.
- To determine the viral titer in infected human embryonic lung (HEL) cells.
Main Methods:
- Inoculation of human KC cell monolayers with concentrated and unconcentrated MPMV.
- Treatment of MPMV with neutralizing antiserum and beta-propiolactone.
- Serial dilution and transfer of MPMV in HEL cells, followed by co-cultivation with KC cells.
Main Results:
- Concentrated MPMV rapidly induced syncytia formation in KC cells, which was inhibited by neutralizing antiserum.
- Beta-propiolactone treatment abolished MPMV infectivity but retained its cell fusion ability.
- Unconcentrated MPMV established chronic infection in KC cells without syncytia formation; these cells became refractory to fusion.
- HEL cells infected with MPMV diluted up to 10(-4) could still induce syncytia formation in co-cultured KC cells.
Conclusions:
- MPMV's ability to induce cell fusion is separable from its infectivity.
- Chronic MPMV infection in KC cells leads to refractoriness to viral-induced cell fusion.
- The end-point dilution titer of MPMV in HEL cells can be determined by assessing syncytia formation in co-cultured KC cells.