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Mutagenesis by simian virus 40. I. detection of mutations in Chinese hamster cell lines using different resistance

Mutation Research
|October 1, 1976
PubMed

Insights

Simian virus 40 (SV40) demonstrated mutagenic effects in Chinese hamster cells, increasing mutation frequencies for specific drug resistances. However, it did not increase resistance to 5-bromodeoxyuridine (BUdR) but could induce resistance in some BUdR-resistant cells.

Area of Science:

  • * Virology
  • * Molecular Biology
  • * Cell Biology

Background:

  • * Simian virus 40 (SV40) is a well-characterized DNA tumor virus with known oncogenic properties.
  • * Understanding the mutagenic potential of viruses like SV40 is crucial for assessing their role in cellular transformation and disease.
  • * Previous studies have explored the interaction of SV40 with host cell DNA and its effects on cellular processes.

Purpose of the Study:

  • * To investigate the mutagenic action of SV40 in permanent Chinese hamster cell lines (CHO-K1 and V79).
  • * To assess the frequency of mutations induced by SV40 using various drug resistance markers.
  • * To explore the potential of SV40 to induce or alter drug resistance phenotypes in mammalian cells.

Main Methods:

  • * Infection of Chinese hamster cells (CHO-K1 and V79) with SV40.
  • * Measurement of mutation frequencies using resistance markers for 8-azaguanine, aminopterin, colchicine, and 5-bromodeoxyuridine (BUdR).
  • * Culture of isolated resistant cell clones under non-selective conditions to assess stability of induced resistance.

Main Results:

  • * SV40 infection significantly increased mutation frequencies for 8-azaguanine, aminopterin, and colchicine resistance by one to two orders of magnitude compared to spontaneous frequencies.
  • * SV40 infection did not enhance the frequency of mutations conferring resistance to 5-bromodeoxyuridine (BUdR).
  • * Infection with SV40 induced the ability to proliferate in HAT medium in three out of five BUdR-resistant cell clones, indicating induced resistance.

Conclusions:

  • * SV40 exhibits mutagenic activity in Chinese hamster cells, particularly for certain drug resistance markers.
  • * The virus's effect on BUdR resistance is complex, not directly increasing mutation frequency but capable of inducing resistance phenotypes.
  • * The induced resistance to HAT medium by SV40 was stable, suggesting potential mechanisms for viral-mediated genetic alteration.

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