Key result
Treatment of MHV-infected cells with an antisense oligonucleotide against the leader RNA at 5-25 microM inhibited viral multiplication and reduced viral mRNA and protein synthesis.
An antisense oligonucleotide targeting the leader RNA of mouse hepatitis virus effectively inhibits viral multiplication in vitro.
Antisense targeting of MHV leader RNA inhibits replication in vitro; leaves open translation to animal models or human coronaviruses.
An oligonucleotide complementary to a leader RNA of positive-stranded mouse hepatitis virus (MHV) was tested for the effect on the viral multiplication in mouse DBT cells. A 14-mer antisense oligonucleotide contained a sequence complementary to the conserved pentanucleotide sequence, UCUAA, of the leader RNA. A treatment of MHV-infected cells with the antisense oligonucleotide at concentrations from 5 to 25 microM had an inhibitory effect on the viral multiplication and reduced the synthesis of viral specific mRNA and proteins. No inhibitory effect was observed when the cells were treated with sense oligonucleotide and oligonucleotide which contained unrelated sequences at concentrations from 1 to 10 microM. These results showed that antisense oligonucleotide against the leader RNA reduced the multiplication of positive-stranded RNA virus, MHV.
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Mizutani et al. (1992) studied Mouse hepatitis virus (MHV) infection. 14-mer antisense oligonucleotide complementary to the leader RNA vs. Sense oligonucleotide and unrelated sequence oligonucleotides (1 to 10 microM) was evaluated on Viral multiplication and synthesis of viral specific mRNA and proteins. Treatment of MHV-infected cells with an antisense oligonucleotide against the leader RNA at 5-25 microM inhibited viral multiplication and reduced viral mRNA and protein synthesis.
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