Key result
Shifts to supraoptimal temperatures in poliovirus-infected HeLa cells resulted in extensive degradation of newly made virus RNA, potentially due to the release or activation of a ribonuclease.
Answers are grounded in this paper and cite their sources.
Supraoptimal temperatures inhibit poliovirus RNA synthesis in HeLa cells by inducing degradation of newly made viral RNA, possibly due to the release or activation of a ribonuclease.
Summary In HeLa cells infected with poliovirus, shifts from optimal to supraoptimal temperatures in the middle of the infectious cycle resulted in extensive degradation of newly made virus RNA. This temperature-induced degradation was not observed until about 3 hr after infection. It did not require simultaneous synthesis of proteins. During the first 3 hr of infection at 39·5°, RNA of temperature-resistant poliovirus strains replicated much faster than at 36°. Subsequently, degradation became predominant. Thus, temperature-resistant strains partially escaped the effects of degradation by faster replication. During the first 150 min. approximately, the RNA of temperature-sensitive strains replicated as well at supraoptimal as at optimal temperatures. Subsequently, newly made virus RNA was degraded. The inhibitory effect of supraoptimal temperatures may be due to release, or activation, of a ribonuclease.
No takes yet. Share an insight, caveat, or question.
Fiszman et al. (1970) studied Poliovirus infection. Supraoptimal temperatures vs. Optimal temperatures was evaluated on Poliovirus RNA synthesis and degradation. Shifts to supraoptimal temperatures in poliovirus-infected HeLa cells resulted in extensive degradation of newly made virus RNA, potentially due to the release or activation of a ribonuclease.
Synapse has enriched 10 related papers. Consider them for comparative context: