Patterns of Cytopathology and Lysosomal Enzyme Release in Poliovirus-infected HEp-2 Cells Treated With Either 2-( -Hydroxybenzyl)-Benzimidazole or Guanidine HCl

Abstract

SUMMARYThe viral inhibitors guanidine hydrochloride and 2-(~-hydroxybenzyl)-benzimidazole (HBB) were used to study the relationship between lysosomal enzyme release and the development of poliovirus-induced cytopathic effect (CPE) in HEp-2 cells. Lysosomal enzyme release, the development of CPE and virus replication were inhibited or delayed if these antiviral agents were added up to 2 to 3 hr after infection. When added later the agents were no longer effective. It is suggested that a virus-induced protein produced during 3 hr after infection is responsible for lysosomal enzyme release.

Remodeling the Endoplasmic Reticulum by Poliovirus Infection and by Individual Viral Proteins: an Autophagy-Like Origin for Virus-Induced Vesicles

“…A lysosomal origin for poliovirus-induced vesicles would be consistent with immunoelectron microscopic analysis that showed staining of poliovirus-induced vesicles with LAMP-1, a marker of endosomes and lysosomes (41), and with the documented increases in lysosomal enzymes in the cytoplasm of poliovirus-infected cells (21). All fractions from uninfected and virus-infected cells were assayed for ␤-hexosaminidase activity (Fig.…”

Effect of Double Infection of Cowpox Virus‐Infected Cells with Paramyxovirus (Sendai Virus) on Formation of Cowpox Virus‐Specific Cell Surface Antigen

“…Moreover, the increase in these activities was similarly inhibited in the presence of puromycin coincident with loss of the enhancement of the CPV S-ag formation. A general increase in lysosomal enzyme activities after lytic virus infection is well known (1,2,5,11). In our present study, a close correlation between the activation of these lysosomal enzymes and the CPV degrading activity or a subsequent enhancement of the CPV S-ag formation was observed.…”

Cytopathic Effects of Viruses: A General Survey

“…In a subsequent study, Bablanian et al (1966) found that HBB markedly delayed the development of cytopathic effects caused by echovirus 12 and coxsackie-virus B4 infection of monkey kidney cells; once again, the HBB did not prevent ultimate degeneration of infected cells even though viral multiplication was inhibited. Guskey et al (1970) confirmed and extended these studies somewhat by testing the effect of guanidine and HBB on the release of lysosomal enzymes as well as cytopathology of HEp-2 cells infected with poliovirus 1. Poliovirus replication, cytopathology, and lysosomal enzyme release were all inhibited or delayed if the antiviral agents were present up to 2-3 hr postinfection but not thereafter.…”

“…To test the hypothesis proposed by Amako and Dales (1967b) that a cytotoxic protein synthesized by mengovirus alters the permeability of lysosomes, Thacore and Wolff (1968) ex-amined cytoplasmic extracts from poliovirus-infected HEp-2 cells and found that they contained twice as much f3-glucuronidase from lysosomes than did cytoplasmic extracts of uninfected cells; any interpretation of such an experiment might be considered dangerous. Guskey et al (1970) used guanidine-Hel and HBB to study the relationship between lysosomal enzyme release and cytopathic effects in HEp-2 cells infected with poliovirus type 1. Lysosomal enzyme release, cytopathic effect, and virus release were all inhibited or delayed if the antiviral agents were added up to 2-3 hr postinfection, but not later; an hypothesis implicating a newly synthesized poliovirus protein as the lysosome enzyme-releasing factor was not tested.…”