pH-dependent solubility shift of rubella virus capsid protein

Mauracher, Christoph A.; Gillam, Shirley; Shukin, Robert; Tingle, Aubrey J.

doi:10.1016/0042-6822(91)90916-y

Cited by 28 publications

(12 citation statements)

References 15 publications

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“…For JV entry, fusion seems to occur in endosomes where the pH is 6.1 or lower. The acid environment may be responsible for structural changes in JV external proteins allowing membrane fusion and facilitating viral uncoating as described for Influenza virus [7], Rubella virus [17], West Nile virus [13] and tick-borne encephalitis virus [11].…”

Section: Discussionmentioning

confidence: 99%

The entry of Junin virus into Vero cells

Castilla

Mersich

Candurra

et al. 1994

Archives of Virology

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The entry mechanism of Junin virus (JV) into Vero cells was studied analyzing the effect of lysosomotropic compounds and acid pH on JV infection. Ammonium chloride, amantadine, chlorpheniramine and procaine inhibited JV production. The action of ammonium chloride was exerted at early times of infection. Virus internalization was inhibited and viral protein expression was not detected. When the extracellular medium was buffered at low pH, the ammonium chloride induced block on JV infection was overcome. Furthermore, JV was able to induce fusion of infected cells at pH 5.5 leading to polykaryocyte formation. Taken together, these results demonstrate that JV entry occurs through an endocytic mechanism requiring a low pH dependent membrane fusion.

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Section: Discussionmentioning

confidence: 99%

The entry of Junin virus into Vero cells

Castilla

Mersich

Candurra

et al. 1994

Archives of Virology

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“…It has been shown that between pH 5.0 and 5.5, the RV capsid protein undergoes a structural change from having hydrophilic to hydrophobic properties (95). This conformational change in the capsid protein presumably allows uncoating to occur within the endosome, allowing the release of viral genomic RNA into the cytoplasm.…”

Section: Attachment and Entrymentioning

confidence: 99%

“…The virion is then transported into the cell when the coated pit invaginates to form a coated vesicle. The virus is subsequently delivered through a series of endosomes with progressively acidic compartments until it reaches an endosome where the environment is sufficiently acidic (pH 5.3) to induce conformational changes within the E1 and capsid pro- tein, resulting in the release of the genomic RNA into the cytoplasm (95). The events from virus uncoating to early formation of the replication complex are unknown.…”

Section: Replication Complexesmentioning

confidence: 99%

Rubella Virus Replication and Links to Teratogenicity

Lee

Bowden

2000

Clinical Microbiology Reviews

152

115

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“…RV produces haemolysis and fusion of erythrocytes in a mildly acidic pH (Kobayashi, 1978;Vfifin~inen & Kfifiri/iinen, 1980); a brief treatment at a pH below 6.0 causes a conformational change in the viral envelope glycoproteins E1 and E2, resulting in the acquisition of liposome-binding activity of virions and inducing fusion of RV-infected cells (Katow & Sugiura, 1988). RV capsids also undergo a solubility change below pH 5.5, becoming hydrophobic in nature (Mauracher et al, 1991). However the entry pathway of RV has not yet been identified.…”

Section: Introductionmentioning

confidence: 99%

Pathway of rubella virus infectious entry into Vero cells

Petruzziello

Orsi

Macchia

et al. 1996

Journal of General Virology

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The mechanism and the kinetics of rubella virus (RV) penetration into Vero cells were studied. By using pronase or acid treatment to inactivate virus which had adsorbed to cell membrane but had not been internalized, it was found that a period of 7 h was required in order for all of the adsorbed virus to enter the host cells. Lysosomotropic agents (monensin, methylamine, ammonium chloride and chloroquine) were used to study the mechanism by which RV penetrates host cells. Virus replication was inhibited if treatment of cells with these compounds was performed for at least 9 h after infection. However, if extracellular adsorbed virions were eliminated by acid treatment following removal of the lysosomotropic compounds, RV replication was completely inhibited by treatment with these drugs for any time period after adsorption. This indicated that the prolonged period of treatment with these compounds necessary to inhibit virus replication is due to the slow rate of RV internalization. None of the compounds had any effect on infection initiated by transfection of RV RNA, confirming that these drugs were exerting their inhibitory activity at penetration. The inhibition of RV replication by lysosomotropic compounds indicates that RV penetrates host cells by the endosomal pathway.

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pH-dependent solubility shift of rubella virus capsid protein

Cited by 28 publications

References 15 publications

The entry of Junin virus into Vero cells

The entry of Junin virus into Vero cells

Rubella Virus Replication and Links to Teratogenicity

Pathway of rubella virus infectious entry into Vero cells

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