Uncoating of human rhinovirus serotype 2 from late endosomes

Prchla, Elisabeth; Kuechler, Ernst; Blaas, Dieter; Fuchs, Renate

doi:10.1128/jvi.68.6.3713-3723.1994

Cited by 144 publications

(86 citation statements)

References 71 publications

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“…Using NH 4 Cl, we showed that the first viruses reached the acid-dependent step 5 min after cell warming, and that half of the incoming, infectious particles passed the NH 4 Cl-sensitive step within 12 min. The time course resembled that of other viruses penetrating from LE, such as lymphocytic choriomeningitis virus (LCMV), influenza A, and minor rhinoviruses (Martin and Helenius, 1991;Prchla et al, 1994;Quirin et al, 2008). These viruses pass the acid-sensitive step typically with a half-time of 10-20 min.…”

Section: Discussionmentioning

confidence: 82%

Entry of Bunyaviruses into Mammalian Cells

Lozach

Mancini

Bitto

et al. 2010

Cell Host & Microbe

135

251

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The Bunyaviridae constitute a large family of enveloped animal viruses, many members of which cause serious diseases. However, early bunyavirus-host cell interactions and entry mechanisms remain largely uncharacterized. Investigating Uukuniemi virus, a bunyavirus of the genus Phlebovirus, we found that virus attachment to the cell surface was specific but inefficient, with 25% of bound viruses being endocytosed within 10 min, mainly via noncoated vesicles. The viruses entered Rab5a+ early endosomes and, subsequently, Rab7a+ and LAMP-1+ late endosomes. Acid-activated penetration, occurring 20-40 min after internalization, required maturation of early to late endosomes. The pH threshold for viral membrane fusion was 5.4, and entry was sensitive to temperatures below 25 degrees C. Together, our results indicate that Uukuniemi virus penetrates host cells by acid-activated membrane fusion from late endosomal compartments. This study also highlights the importance of the degradative branch of the endocytic pathway in facilitating entry of late-penetrating viruses.

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Section: Discussionmentioning

confidence: 82%

Entry of Bunyaviruses into Mammalian Cells

Lozach

Mancini

Bitto

et al. 2010

Cell Host & Microbe

135

251

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“…The opening of the capsid in PV and HRV can be mediated by receptor binding, by low pH, or by the cooperative effect of both factors [71,[74][75][76]. Initial studies with PV and soluble poliovirus receptor (PVR) showed that receptor binding at physiological temperature (37 C) mediates RNA exit from the capsid interior with no additional factors [70].…”

Section: Receptor-mediated Uncoating Of Picornavirusesmentioning

confidence: 99%

“…Minor group HRV are sensitive to mildly acidic pH (5.5-6.0), which can trigger virus uncoating at physiological temperatures. Binding to LDLR does not mediate uncoating, and minor group HRV are thus dependent on endocytosis and endosome acidification for uncoating and host cell entry [16,75]. The major group of HRV, which bind ICAM-1, comprises viruses that differ in stability and sensitivity to receptor binding [12,71,78].…”

Section: Receptor-mediated Uncoating Of Picornavirusesmentioning

confidence: 99%

“…15.1) [3]. Indeed, the mildly acidic pH (5.5-6.0) in endosomal compartments is optimal for uncoating of and infection by minor group HRV [16,75,80]. Exposure to low pH is also necessary for efficient uncoating and cell entry by some major group HRV [16,76], although certain serotypes require only ICAM-1 binding, after which they can infect cells, even in the presence of agents that prevent endosome acidification.…”

Section: Receptor-mediated Uncoating Of Picornavirusesmentioning

confidence: 99%

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Virus-Receptor Interactions and Receptor-Mediated Virus Entry into Host Cells

Casasnovas

2013

Subcellular Biochemistry

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The virus particles described in previous chapters are vehicles that transmit the viral genome and the infection from cell to cell. To initiate the infective cycle, the viral genome must therefore translocate from the viral particle to the cytoplasm. Via distinct proteins or motifs in their outermost shell, the particles attach initially to specific molecules on the host cell surface. These virus receptors thus mediate penetration of the viral genome inside the cell, where the intracellular infective cycle starts. The presence of these receptors on the cell surface is a principal determinant of virus host tropism. Viruses can use diverse types of molecules to attach to and enter into cells. In addition, virus-receptor recognition can evolve over the course of an infection, and virus variants with distinct receptor-binding specificities and tropism can appear. The identification of virus receptors and the characterization of virus-receptor interactions have been major research goals in virology for the last two decades. In this chapter, we will describe, from a structural perspective, several virus-receptor interactions and the active role of receptor molecules in virus entry.

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“…The RV life cycle offers many opportunities for intervention. The initial stage of the viral life cycle involves binding to a cell surface receptor, endocytosis, acidification of the endosome, viral uncoating, and release of viral RNA (vRNA) to the cytoplasm (Prchla et al, 1994). In the next stage, vRNA is translated as a single large polyprotein from an internal ribosomal entry site (IRES) which is located in the 5 0 untranslated region of RV genome.…”

Section: Introductionmentioning

confidence: 99%

Quercetin inhibits rhinovirus replication in vitro and in vivo

et al. 2012

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Highlights ► Rhinovirus is responsible for majority of common colds. ► There are no FDA approved drugs are available to treat rhinovirus infection. ► We show that quercetin, a plant flavonoid blocks viral replication in vitro . ► In addition quercetin inhibits virus-stimulated cytokine expression. ► Quercetin also inhibits viral replication and decreasing lung inflammation in vivo .

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Uncoating of human rhinovirus serotype 2 from late endosomes

Cited by 144 publications

References 71 publications

Entry of Bunyaviruses into Mammalian Cells

Entry of Bunyaviruses into Mammalian Cells

Virus-Receptor Interactions and Receptor-Mediated Virus Entry into Host Cells

Quercetin inhibits rhinovirus replication in vitro and in vivo

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