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Dynamics of virus-receptor interactions in virus binding, signaling, and endocytosis.

Boulant S, Stanifer M, Lozach PY - Viruses (2015)

Bottom Line: During viral infection the first challenge that viruses have to overcome is gaining access to the intracellular compartment.The infection process starts when the virus contacts the surface of the host cell.A complex series of events ensues, including diffusion at the host cell membrane surface, binding to receptors, signaling, internalization, and delivery of the genetic information.

View Article: PubMed Central - PubMed

Affiliation: CellNetworks-Cluster of Excellence and Department of Infectious Diseases, Virology, University Hospital Heidelberg, 69120 Heidelberg, Germany. s.boulant@dkfz-heidelberg.de.

ABSTRACT
During viral infection the first challenge that viruses have to overcome is gaining access to the intracellular compartment. The infection process starts when the virus contacts the surface of the host cell. A complex series of events ensues, including diffusion at the host cell membrane surface, binding to receptors, signaling, internalization, and delivery of the genetic information. The focus of this review is on the very initial steps of virus entry, from receptor binding to particle uptake into the host cell. We will discuss how viruses find their receptor, move to sub-membranous regions permissive for entry, and how they hijack the receptor-mediated signaling pathway to promote their internalization.

No MeSH data available.


Related in: MedlinePlus

Signaling during virus entry. Infections cause profound perturbations of the host cell signaling networks. Signaling likely begins at the plasma membrane, after virus binding to receptors. Here are few examples of signaling during virus entry. (A) Following attachment at the cell surface, influenza A virus (IAV) relies on the activation of epidermal growth factor receptor (EGFR) for the endocytosis of virions. However, no direct interaction has been reported between IAV and EGFR; (B) In the case of vaccinia virus (VV), virions seem to cooperate for entry. In this model, the first incoming virions trigger signaling through binding to primary receptor(s). The signal facilitates the recruitment of other receptors, which all together mediate the attachment and endocytosis of further incoming particles by induction of micropinocytosis; (C) Upon binding of viruses to receptor molecules, receptor-mediated signaling induces the local internalization of the virus/receptor complex. Concrete evidence supporting such receptor-mediated signaling that results in an active internalization is missing. The encircled numbers indicate the sequence of events.
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viruses-07-02747-f003: Signaling during virus entry. Infections cause profound perturbations of the host cell signaling networks. Signaling likely begins at the plasma membrane, after virus binding to receptors. Here are few examples of signaling during virus entry. (A) Following attachment at the cell surface, influenza A virus (IAV) relies on the activation of epidermal growth factor receptor (EGFR) for the endocytosis of virions. However, no direct interaction has been reported between IAV and EGFR; (B) In the case of vaccinia virus (VV), virions seem to cooperate for entry. In this model, the first incoming virions trigger signaling through binding to primary receptor(s). The signal facilitates the recruitment of other receptors, which all together mediate the attachment and endocytosis of further incoming particles by induction of micropinocytosis; (C) Upon binding of viruses to receptor molecules, receptor-mediated signaling induces the local internalization of the virus/receptor complex. Concrete evidence supporting such receptor-mediated signaling that results in an active internalization is missing. The encircled numbers indicate the sequence of events.

Mentions: A more direct role in the entry and internalization of IAV and hepatitis C virus (HCV) has been attributed to EGFR. Following attachment of IAV to the cells, the activation of EGFR and downstream signaling via PI3Ks have been proposed to be required for the endocytosis of the virions (Figure 3A) [60]. The binding of HCV to one of its receptors, CD81, is believed to allow for interactions with EGFR, and subsequently, for internalization of the virus/EGFR complex [61,62]. The activation of EGFR signaling seems to enhance the entry of further HCV particles. In addition to these viruses, human papillomavirus type 16, respiratory syncytial virus, and African swine fever virus have the ability to hijack the EGFR functions to ensure their entry [63,64,65,66]. Many of these viruses share a dependence on membrane blebbing and rapid rearrangement of actin filaments for infectious entry.


Dynamics of virus-receptor interactions in virus binding, signaling, and endocytosis.

Boulant S, Stanifer M, Lozach PY - Viruses (2015)

Signaling during virus entry. Infections cause profound perturbations of the host cell signaling networks. Signaling likely begins at the plasma membrane, after virus binding to receptors. Here are few examples of signaling during virus entry. (A) Following attachment at the cell surface, influenza A virus (IAV) relies on the activation of epidermal growth factor receptor (EGFR) for the endocytosis of virions. However, no direct interaction has been reported between IAV and EGFR; (B) In the case of vaccinia virus (VV), virions seem to cooperate for entry. In this model, the first incoming virions trigger signaling through binding to primary receptor(s). The signal facilitates the recruitment of other receptors, which all together mediate the attachment and endocytosis of further incoming particles by induction of micropinocytosis; (C) Upon binding of viruses to receptor molecules, receptor-mediated signaling induces the local internalization of the virus/receptor complex. Concrete evidence supporting such receptor-mediated signaling that results in an active internalization is missing. The encircled numbers indicate the sequence of events.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4488714&req=5

viruses-07-02747-f003: Signaling during virus entry. Infections cause profound perturbations of the host cell signaling networks. Signaling likely begins at the plasma membrane, after virus binding to receptors. Here are few examples of signaling during virus entry. (A) Following attachment at the cell surface, influenza A virus (IAV) relies on the activation of epidermal growth factor receptor (EGFR) for the endocytosis of virions. However, no direct interaction has been reported between IAV and EGFR; (B) In the case of vaccinia virus (VV), virions seem to cooperate for entry. In this model, the first incoming virions trigger signaling through binding to primary receptor(s). The signal facilitates the recruitment of other receptors, which all together mediate the attachment and endocytosis of further incoming particles by induction of micropinocytosis; (C) Upon binding of viruses to receptor molecules, receptor-mediated signaling induces the local internalization of the virus/receptor complex. Concrete evidence supporting such receptor-mediated signaling that results in an active internalization is missing. The encircled numbers indicate the sequence of events.
Mentions: A more direct role in the entry and internalization of IAV and hepatitis C virus (HCV) has been attributed to EGFR. Following attachment of IAV to the cells, the activation of EGFR and downstream signaling via PI3Ks have been proposed to be required for the endocytosis of the virions (Figure 3A) [60]. The binding of HCV to one of its receptors, CD81, is believed to allow for interactions with EGFR, and subsequently, for internalization of the virus/EGFR complex [61,62]. The activation of EGFR signaling seems to enhance the entry of further HCV particles. In addition to these viruses, human papillomavirus type 16, respiratory syncytial virus, and African swine fever virus have the ability to hijack the EGFR functions to ensure their entry [63,64,65,66]. Many of these viruses share a dependence on membrane blebbing and rapid rearrangement of actin filaments for infectious entry.

Bottom Line: During viral infection the first challenge that viruses have to overcome is gaining access to the intracellular compartment.The infection process starts when the virus contacts the surface of the host cell.A complex series of events ensues, including diffusion at the host cell membrane surface, binding to receptors, signaling, internalization, and delivery of the genetic information.

View Article: PubMed Central - PubMed

Affiliation: CellNetworks-Cluster of Excellence and Department of Infectious Diseases, Virology, University Hospital Heidelberg, 69120 Heidelberg, Germany. s.boulant@dkfz-heidelberg.de.

ABSTRACT
During viral infection the first challenge that viruses have to overcome is gaining access to the intracellular compartment. The infection process starts when the virus contacts the surface of the host cell. A complex series of events ensues, including diffusion at the host cell membrane surface, binding to receptors, signaling, internalization, and delivery of the genetic information. The focus of this review is on the very initial steps of virus entry, from receptor binding to particle uptake into the host cell. We will discuss how viruses find their receptor, move to sub-membranous regions permissive for entry, and how they hijack the receptor-mediated signaling pathway to promote their internalization.

No MeSH data available.


Related in: MedlinePlus