Monitoring of S Protein Maturation in the Endoplasmic Reticulum by Calnexin Is Important for the Infectivity of Severe Acute Respiratory Syndrome Coronavirus
Identifieur interne : 000043 ( PascalFrancis/Corpus ); précédent : 000042; suivant : 000044Monitoring of S Protein Maturation in the Endoplasmic Reticulum by Calnexin Is Important for the Infectivity of Severe Acute Respiratory Syndrome Coronavirus
Auteurs : Masaya Fukushi ; Yoshiyuki Yoshinaka ; Yusuke Matsuoka ; Seisuke Hatakeyama ; Yukihito Ishizaka ; Teruo Kirikae ; Takehiko Sasazuki ; Tohru Miyoshi-AkiyamaSource :
- Journal of virology [ 0022-538X ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of SARS, a fatal pulmonary disorder with no effective treatment. We found that SARS-CoV spike glycoprotein (S protein), a key molecule for viral entry, binds to calnexin, a molecular chaperone in the endoplasmic reticulum (ER), but not to calreticulin, a homolog of calnexin. Calnexin bound to most truncated mutants of S protein, and S protein bound to all mutants of calnexin. Pseudotyped virus carrying S protein (S-pseudovirus) produced by human cells that were treated with small interfering RNA (siRNA) for calnexin expression (calnexin siRNA-treated cells) showed significantly lower infectivity than S-pseudoviruses produced by untreated and control siRNA-treated cells. S-pseudovirus produced by calnexin siRNA-treated cells contained S protein modified with N-glycan side chains differently from other two S proteins and consisted of two kinds of viral particles: those of normal density with little S protein and those of high density with abundant S protein. Treatment with peptide-N-glycosidase F (PNGase F), which removes all types of N-glycan side chains from glycoproteins, eliminated the infectivity of S-pseudovirus. S-pseudovirus and SARS-CoV produced in the presence of α-glucosidase inhibitors, which disrupt the interaction between calnexin and its substrates, showed significantly lower infectivity than each virus produced in the absence of those compounds. In S-pseudovirus, the incorporation of S protein into viral particles was obviously inhibited. In SARS-CoV, viral production was obviously inhibited. These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding, resulting in conferring infectivity on SARS-CoV.
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Format Inist (serveur)
NO : | PASCAL 12-0410005 INIST |
---|---|
ET : | Monitoring of S Protein Maturation in the Endoplasmic Reticulum by Calnexin Is Important for the Infectivity of Severe Acute Respiratory Syndrome Coronavirus |
AU : | FUKUSHI (Masaya); YOSHINAKA (Yoshiyuki); MATSUOKA (Yusuke); HATAKEYAMA (Seisuke); ISHIZAKA (Yukihito); KIRIKAE (Teruo); SASAZUKI (Takehiko); MIYOSHI-AKIYAMA (Tohru) |
AF : | Department of Infectious Diseases, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (1 aut., 3 aut., 4 aut., 6 aut., 8 aut.); Disease Control and Prevention Center, National Center for Global Health and Medicine/Tokyo/Japon (1 aut.); Deputy Director-General's Laboratory, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (1 aut.); Department of Virology, Institute of Biomedical & Health Sciences, Hiroshima University/Hiroshima/Japon (1 aut.); Department of Molecular Virology, Bio-Response, Graduate School, Tokyo Medical and Dental University/Tokyo/Japon (2 aut.); Department of Intractable Diseases, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (5 aut.); National Center for Global Health and Medicine/Tokyo/Japon (7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 21; Pp. 11745-11753; Bibl. 49 ref. |
LA : | Anglais |
EA : | Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of SARS, a fatal pulmonary disorder with no effective treatment. We found that SARS-CoV spike glycoprotein (S protein), a key molecule for viral entry, binds to calnexin, a molecular chaperone in the endoplasmic reticulum (ER), but not to calreticulin, a homolog of calnexin. Calnexin bound to most truncated mutants of S protein, and S protein bound to all mutants of calnexin. Pseudotyped virus carrying S protein (S-pseudovirus) produced by human cells that were treated with small interfering RNA (siRNA) for calnexin expression (calnexin siRNA-treated cells) showed significantly lower infectivity than S-pseudoviruses produced by untreated and control siRNA-treated cells. S-pseudovirus produced by calnexin siRNA-treated cells contained S protein modified with N-glycan side chains differently from other two S proteins and consisted of two kinds of viral particles: those of normal density with little S protein and those of high density with abundant S protein. Treatment with peptide-N-glycosidase F (PNGase F), which removes all types of N-glycan side chains from glycoproteins, eliminated the infectivity of S-pseudovirus. S-pseudovirus and SARS-CoV produced in the presence of α-glucosidase inhibitors, which disrupt the interaction between calnexin and its substrates, showed significantly lower infectivity than each virus produced in the absence of those compounds. In S-pseudovirus, the incorporation of S protein into viral particles was obviously inhibited. In SARS-CoV, viral production was obviously inhibited. These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding, resulting in conferring infectivity on SARS-CoV. |
CC : | 002A05C10 |
FD : | Coronavirus; Protéine; Réticulum endoplasmique; Pouvoir infectant; Syndrome respiratoire aigu sévère |
FG : | Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons |
ED : | Coronavirus; Protein; Endoplasmic reticulum; Infectivity; Severe acute respiratory syndrome |
EG : | Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease |
SD : | Coronavirus; Proteína; Retículo endoplásmico; Poder infectante; Síndrome respiratorio agudo severo |
LO : | INIST-13592.354000506814370320 |
ID : | 12-0410005 |
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Pascal:12-0410005Le document en format XML
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of SARS, a fatal pulmonary disorder with no effective treatment. We found that SARS-CoV spike glycoprotein (S protein), a key molecule for viral entry, binds to calnexin, a molecular chaperone in the endoplasmic reticulum (ER), but not to calreticulin, a homolog of calnexin. Calnexin bound to most truncated mutants of S protein, and S protein bound to all mutants of calnexin. Pseudotyped virus carrying S protein (S-pseudovirus) produced by human cells that were treated with small interfering RNA (siRNA) for calnexin expression (calnexin siRNA-treated cells) showed significantly lower infectivity than S-pseudoviruses produced by untreated and control siRNA-treated cells. S-pseudovirus produced by calnexin siRNA-treated cells contained S protein modified with N-glycan side chains differently from other two S proteins and consisted of two kinds of viral particles: those of normal density with little S protein and those of high density with abundant S protein. Treatment with peptide-N-glycosidase F (PNGase F), which removes all types of N-glycan side chains from glycoproteins, eliminated the infectivity of S-pseudovirus. S-pseudovirus and SARS-CoV produced in the presence of α-glucosidase inhibitors, which disrupt the interaction between calnexin and its substrates, showed significantly lower infectivity than each virus produced in the absence of those compounds. In S-pseudovirus, the incorporation of S protein into viral particles was obviously inhibited. In SARS-CoV, viral production was obviously inhibited. These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding, resulting in conferring infectivity on SARS-CoV.</div>
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<fC03 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Protéine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Protein</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Proteína</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Réticulum endoplasmique</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Endoplasmic reticulum</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Retículo endoplásmico</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Pouvoir infectant</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Infectivity</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Poder infectante</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>317</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
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<server><NO>PASCAL 12-0410005 INIST</NO>
<ET>Monitoring of S Protein Maturation in the Endoplasmic Reticulum by Calnexin Is Important for the Infectivity of Severe Acute Respiratory Syndrome Coronavirus</ET>
<AU>FUKUSHI (Masaya); YOSHINAKA (Yoshiyuki); MATSUOKA (Yusuke); HATAKEYAMA (Seisuke); ISHIZAKA (Yukihito); KIRIKAE (Teruo); SASAZUKI (Takehiko); MIYOSHI-AKIYAMA (Tohru)</AU>
<AF>Department of Infectious Diseases, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (1 aut., 3 aut., 4 aut., 6 aut., 8 aut.); Disease Control and Prevention Center, National Center for Global Health and Medicine/Tokyo/Japon (1 aut.); Deputy Director-General's Laboratory, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (1 aut.); Department of Virology, Institute of Biomedical & Health Sciences, Hiroshima University/Hiroshima/Japon (1 aut.); Department of Molecular Virology, Bio-Response, Graduate School, Tokyo Medical and Dental University/Tokyo/Japon (2 aut.); Department of Intractable Diseases, Research Institute, National Center for Global Health and Medicine/Tokyo/Japon (5 aut.); National Center for Global Health and Medicine/Tokyo/Japon (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 21; Pp. 11745-11753; Bibl. 49 ref.</SO>
<LA>Anglais</LA>
<EA>Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of SARS, a fatal pulmonary disorder with no effective treatment. We found that SARS-CoV spike glycoprotein (S protein), a key molecule for viral entry, binds to calnexin, a molecular chaperone in the endoplasmic reticulum (ER), but not to calreticulin, a homolog of calnexin. Calnexin bound to most truncated mutants of S protein, and S protein bound to all mutants of calnexin. Pseudotyped virus carrying S protein (S-pseudovirus) produced by human cells that were treated with small interfering RNA (siRNA) for calnexin expression (calnexin siRNA-treated cells) showed significantly lower infectivity than S-pseudoviruses produced by untreated and control siRNA-treated cells. S-pseudovirus produced by calnexin siRNA-treated cells contained S protein modified with N-glycan side chains differently from other two S proteins and consisted of two kinds of viral particles: those of normal density with little S protein and those of high density with abundant S protein. Treatment with peptide-N-glycosidase F (PNGase F), which removes all types of N-glycan side chains from glycoproteins, eliminated the infectivity of S-pseudovirus. S-pseudovirus and SARS-CoV produced in the presence of α-glucosidase inhibitors, which disrupt the interaction between calnexin and its substrates, showed significantly lower infectivity than each virus produced in the absence of those compounds. In S-pseudovirus, the incorporation of S protein into viral particles was obviously inhibited. In SARS-CoV, viral production was obviously inhibited. These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding, resulting in conferring infectivity on SARS-CoV.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Protéine; Réticulum endoplasmique; Pouvoir infectant; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons</FG>
<ED>Coronavirus; Protein; Endoplasmic reticulum; Infectivity; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Proteína; Retículo endoplásmico; Poder infectante; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000506814370320</LO>
<ID>12-0410005</ID>
</server>
</inist>
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