Mutations in Sendai virus variant F1-R that correlate with plaque formation in the absence of trypsin.
Identifieur interne : 000E98 ( Ncbi/Curation ); précédent : 000E97; suivant : 000E99Mutations in Sendai virus variant F1-R that correlate with plaque formation in the absence of trypsin.
Auteurs : Xiaogang Hou [États-Unis] ; Edgar Suquilanda ; Ana Zeledon ; Apollo Kacsinta ; Akila Moore ; Joseph Seto ; Nancy McqueenSource :
- Medical microbiology and immunology [ 0300-8584 ] ; 2005.
Descripteurs français
- KwdFr :
- Mutation, Méthode des plages virales, Protéines de fusion virale (génétique), Protéines de fusion virale (physiologie), Protéines de la matrice virale (génétique), Protéines de la matrice virale (physiologie), Recombinaison génétique, Réplication virale, Trypsine (métabolisme), Virus Sendai (croissance et développement), Virus Sendai (génétique).
- MESH :
- croissance et développement : Virus Sendai.
- génétique : Protéines de fusion virale, Protéines de la matrice virale, Virus Sendai.
- métabolisme : Trypsine.
- physiologie : Protéines de fusion virale, Protéines de la matrice virale.
- Mutation, Méthode des plages virales, Recombinaison génétique, Réplication virale.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Viral Fusion Proteins, Viral Matrix Proteins.
- chemical , metabolism : Trypsin.
- genetics : Sendai virus.
- growth & development : Sendai virus.
- chemical , physiology : Viral Fusion Proteins, Viral Matrix Proteins.
- Mutation, Recombination, Genetic, Viral Plaque Assay, Virus Replication.
Abstract
With the emergence of new viruses, such as the SARS virus and the avian influenza virus, the importance of investigations on the genetic basis of viral infections becomes clear. Sendai virus causes a localized respiratory tract infection in rodents, while a mutant, F1-R, causes a systemic infection. It has been suggested that two determinants are responsible for the systemic infection caused by F1-R [Okada et al (1998) Arch Virol 143:2343-2352]. The primary determinant of the pantropism is the enhanced proteolytic cleavability of the fusion (F) protein of F1-R, which allows the virus to undergo multiple rounds of replication in many different organs, whereas wild-type virus can only undergo multiple rounds of replication in the lungs. The enhanced cleavability of F1-R F was previously attributed to an amino acid change at F115 that is adjacent to the cleavage site at amino acid 116. Secondly, wild-type virus buds only from the apical domain of bronchial epithelium, releasing virus into the lumen of the respiratory tract, whereas F1-R buds from both apical and basolateral domains. Thus, virus is released into the basement membrane where it can easily gain access to the bloodstream for dissemination. The microtubule disruption is attributed to two amino acid differences in M protein. To confirm that the F and M gene mutations described above are solely responsible for the phenotypic differences seen in wild-type versus F1-R infections, reverse genetics was used to construct recombinant Sendai viruses with various combinations of the mutations found in the M and F genes of F1-R. Plaque assays were performed with or without trypsin addition. A recombinant virus containing all F1-R M and F mutations formed plaques in LLC-MK2 cells and underwent multiple cycles of replication without trypsin addition. To clarify which mutation(s) are necessary for plaque formation, plaque assays were done using other recombinant viruses. A virus with only the F115 change, which was previously thought to be the only change important for plaque formation of F 1-R F, did not confer upon the virus the ability to form plaques without the addition of trypsin. Another virus with the F115 and both M changes gave the same result. Therefore, more than one mutation in the F gene contributes to the ability of F1-R to form plaques without trypsin addition.
DOI: 10.1007/s00430-004-0224-3
PubMed: 15834752
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pubmed:15834752Le document en format XML
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<affiliation wicri:level="2"><nlm:affiliation>Department of Biological Sciences, California State University, Los Angeles, 5151 State University Drive, Los Angeles, CA 90032, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Suquilanda, Edgar" sort="Suquilanda, Edgar" uniqKey="Suquilanda E" first="Edgar" last="Suquilanda">Edgar Suquilanda</name>
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<author><name sortKey="Seto, Joseph" sort="Seto, Joseph" uniqKey="Seto J" first="Joseph" last="Seto">Joseph Seto</name>
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<term>Recombination, Genetic</term>
<term>Sendai virus (genetics)</term>
<term>Sendai virus (growth & development)</term>
<term>Trypsin (metabolism)</term>
<term>Viral Fusion Proteins (genetics)</term>
<term>Viral Fusion Proteins (physiology)</term>
<term>Viral Matrix Proteins (genetics)</term>
<term>Viral Matrix Proteins (physiology)</term>
<term>Viral Plaque Assay</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Mutation</term>
<term>Méthode des plages virales</term>
<term>Protéines de fusion virale (génétique)</term>
<term>Protéines de fusion virale (physiologie)</term>
<term>Protéines de la matrice virale (génétique)</term>
<term>Protéines de la matrice virale (physiologie)</term>
<term>Recombinaison génétique</term>
<term>Réplication virale</term>
<term>Trypsine (métabolisme)</term>
<term>Virus Sendai (croissance et développement)</term>
<term>Virus Sendai (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Fusion Proteins</term>
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Trypsin</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Virus Sendai</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Sendai virus</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Sendai virus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de fusion virale</term>
<term>Protéines de la matrice virale</term>
<term>Virus Sendai</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Trypsine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Protéines de fusion virale</term>
<term>Protéines de la matrice virale</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Viral Fusion Proteins</term>
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Mutation</term>
<term>Recombination, Genetic</term>
<term>Viral Plaque Assay</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Mutation</term>
<term>Méthode des plages virales</term>
<term>Recombinaison génétique</term>
<term>Réplication virale</term>
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<front><div type="abstract" xml:lang="en">With the emergence of new viruses, such as the SARS virus and the avian influenza virus, the importance of investigations on the genetic basis of viral infections becomes clear. Sendai virus causes a localized respiratory tract infection in rodents, while a mutant, F1-R, causes a systemic infection. It has been suggested that two determinants are responsible for the systemic infection caused by F1-R [Okada et al (1998) Arch Virol 143:2343-2352]. The primary determinant of the pantropism is the enhanced proteolytic cleavability of the fusion (F) protein of F1-R, which allows the virus to undergo multiple rounds of replication in many different organs, whereas wild-type virus can only undergo multiple rounds of replication in the lungs. The enhanced cleavability of F1-R F was previously attributed to an amino acid change at F115 that is adjacent to the cleavage site at amino acid 116. Secondly, wild-type virus buds only from the apical domain of bronchial epithelium, releasing virus into the lumen of the respiratory tract, whereas F1-R buds from both apical and basolateral domains. Thus, virus is released into the basement membrane where it can easily gain access to the bloodstream for dissemination. The microtubule disruption is attributed to two amino acid differences in M protein. To confirm that the F and M gene mutations described above are solely responsible for the phenotypic differences seen in wild-type versus F1-R infections, reverse genetics was used to construct recombinant Sendai viruses with various combinations of the mutations found in the M and F genes of F1-R. Plaque assays were performed with or without trypsin addition. A recombinant virus containing all F1-R M and F mutations formed plaques in LLC-MK2 cells and underwent multiple cycles of replication without trypsin addition. To clarify which mutation(s) are necessary for plaque formation, plaque assays were done using other recombinant viruses. A virus with only the F115 change, which was previously thought to be the only change important for plaque formation of F 1-R F, did not confer upon the virus the ability to form plaques without the addition of trypsin. Another virus with the F115 and both M changes gave the same result. Therefore, more than one mutation in the F gene contributes to the ability of F1-R to form plaques without trypsin addition.</div>
</front>
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