Genome packaging in influenza A virus

被引:219
作者
Hutchinson, Edward C. [1 ]
von Kirchbach, Johann C. [2 ]
Gog, Julia R. [2 ]
Digard, Paul [1 ]
机构
[1] Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England
[2] Univ Cambridge, DAMTP, Ctr Math Sci, Cambridge CB3 0WA, England
基金
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词
DEFECTIVE-INTERFERING PARTICLES; TEMPERATURE-SENSITIVE MUTANTS; VIRAL-RNA MOLECULES; ELECTRON-MICROSCOPY; POLYMERASE GENE; RIBONUCLEOPROTEIN COMPLEXES; VONMAGNUS PARTICLES; NONCODING SEQUENCES; MUTATIONAL ANALYSIS; INTERNAL DELETION;
D O I
10.1099/vir.0.017608-0
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The negative-sense RNA genome of influenza A virus is composed of eight segments, which encode 12 proteins between them. At the final stage of viral assembly, these genomic virion (v)RNAs are incorporated into the virion as it buds from the apical plasma membrane of the cell. Genome segmentation confers evolutionary advantages on the virus, but also poses a problem during virion assembly as at least one copy of each of the eight segments is required to produce a fully infectious virus particle. Historically, arguments have been presented in favour of a specific packaging mechanism that ensures incorporation of a full genome complement, as well as for an alternative model in which segments are chosen at random but packaged in sufficient numbers to ensure that a reasonable proportion of virions are viable. The question has seen a resurgence of interest in recent years leading to a consensus that the vast majority of virions contain no more than eight segments and that a specific mechanism does indeed function to select one copy of each vRNA. This review summarizes work leading to this conclusion. In addition, we describe recent progress in identifying the specific packaging signals and discuss likely mechanisms by which these RNA elements might operate.
引用
收藏
页码:313 / 328
页数:16
相关论文
共 136 条
[1]   The generation of recombinant influenza A viruses expressing a PB2 fusion protein requires the conservation of a packaging signal overlapping the coding and noncoding regions at the 5′ end of the PB2 segment [J].
Afonso, EDS ;
Escriou, N ;
Leclercq, I ;
van der Werf, S ;
Naffakh, N .
VIROLOGY, 2005, 341 (01) :34-46
[2]   MECHANISM OF INTERFERENCE BY DEFECTIVE-INTERFERING PARTICLES OF INFLUENZA-VIRUS - DIFFERENTIAL REDUCTION OF INTRACELLULAR SYNTHESIS OF SPECIFIC POLYMERASE PROTEINS [J].
AKKINA, RK ;
CHAMBERS, TM ;
NAYAK, DP .
VIRUS RESEARCH, 1984, 1 (08) :687-702
[3]   MORPHOLOGICAL STUDY OF INTERNAL COMPONENT OF INFLUENZA-VIRUS [J].
ALMEIDA, JD ;
BRAND, CM .
JOURNAL OF GENERAL VIROLOGY, 1975, 27 (JUN) :313-318
[4]   FURTHER OBSERVATIONS ON STRUCTURE OF INFLUENZA VIRUSES A AND C [J].
APOSTOLOV, K ;
FLEWETT, TH .
JOURNAL OF GENERAL VIROLOGY, 1969, 4 :365-+
[5]  
BACHI T, 1969, J VIROL, V4, P769
[6]  
BALL LA, 2007, FIELDS VIROLOGY, P119
[7]   Evidence for segment-nonspecific packaging of the influenza A virus genome [J].
Bancroft, CT ;
Parslow, TG .
JOURNAL OF VIROLOGY, 2002, 76 (14) :7133-7139
[9]   Pacing a small cage: mutation and RNA viruses [J].
Belshaw, Robert ;
Gardner, Andy ;
RarnbaUt, Andrew ;
Pybus, Oliver G. .
TRENDS IN ECOLOGY & EVOLUTION, 2008, 23 (04) :188-193
[10]   Mutations in the nonconserved noncoding sequences of the influenza A virus segments affect viral vRNA formation [J].
Bergmann, M ;
Muster, T .
VIRUS RESEARCH, 1996, 44 (01) :23-31