Influenza virus genetics

Brown, Earl G.

doi:10.1016/s0753-3322(00)89026-5

Cited by 74 publications

(73 citation statements)

References 40 publications

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“…The amino acid at position 627 has been reported to affect the replicative efficiency of Hong Kong H5N1 influenza A viruses in mice (23). The amino acid at position 701 is located between the cap-binding motif at positions 634 to 650 and the second nuclear localization signal at positions 736 to 739 (2). It remains to be determined whether this mutation affects polymerase function.…”

Section: Discussionmentioning

confidence: 99%

Molecular Basis of Replication of Duck H5N1 Influenza Viruses in a Mammalian Mouse Model

Chen

Jiao

et al. 2005

J Virol

499

482

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We recently analyzed a series of H5N1 viruses isolated from healthy ducks in southern China since 1999 and found that these viruses had progressively acquired the ability to replicate and cause disease in mice. In the present study, we explored the genetic basis of this change in host range by comparing two of the viruses that are genetically similar but differ in their ability to infect mice and have different pathogenicity in mice.

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Section: Discussionmentioning

confidence: 99%

Molecular Basis of Replication of Duck H5N1 Influenza Viruses in a Mammalian Mouse Model

Chen

Jiao

et al. 2005

J Virol

499

482

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“…Influenza viruses cause annually recurrent epidemics of moderate-to-severe respiratory disease, frequently associated with genetic variation termed drift and shift (5,27). These viruses present an important diagnostic problem, and the rapid detection, typing, and subtyping of influenza A and B virus strains are of both clinical and epidemiological value.…”

mentioning

confidence: 99%

Typing and Subtyping Influenza Virus Using DNA Microarrays and Multiplex Reverse Transcriptase PCR

Chen

Evans³

2001

J Clin Microbiol

152

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A model DNA microarray has been prepared and shown to facilitate typing and subtyping of human influenza A and B viruses. Reverse transcriptase PCR was used to prepare cDNAs encoding ϳ500-bp influenza virus gene fragments, which were then cloned, sequenced, reamplified, and spotted to form a glass-bound microarray. These target DNAs included multiple fragments of the hemagglutinin, neuraminidase, and matrix protein genes. Cy3-or Cy5-labeled fluorescent probes were then hybridized to these target DNAs, and the arrays were scanned to determine the probe binding site(s). The hybridization pattern agreed perfectly with the known grid location of each target, and the signal-to-background ratio varied from 5 to 30. No crosshybridization could be detected beyond that expected from the limited degree of sequence overlap between different probes and targets. At least 100 to 150 bp of homology was required for hybridization under the conditions used in this study. Combinations of Cy3-and Cy5-labeled DNAs can also be hybridized to the same chip, permitting further differentiation of amplified molecules in complex mixtures. In a more realistic test of the technology, several sets of multiplex PCR primers that collectively target influenza A and B virus strains were identified and were used to type and subtype several previously unsequenced influenza virus isolates. The results show that DNA microarray technology provides a useful supplement to PCR-based diagnostic methods.

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“…They contain a singlestranded RNA genome composed of eight gene segments encoding at least 10 viral proteins (1 (1,2). Currently, AIV are classified into 16 HA (H1 to H16) and 9 NA (N1 to N9) subtypes, which are known to infect birds, whereas influenza viruses of subtypes H17N10 and H18N11 have been identified in bats (3).…”

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confidence: 99%

A Unique Multibasic Proteolytic Cleavage Site and Three Mutations in the HA2 Domain Confer High Virulence of H7N1 Avian Influenza Virus in Chickens

Mostafa

Veits

Tauscher

et al. 2016

J Virol

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In 1999, after circulation for a few months in poultry in Italy, low-pathogenic (LP) avian influenza (AI) H7N1 virus mutated into a highly pathogenic (HP) form by acquisition of a unique multibasic cleavage site (mCS), PEIPKGSRVRR*GLF (asterisk indicates the cleavage site), in the hemagglutinin (HA) and additional alterations with hitherto unknown biological function. To elucidate these virulence-determining alterations, recombinant H7N1 viruses carrying specific mutations in the HA of LPAI A/chicken/Italy/473/1999 virus (Lp) and HPAI A/chicken/Italy/445/1999 virus (Hp) were generated. Hp with a monobasic CS or carrying the HA of Lp induced only mild or no disease in chickens, thus resembling Lp. Conversely, Lp with the HA of Hp was as virulent and transmissible as Hp. While Lp with a multibasic cleavage site (Lp_CS445) was less virulent than Hp, full virulence was exhibited when HA2 was replaced by that of Hp. In HA2, three amino acid differences consistently detected between LP and HP H7N1 viruses were successively introduced into Lp_CS445. Q450L in the HA2 stem domain increased virulence and transmission but was detrimental to replication in cell culture, probably due to low-pH activation of HA. A436T and/or K536R restored viral replication in vitro and in vivo. Viruses possessing A436T and K536R were observed early in the HPAI outbreak but were later superseded by viruses carrying all three mutations. Together, besides the mCS, stepwise mutations in HA2 increased the fitness of the Italian H7N1 virus in vivo. The shift toward higher virulence in the field was most likely gradual with rapid optimization. IMPORTANCEIn 1999, after 9 months of circulation of low-pathogenic (LP) avian influenza virus (AIV), a devastating highly pathogenic (HP) H7N1 AIV emerged in poultry, marking the largest epidemic of AIV reported in a Western country. The HPAIV possessed a unique multibasic cleavage site (mCS) complying with the minimum motif for HPAIV. The main finding in this report is the identification of three mutations in the HA2 domain that are required for replication and stability, as well as for virulence, transmission, and tropism of H7N1 in chickens. In addition to the mCS, Q450L was required for full virulence and transmissibility of the virus. Nonetheless, it was detrimental to virus replication and required A436T and/or K536R to restore replication, systemic spread, and stability. These results are important for better understanding of the evolution of highly pathogenic avian influenza viruses from low-pathogenic precursors. PB1-F2) (1, 2). Currently, AIV are classified into 16 HA (H1 to H16) and 9 NA (N1 to N9) subtypes, which are known to infect birds, whereas influenza viruses of subtypes H17N10 and H18N11 have been identified in bats (3). While AIV of all subtypes induce subclinical or only mild disease in poultry, the virulence of H5 and H7 subtypes varies from asymptomatic to highly lethal infections (4). Major outbreaks of fowl plague are caused by highly pathogenic (HP) AIV subtypes that evolve ...

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Influenza virus genetics

Cited by 74 publications

References 40 publications

Molecular Basis of Replication of Duck H5N1 Influenza Viruses in a Mammalian Mouse Model

Molecular Basis of Replication of Duck H5N1 Influenza Viruses in a Mammalian Mouse Model

Typing and Subtyping Influenza Virus Using DNA Microarrays and Multiplex Reverse Transcriptase PCR

A Unique Multibasic Proteolytic Cleavage Site and Three Mutations in the HA2 Domain Confer High Virulence of H7N1 Avian Influenza Virus in Chickens

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