(Q39680790)

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In vitro characterization of naturally occurring influenza H3NA- viruses lacking the NA gene segment: toward a new mechanism of viral resistance?

scientific article published on September 2010

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:20627352%20AND%20SRC:MED&resulttype=core&format=json

7 February 2020

In vitro characterization of naturally occurring influenza H3NA- viruses lacking the NA gene segment: toward a new mechanism of viral resistance? (English)

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7 February 2020

20

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7 February 2020

Olivier Terrier

3

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7 February 2020

Aurélien Traversier

11

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7 February 2020

17

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7 February 2020

Manuel Rosa-Calatrava

18

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7 February 2020

19

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7 February 2020

22

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7 February 2020

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V Moules

1

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7 February 2020

O Ferraris

2

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7 February 2020

E Giudice

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7 February 2020

M Yver

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7 February 2020

J P Rolland

6

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7 February 2020

M Bouscambert-Duchamp

7

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7 February 2020

C Bergeron

8

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7 February 2020

M Ottmann

9

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7 February 2020

E Fournier

10

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7 February 2020

C Boule

12

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7 February 2020

A Rivoire

13

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7 February 2020

Y Lin

14

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7 February 2020

A Hay

15

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7 February 2020

M Valette

16

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7 February 2020

D Thomas

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7 February 2020

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1 September 2010

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7 February 2020

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7 February 2020

404

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7 February 2020

2

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7 February 2020

215-224

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7 February 2020

Characterization of 2 influenza A(H3N2) clinical isolates with reduced susceptibility to neuraminidase inhibitors due to mutations in the hemagglutinin gene

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Mutations of neuraminidase implicated in neuraminidase inhibitors resistance

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The PA subunit is required for efficient nuclear accumulation of the PB1 subunit of the influenza A virus RNA polymerase complex

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7 January 2021

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Influenza A viruses lacking sialidase activity can undergo multiple cycles of replication in cell culture, eggs, or mice

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Genome packaging in influenza A virus

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Host-range determinants on the PB2 protein of influenza A viruses control the interaction between the viral polymerase and nucleoprotein in human cells

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Accumulation of defective neuraminidase (NA) genes by influenza A viruses in the presence of NA inhibitors as a marker of reduced dependence on NA.

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