Accumulation of segment 6 sgRNAs of influenza A viruses in the presence of neuraminidase inhibitors

2001 ◽  
Vol 1219 ◽  
pp. 845-853 ◽  
Author(s):  
Marina S Nedyalkova ◽  
Frederick G Hayden ◽  
Robert G Webster ◽  
Larisa V Gubareva
2011 ◽  
Vol 32 (1) ◽  
pp. 26
Author(s):  
Aeron C Hurt

Two classes of anti-influenza drugs are currently available for the treatment or prophylaxis of influenza. These are the adamantanes (amantadine and rimantadine), which block the activity of the M2 ion channel of influenza A viruses (but not influenza B viruses), and the neuraminidase inhibitors (NAIs), which act by binding to the enzymatic site of the influenza neuraminidase (NA) thereby preventing progeny virions from being released from the host cell during viral replication. Antiviral resistance can occur in influenza viruses and render the drug ineffective for the treatment of patients. Virtually all influenza A viruses currently circulating in the human population are resistant to the adamantanes, while in comparison these viruses remain susceptible to the NAIs. In particular, very low NAI resistance has been observed in pandemic A(H1N1) 2009 viruses, even though unprecedented amounts of these drugs were used.


2015 ◽  
Vol 117 ◽  
pp. 10-19 ◽  
Author(s):  
Tatiana Baranovich ◽  
Justin Bahl ◽  
Bindumadhav M. Marathe ◽  
Marie Culhane ◽  
Evelyn Stigger-Rosser ◽  
...  

Viruses ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1066 ◽  
Author(s):  
Maki Kiso ◽  
Seiya Yamayoshi ◽  
Yuri Furusawa ◽  
Masaki Imai ◽  
Yoshihiro Kawaoka

Viral neuraminidase inhibitors show limited efficacy in mice infected with H7N9 influenza A viruses isolated from humans. Although baloxavir marboxil protected mice from lethal challenge infection with a low pathogenic avian influenza H7N9 virus isolated from a human, its efficacy in mice infected with a recent highly pathogenic version of H7N9 human isolates is unknown. Here, we examined the efficacy of baloxavir marboxil in mice infected with a highly pathogenic human H7N9 virus, A/Guangdong/17SF003/2016. Treatment of infected mice with a single 1.5 mg/kg dose of baloxavir marboxil protected mice from the highly pathogenic human H7N9 virus infection as effectively as oseltamivir treatment at 50 mg/kg twice a day for five days. Daily treatment for five days at 15 or 50 mg/kg of baloxavir marboxil showed superior therapeutic efficacy, largely preventing virus replication in respiratory organs. These results indicate that baloxavir marboxil is a valuable candidate treatment for human patients suffering from highly pathogenic H7N9 virus infection.


2009 ◽  
Vol 81 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Varough M. Deyde ◽  
Margaret Okomo-Adhiambo ◽  
Tiffany G. Sheu ◽  
Teresa R. Wallis ◽  
Alicia Fry ◽  
...  

2009 ◽  
Vol 14 (38) ◽  
Author(s):  
S Burrel ◽  
L Roncin ◽  
M E Lafon ◽  
H Fleury

The recent emergence of seasonal influenza A(H1N1) strains resistant to oseltamivir makes it necessary to monitoring carefully the susceptibility of human influenza viruses to neuraminidase inhibitors. We report the prevalence of the oseltamivir resistance among influenza A viruses circulating in south-western France over the past three years: seasonal influenza A(H1N1), seasonal influenza A(H3N2), and the influenza A(H1N1)v viruses associated with the ongoing 2009 pandemic. The main result of the study is the absence of oseltamivir resistance in the pandemic H1N1 strains studied so far (n=129).


2008 ◽  
Vol 82 (10) ◽  
pp. 4834-4843 ◽  
Author(s):  
I-Chueh Huang ◽  
Wenhui Li ◽  
Jianhua Sui ◽  
Wayne Marasco ◽  
Hyeryun Choe ◽  
...  

ABSTRACT Enveloped viruses use multiple mechanisms to inhibit infection of a target cell by more than one virion. These mechanisms may be of particular importance for the evolution of segmented viruses, because superinfection exclusion may limit the frequency of reassortment of viral genes. Here, we show that cellular expression of influenza A virus neuraminidase (NA), but not hemagglutinin (HA) or the M2 proton pump, inhibits entry of HA-pseudotyped retroviruses. Cells infected with H1N1 or H3N2 influenza A virus were similarly refractory to HA-mediated infection and to superinfection with a second influenza A virus. Both HA-mediated entry and viral superinfection were rescued by the neuraminidase inhibitors oseltamivir carboxylate and zanamivir. These inhibitors also prevented the removal of α-2,3- and α-2,6-linked sialic acid observed in cells expressing NA or infected with influenza A viruses. Our data indicate that NA alone among viral proteins limits influenza A virus superinfection.


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