scholarly journals Overcoming amantadine resistance

2013 ◽  
Vol 6 (2) ◽  
pp. 27-27
Author(s):  
Lauren Martz
Keyword(s):  
Amantadine Resistance

scholarly journals Large-Scale Sequence Analysis of M Gene of Influenza A Viruses from Different Species: Mechanisms for Emergence and Spread of Amantadine Resistance

2009 ◽  
Vol 53 (10) ◽  
pp. 4457-4463 ◽  
Author(s):  
Yuki Furuse ◽  
Akira Suzuki ◽  
Hitoshi Oshitani
Keyword(s):  
Influenza Virus ◽  
Influenza A ◽  
Drug Resistant ◽  
Human Influenza ◽  
Influenza A Viruses ◽  
M Gene ◽  
Drug Pressure ◽  
Human Influenza Virus ◽  
Selective Pressures ◽  
Amantadine Resistance

ABSTRACT Influenza A virus infects many species, and amantadine is used as an antiviral agent. Recently, a substantial increase in amantadine-resistant strains has been reported, most of which have a substitution at amino acid position 31 in the M2 gene. Understanding the mechanism responsible for the emergence and spread of antiviral resistance is important for developing a treatment protocol for seasonal influenza and for deciding on a policy for antiviral stockpiling for pandemic influenza. The present study was conducted to identify the existence of drug pressure on the emergence and spread of amantadine-resistant influenza A viruses. We analyzed data on more than 5,000 virus sequences and constructed a phylogenetic tree to calculate selective pressures on sites in the M2 gene associated with amantadine resistance (positions 26, 27, 30, and 31) among different hosts. The phylogenetic tree revealed that the emergence and spread of the drug-resistant M gene in different hosts and subtypes were independent and not through reassortment. For human influenza virus, positive selection was detected only at position 27. Selective pressures on the sites were not always higher for human influenza virus than for viruses of other hosts. Additionally, selective pressure on position 31 did not increase after the introduction of amantadine. Although there is a possibility of drug pressure on human influenza virus, we could not find positive pressure on position 31. Because the recent rapid increase in drug-resistant virus is associated with the substitution at position 31, the resistance may not be related to drug use.

Amantadine Resistance among Hemagglutinin Subtype 5 Strains of Avian Influenza Virus

1991 ◽  
Vol 35 (1) ◽  
pp. 31 ◽  
Author(s):  
Patricia O. Wainright ◽  
Michael L. Perdue ◽  
Max Brugh ◽  
Charles W. Beard
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Amantadine Resistance

Amantadine Resistance among Porcine H1N1, H1N2, and H3N2 Influenza A Viruses Isolated in Germany between 1981 and 2001

Intervirology ◽  
2006 ◽  
Vol 49 (5) ◽  
pp. 286-293 ◽  
Author(s):  
Michaela Schmidtke ◽  
Roland Zell ◽  
Katja Bauer ◽  
Andi Krumbholz ◽  
Christina Schrader ◽  
...  
Keyword(s):  
Influenza A ◽  
Influenza A Viruses ◽  
Amantadine Resistance ◽  
H3n2 Influenza

Amantadine-resistance among H5N1 avian influenza viruses isolated in Northern China

2008 ◽  
Vol 77 (1) ◽  
pp. 72-76 ◽  
Author(s):  
Guimei He ◽  
Jian Qiao ◽  
Changgui Dong ◽  
Cheng He ◽  
Lihong Zhao ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Northern China ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
H5n1 Avian Influenza ◽  
Amantadine Resistance

scholarly journals Efficacy, Mechanism and Antiviral Resistance of Neuraminidase Inhibitors and Adamantane against Avian Influenza

2019 ◽  
Vol 29 (2) ◽  
pp. 61
Author(s):  
Dyah Ayu Hewajuli ◽  
NLPI Dharmayanti
Keyword(s):  
Avian Influenza ◽  
Ion Channel ◽  
Influenza A ◽  
Influenza Infection ◽  
Antiviral Drug ◽  
Neuraminidase Inhibitor ◽  
M2 Protein ◽  
New Variant ◽  
Amantadine Resistance ◽  
Ion Channel Inhibitors

Vaccination and antiviral drug are often used to control influenza. However, the effectiveness of vaccine was impaired due to the emergence of new variant of virus strain. Antiviral drug consists of prophylactic and curative substances, namely M2 ion channel inhibitors (adamantane; amantadine and rimantadine) and neuraminidase (NA) inhibitors (NAIs; oseltamivir, zanamivir, peramivir, laninamivir). The synthesis and modification of antiviral neuraminidase (NA) inhibitors (NAIs) and adamantanes increased the antiviral effectiveness. The mechanism of the neuraminidase inhibitor is to prevent influenza infection by inhibiting the release of the virus from internal cells. Adamantane is antiviral drug that selectively inhibits the flow of H+ ions through M2 protein to prevent the uncoating virus particles getting into the endosome. The substitution of (H275Y, S247N, I223L, K150N, R292K, I222T, R152K, R118K, E119V) on NA protein caused resistance of avian influenza virus against the neuraminidase inhibitor. The combination of mutations (S247N, I223L, K150N) increased the resistance of influenza A (H5N1) virus. The diffusion of adamantane resistance varies among HA subtypes, the species of host, the period of isolation, and region. Mutations at residues of 26, 27, 30, 31 or 34 transmembrane M2 protein caused adamantane resistance. The unique substitution (V27I) of M2 protein of clade 2.3.2 H5N1 subtype isolated in Indonesia in 2016 has been contributed to the amantadine resistance. Antiviral combination of M2 ion channel inhibitors and neuraminidase (NA) inhibitors is effective treatments for the resistance.

Differential patterns of amantadine-resistance in influenza A (H3N2) and (H1N1) isolates in Toronto, Canada

2009 ◽  
Vol 44 (1) ◽  
pp. 91-93 ◽  
Author(s):  
Rachel R. Higgins ◽  
A. Eshaghi ◽  
L. Burton ◽  
T. Mazzulli ◽  
S.J. Drews
Keyword(s):  
Influenza A ◽  
Amantadine Resistance

scholarly journals Viral Factors Associated With the High Mortality Related to Human Infections With Clade 2.1 Influenza A/H5N1 Virus in Indonesia

2019 ◽  
Vol 70 (6) ◽  
pp. 1139-1146 ◽  
Author(s):  
Hana A Pawestri ◽  
Dirk Eggink ◽  
Siti Isfandari ◽  
Tran Tan Thanh ◽  
H Rogier van Doorn ◽  
...  
Keyword(s):  
High Mortality ◽  
Influenza A ◽  
H5n1 Virus ◽  
Fatal Outcome ◽  
Viral Rna ◽  
Viral Loads ◽  
Antiviral Responses ◽  
Amantadine Resistance ◽  
Human Infections ◽  
Over Time

Abstract Background Since their emergence in Indonesia in 2005, 200 human infections with clade 2.1 highly pathogenic avian influenza A/H5N1 virus have been reported, associated with exceptionally high mortality (84%) compared to regions affected by other genetic clades of this virus. To provide potential clues towards understanding this high mortality, detailed clinical virological analyses were performed in specimens from 180 H5N1 patients, representing 90% of all Indonesian patients and 20% of reported H5N1-infected patients globally. Methods H5N1 RNA was quantified in available upper- and lower-respiratory tract specimens as well as fecal and blood samples from 180 patients with confirmed infection between 2005 and 2017. Mutations in the neuraminidase and M2 genes that confer resistance to oseltamivir and adamantanes were assessed. Fatal and nonfatal cases were compared. Results High viral RNA loads in nasal and pharyngeal specimens were associated with fatal outcome. Mortality increased over time during the study period, which correlated with increasing viral RNA loads on admission. Furthermore, the prevalence of amantadine resistance–conferring M2 mutations increased over time, and viral loads were higher in patients infected with viruses that harbored these mutations. Compared to observations from other regions, viral RNA was detected more frequently in feces (80%) and particularly in blood (85%), and antiviral responses to oseltamivir appeared less pronounced. Conclusions These observations confirm the association of viral load with outcome of human H5N1 infections and suggest potential differences in virulence and antiviral responses to oseltamivir that may explain the exceptionally high mortality related to clade 2.1 H5N1 infections in Indonesia.

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