Emergence of amantadine-resistant influenza A viruses: epidemiological study

An Off-Seasonal Amantadine-Resistant H3N2 Influenza Outbreak in Japan

“…It is generally accepted that amantadine resistant viruses emerges under the pressure of the drug, but are less virulent or transmissible than susceptible viruses (Harper et al 2005). In Japan, the prevalence of resistance remained 0-3% in pre-treatment samples until the 2004-05 season in our survey (Suzuki et al 2001(Suzuki et al , 2003, and less than 1% in USA and other countries (Ziegler et al 1999;Tooley 2002). However, Bight and colleague's (Bright et al 2005;Guan and Chen 2005) study recently highlighted a dramatic increase in the prevalence of resistant H3N2 strains in Asian countries, suggesting association with inappropriate drug administration.…”

“…The medicines are economical and chemically stable, but emergence of resistance and adverse effect are matters of concern (Suzuki et al 2003). The genetic basis for resistance to these drugs is associated with amino acid substitutions at positions 26, 27, 30, 31 or 34 in the transmembrane region of the M2 protein (Pinto et al 1992;Holsinger et al 1994).…”

“…The genetic basis for resistance to these drugs is associated with amino acid substitutions at positions 26, 27, 30, 31 or 34 in the transmembrane region of the M2 protein (Pinto et al 1992;Holsinger et al 1994). It was reported that roughly 1/3 of patients develops resistance after treatment (Hayden and Hay 1992;Saito et al 2002), but resistance in pre-treatment samples, or community prevalence, remained low in the past, as 0-3% in Japan (Suzuki et al 2001(Suzuki et al , 2003, and roughly 1% in the United States and the United Kingdom (Ziegler et al 1999;Tooley 2002). However, Bight and colleagues (Bright et al 2005(Bright et al , 2006 recently highlighted a dramatic increase in the prevalence of amantadine resistant H3N2 influenza strains in Asian countries and USA.…”

Influenza Virus Shedding in Laninamivir-Treated Children upon Returning to School

“…Isolates were screened for influenza using a previously reported cycling probe real-time polymerase chain reaction (PCR) method that allows typing and subtyping of influenza (Suzuki et al , 2011Dapat et al 2012). Viral load was determined by using 50% tissue culture infectious dose (TCID 50 ) and by quantification of the influenza virus M gene using real-time PCR (Suzuki et al 2003;Daum et al 2007). …”

Genetic characterization of an H5N1 avian influenza virus from a vaccinated duck flock in Vietnam

“…In the M2 protein of Dk/VN/QB1207/12, the S31A mutation known to be involved in amantadine resistance was also not seen. However, the M2 of Dk/VN/QB1207/12 contained an amino acid substitution at position 27 (V27I), which may suggest a reduced susceptibility to amantadine (Table 4) [37,38]. Recently, Govorkova et al [36] systematically examined the prevalence of NA inhibitor and amantadine resistance among the HPAIVs circulating worldwide, and reported that most of the HPAIVs are likely to be susceptible to NA inhibitors while some proportion will also be susceptible to amantadine.…”