Isolation of influenza A H1N2 virus from a returning traveller at Nagoya International Airport

A reassortant influenza A H1N2 virus was isolated from a returning traveller arriving at Nagoya International Airport, Japan from Indonesia in May, 2002. A Hemagglutination inhibition test revealed that the virus was similar to a vaccine strain of A/NewCaledonia/20/99. A phylogenetic analysis demonstrated that the virus forms a cluster with other influenza A H1N2 viruses isolated in other countries. The reassortment event was theoretically assumed to have occurred between the 1999/2000 and 2000/2001 influenza seasons. Neither A H1N2 nor A H3N1 virus was detected from 256 isolates of AH1 or 177 of AH3 influenza viruses isolated in Aichi Prefecture, Japan between the 1999/2000 and 2001/2002 influenza seasons. This finding suggests the importance of influenza surveillance at an airport quarantine office to detect promptly a novel influenza virus penetrating to Japan.     

Mild to moderate influenza activity in Europe and the detection of novel A(H1N2) and B viruses during the winter of 2001-02

Influenza activity in Europe during the 2001-02 influenza season was mild to moderate. Compared to historical data, the intensity was low in six countries, medium in eleven and high in one country (Spain). The dominant virus circulating in Europe was influenza A(H3N2). Two novel influenza virus strains were isolated during the 2001-02 season: influenza A(H1N2) viruses (mainly isolated in the United Kingdom and Ireland, but also in Belgium, France, Germany, the Netherlands, Portugal, Sweden, Switzerland and Romania), and influenza B viruses belonging to the B/Victoria/2/87 lineage (mainly isolated in Germany, but also sporadically in France, Italy, the Netherlands and Norway). With the exception of H1N2 virus detections in England, and Ireland and the influenza B viruses belonging to the B/Victoria/2/87 lineage in Germany, these two viruses did not circulate widely in Europe and did not play an important role in influenza activity during the 2001-02 season. An influenza B virus belonging to the B/Victoria/2/87 lineage will be included in the 2002-03 influenza vaccine. The new subtype influenza A(H1N2) is covered by the 2002-03 vaccine, as the haemagglutinin and neuraminidase components of the H1N2 viruses are antigenically similar to the vaccine components (H1N1 and H3N2).     

Intercontinental circulation of human influenza A(H1N2) reassortant viruses during the 2001-2002 influenza season

Reassortant influenza A viruses bearing the H1 subtype of hemagglutinin (HA) and the N2 subtype of neuraminidase (NA) were isolated from humans in the United States, Canada, Singapore, Malaysia, India, Oman, Egypt, and several countries in Europe during the 2001-2002 influenza season. The HAs of these H1N2 viruses were similar to that of the A/New Caledonia/20/99(H1N1) vaccine strain both antigenically and genetically, and the NAs were antigenically and genetically related to those of recent human H3N2 reference strains, such as A/Moscow/10/99(H3N2). All 6 internal genes of the H1N2 reassortants examined originated from an H3N2 virus. This article documents the first widespread circulation of H1N2 reassortants on 4 continents. The current influenza vaccine is expected to provide good protection against H1N2 viruses, because it contains the A/New Caledonia/20/99(H1N1) and A/Moscow/10/99(H3N2)-like viruses, which have H1 and N2 antigens that are similar to those of recent H1N2 viruses.     

Surveillance of resistance to adamantanes among influenza A(H3N2) and A(H1N1) viruses isolated worldwide

Our previous reports demonstrated an alarming increase in resistance to adamantanes among influenza A(H3N2) viruses isolated in 2001-2005. To continue monitoring drug resistance, we conducted a comprehensive analysis of influenza A(H3N2) and A(H1N1) viruses isolated globally in 2005-2006. The results obtained by pyrosequencing indicate that 96.4% (n=761) of A(H3N2) viruses circulating in the United States were adamantane resistant. Drug resistance has reached 100% among isolates from some Asian countries. Analysis of correlation between the appearance of drug resistance and the evolutionary pathway of the hemagglutinin (HA) gene suggests at least 2 separate introductions of resistance into circulating populations that gave rise to identifiable subclades. It also indicates that resistant A(H3N2) viruses may have emerged in Asia in late 2001. Among A(H1N1) viruses isolated worldwide, resistance reached 15.5% in 2005-2006; in the United States alone, it was 4.0%. Phylogenetic analysis of the HA and M genes indicates that the acquisition of resistance in A(H1N1) viruses can be linked to a specific genetic group and was not a result of reassortment between A(H3N2) and A(H1N1) viruses. The results of the study highlight the necessity of close monitoring of resistance to existing antivirals as wells as the need for new therapeutics.     

H5N1 influenza: a protean pandemic threat

Infection with avian influenza A virus of the H5N1 subtype (isolates A/HK/212/03 and A/HK/213/03) was fatal to one of two members of a family in southern China in 2003. This incident was preceded by lethal outbreaks of H5N1 influenza in waterfowl, which are the natural hosts of these viruses and, therefore, normally have asymptomatic infection. The hemagglutinin genes of the A/HK/212/03-like viruses isolated from humans and waterfowl share the lineage of the H5N1 viruses that caused the first known cases of human disease in Hong Kong in 1997, but their internal protein genes originated elsewhere. The hemagglutinin of the recent human isolates has undergone significant antigenic drift. Like the 1997 human H5N1 isolates, the 2003 human H5N1 isolates induced the overproduction of proinflammatory cytokines by primary human macrophages in vitro, whereas the precursor H5N1 viruses and other H5N1 reassortants isolated in 2001 did not. The acquisition by the viruses of characteristics that enhance virulence in humans and waterfowl and their potential for wider distribution by infected migrating birds are causes for renewed pandemic concern.     

Relationship between absolute humidity and influenza prevalence in Odate and Akita cities, Akita Prefecture, in 2001 and 2002

The dynamics of influenza viruses in relation to one meteorological factor, absolute humidity, was investigated. The number of influenza patients, absolute humidity, and isolation of influenza viruses were compared between Odate City the north and Akita City in central Akita Prefecture from 2001 to 2002. The results were as follows: 1) In both Odate and Akita cities, Influenza A (H1N1 and H3N2) and Influenza B (Victoria and Yamagata) viruses were isolated when absolute humidity ranged between 2.7 and 8.8 g/m3. 2) In Akita City in 2002, the influenza viruses were isolated in May (weeks 20 and 22), and the absolute humidity was below 9 g/m3, suggesting that the influenza season lasted until May in this year. 3) A correlation between absolute humidity and isolation of influenza viruses was observed, and the influenza prevalence may occur below 9 g/m3 of absolute humidity. 4) In Odate and Akita cities, the absolute humidity of 10 g/m3, a level at which 5% of influenza viruses can survive after six hours, was observed from January to June and October to December. 5) Influenza prevalence show differential occurrence by time and place. Therefore, further research is required to clarify the absolute humidity related to influenza prevalence.     

Characterization of H9N2 Avian Influenza Viruses Isolated from Poultry Products in a Mouse Model

Low pathogenic H9N2 avian influenza viruses have spread in wild birds and poultry worldwide. Recently, the number of human cases of H9N2 virus infection has increased in China and other countries, heightening pandemic concerns. In Japan, H9N2 viruses are not yet enzootic; however, avian influenza viruses, including H5N1, H7N9, H5N6, and H9N2, have been repeatedly detected in raw poultry meat carried by international flight passengers from Asian countries to Japan. Although H9N2 virus-contaminated poultry products intercepted by the animal quarantine service at the Japan border have been characterized in chickens and ducks, the biological properties of those H9N2 viruses in mammals remain unclear. Here, we characterized the biological features of two H9N2 virus isolates [A/chicken/Japan/AQ-HE28-50/2016 (Ck/HE28-50) and A/chicken/Japan/AQ-HE28-57/2016 (Ck/HE28-57)] in a mouse model. We found that these H9N2 viruses replicate well in the respiratory tract of infected mice without adaptation, and that Ck/HE28-57 caused body weight loss in the infected mice. Our results indicate that H9N2 avian influenza viruses isolated from raw chicken meat products illegally brought to Japan can potentially infect and cause disease in mammals.     

Avian influenza and human health

Natural infections with influenza A viruses have been reported in a variety of animal species including humans, pigs, horses, sea mammals, mustelids and birds. Occasionally devastating pandemics occur in humans. Although viruses of relatively few HA and NA subtype combinations have been isolated from mammalian species, all 15 HA subtypes and all 9 NA subtypes, in most combinations, have been isolated from birds.In the 20th century the sudden emergence of antigenically different strains transmissible in humans, termed antigenic shift, has occurred on four occasions, 1918 (H1N1), 1957 (H2N2), 1968 (H3N2) and 1977 (H1N1), each time resulting in a pandemic. Genetic analysis of the isolates demonstrated that 'new' strains most certainly emerged after reassortment of genes of viruses of avian and human origin in a permissive host. The leading theory is that the pig represents the 'mixing vessel' where this genetic reassortment may occur.In 1996, an H7N7 influenza virus of avian origin was isolated from a woman with a self-limiting conjunctivitis. During 1997 in Hong Kong, an H5N1 avian influenza virus was recognised as the cause of death of 6 of 18 infected patients. Genetic analysis revealed these human isolates of H5N1 subtype to be indistinguishable from a highly pathogenic avian influenza virus that was endemic in the local poultry population. More recently, in March 1999, two independent isolations of influenza virus subtype H9N2 were made from girls aged one to four who recovered from flu-like illnesses in Hong Kong. Subsequently, five isolations of H9N2 virus from humans on mainland China in August 1998 were reported. H9N2 viruses were known to be widespread in poultry in China and other Asian countries.In all these cases there was no evidence of human to human spread except with the H5N1 infections where there was evidence of very limited spread. This is in keeping with the finding that all these viruses possessed all eight genes of avian origin. It may well be that infection of humans with avian influenza viruses occurs much more frequently than originally assumed, but due to their limited effect go unrecognised.For the human population as a whole the main danger of direct infection with avian influenza viruses appears to be if people infected with an 'avian' virus are infected simultaneously with a 'human' influenza virus. In such circumstances reassortment could occur with the potential emergence of a virus fully capable of spread in the human population, but with antigenic characteristics for which the human population was immunologically naive. Presumably this represents a very rare coincidence, but one which could result in a true influenza pandemic.     

Isolation and identification of influenza virus strains circulating in Thailand in 2001

Local influenza surveillance plays an important role in preparing for, and responding to, epidemics and pandemics. Between January and December 2001, the National Institute of Health of Thailand collected a total of 711 throat swab specimens from outpatients affected with acute respiratory symptoms from several centers throughout Thailand, of which 374 were virus-positive. Of these, 338 (90.4%) were positive for influenza virus by immunofluorescence testing. By hemagglutination-inhibition (HI) testing, 155 of the type A viruses were found to be subtype H1N1 strains closely related to A/New Caledonia/20/99, and 70 were subtype H3N2 A/Moscow/ 10/99-like viruses. For type B, the isolates were antigenically B/Sichuan/379/9-like by HI, although a number of the strains could be shown to be more closely related to earlier influenza B strains by genetic analysis. The strains circulating in Thailand were antigenically similar to strains isolated worldwide during the same period and to strains recommended by the WHO for inclusion in the vaccines for use in 2001-2002.     

2009H1N1流感病毒对A549细胞和BEAS-2B细胞作用的初步研究

目的 探求2009H1N1流感病毒对A549细胞和BEAS-2B细胞作用,为研究2009H1N1流感病毒的致病机理提供线索。方法 不同来源(死亡、重症、普通病例分离)的2009H1N1流感病毒和季节性H1N1流感病毒分别感染A549和BEAS-2B细胞12、24、48、72 h后用流式细胞术检测细胞凋亡和细胞周期。结果 感染A549细胞12和24 h,普通病例分离的2009H1N1流感病毒组的细胞凋亡率最高(P<0.05),重症组的细胞凋亡率最低(P<0.05);48 h和72 h,死亡组细胞凋亡率最高(P<0.05)。感染BEAS-2B细胞12 h,重症组细胞凋亡率最高(P<0.05);48 h,死亡组和重症组细胞凋亡率高(P<0.05);72 h,死亡组和普通组细胞凋亡率高(P<0.05)。4株病毒主要将A549细胞阻滞在S期,将BEAS-2B细胞阻滞在G0/G1期。结论 在细胞凋亡和细胞周期的细胞学观察水平上2009H1N1流感病毒和季节性H1N1流感病毒之间存在差异,不同来源的2009H1N1流感病毒之间也存在差异。     

T-705 (favipiravir) activity against lethal H5N1 influenza A viruses

The neuraminidase inhibitors oseltamivir and zanamivi are used to treat H5N1 influenza. However, oseltamivir-resistant H5N1 viruses have been isolated from oseltamivir-treated patients. Moreover, reassortment between H5N1 viruses and oseltamvir-resistant human H1N1 viruses currently circulating could create oseltamivir-resistant H5N1 viruses, rendering the oseltamivir stockpile obsolete. Therefore, there is a need for unique and effective antivirals to combat H5N1 influenza viruses. The investigational drug T-705 (favipiravir; 6-fluoro-3-hydroxy-2-pyrazinecarboxamide) has antiviral activity against seasonal influenza viruses and a mouse-adapted H5N1 influenza virus derived from a benign duck virus. However, its efficacy against highly pathogenic H5N1 viruses, which are substantially more virulent, remains unclear. Here, we demonstrate that T-705 effectively protects mice from lethal infection with oseltamivir-sensitive or -resistant highly pathogenic H5N1 viruses. Furthermore, our biochemical analysis suggests that T-705 ribofuranosyl triphosphate, an active form of T-705, acts like purines or purine nucleosides in human cells and does not inhibit human DNA synthesis. We conclude that T-705 shows promise as a therapeutic agent for the treatment of highly pathogenic H5N1 influenza patients.     

Results of the influenza virus surveillance in wild birds in Western part of Mongolia

ObjectiveTo present results of virological study of wild birds inhabiting Western Mongolia.MethodsOver a period of 2003–2008, we isolated 13 influenza A viruses: H1N1, H3N6, H13N8 and H4N6 subtypes. We did not isolate any H5N1 subtype, that still cause epizooty in wild birds and poultry.ResultsWe revealed taxonomic and ecological heterogeneity of the birds involved in maintenance of circulation of influenza viruses in the given territory. Influenza viruses were isolated from birds of 6 orders; among them there are species preferring water and semi-aquatic biotopes, one species preferring dry plain region, and also one species which can inhabit both dry and water biotopes.ConclusionsRepresentatives of all main orders of Western Mongolia avifauna are involved in support of influenza A virus circulation, highly pathogenic H5N1 influenza viruses were registered in Mongolia thus it's necessary to continue permanent influenza virus surveillance in wild birds' populations.     

The evolution of H5N1 influenza viruses in ducks in southern China

The pathogenicity of avian H5N1 influenza viruses to mammals has been evolving since the mid-1980s. Here, we demonstrate that H5N1 influenza viruses, isolated from apparently healthy domestic ducks in mainland China from 1999 through 2002, were becoming progressively more pathogenic for mammals, and we present a hypothesis explaining the mechanism of this evolutionary direction. Twenty-one viruses isolated from apparently healthy ducks in southern China from 1999 through 2002 were confirmed to be H5N1 subtype influenza A viruses. These isolates are antigenically similar to A/Goose/Guangdong/1/96 (H5N1) virus, which was the source of the 1997 Hong Kong "bird flu" hemagglutinin gene, and all are highly pathogenic in chickens. The viruses form four pathotypes on the basis of their replication and lethality in mice. There is a clear temporal pattern in the progressively increasing pathogenicity of these isolates in the mammalian model. Five of six H5N1 isolates tested replicated in inoculated ducks and were shed from trachea or cloaca, but none caused disease signs or death. Phylogenetic analysis of the full genome indicated that most of the viruses are reassortants containing the A/Goose/Guangdong/1/96-like hemagglutinin gene and the other genes from unknown Eurasian avian influenza viruses. This study is a characterization of the H5N1 avian influenza viruses recently circulating in ducks in mainland China. Our findings suggest that immediate action is needed to prevent the transmission of highly pathogenic avian influenza viruses from the apparently healthy ducks into chickens or mammalian hosts.     

Transmission of influenza A(H1N1) 2009 pandemic viruses in Australian swine

Please cite this paper as: Deng et al. (2012). Transmission of influenza A(H1N1) 2009 pandemic viruses in Australian swine. Influenza and Other Respiratory Viruses 6(3), e42–e47. Background Swine have receptors for both human and avian influenza viruses and are a natural host for influenza A viruses. The 2009 influenza A(H1N1) pandemic (H1N1pdm) virus that was derived from avian, human and swine influenza viruses has infected pigs in various countries. Objectives To investigate the relationship between the H1N1pdm viruses isolated from piggery outbreaks in Australia and human samples associated with one of the outbreaks by phylogenetic analysis, and to determine whether there was any reassortment event occurring during the human‐pig interspecies transmission. Methods Real‐time RT‐PCR and full genome sequencing were carried out on RNA isolated from nasal swabs and/or virus cultures. Phylogenetic analysis was performed using the Geneious package. Results The influenza H1N1pdm outbreaks were detected in three pig farms located in three different states in Australia. Further analysis of the Queensland outbreak led to the identification of two distinct virus strains in the pigs. Two staff working in the same piggery were also infected with the same two strains found in the pigs. Full genome sequence analysis on the viruses isolated from pigs and humans did not identify any reassortment of these H1N1pdm viruses with seasonal or avian influenza A viruses. Conclusions This is the first report of swine infected with influenza in Australia and marked the end of the influenza‐free era for the Australian swine industry. Although no reassortment was detected in these cases, the ability of these viruses to cross between pigs and humans highlights the importance of monitoring swine for novel influenza infections.     

Identification of H2N3 influenza A viruses from swine in the United States

Although viruses of each of the 16 influenza A HA subtypes are potential human pathogens, only viruses of the H1, H2, and H3 subtype are known to have been successfully established in humans. H2 influenza viruses have been absent from human circulation since 1968, and as such they pose a substantial human pandemic risk. In this report, we isolate and characterize genetically similar avian/swine virus reassortant H2N3 influenza A viruses isolated from diseased swine from two farms in the United States. These viruses contained leucine at position 226 of the H2 protein, which has been associated with increased binding affinity to the mammalian α2,6Gal-linked sialic acid virus receptor. Correspondingly, the H2N3 viruses were able to cause disease in experimentally infected swine and mice without prior adaptation. In addition, the swine H2N3 virus was infectious and highly transmissible in swine and ferrets. Taken together, these findings suggest that the H2N3 virus has undergone some adaptation to the mammalian host and that their spread should be very closely monitored.     

2007--2008年上海市H9N2亚型禽流感病毒的遗传演化

目的对分离自上海活禽批发市场的11株H9N2亚型AIV（2007年5株、2008年6株）进行了PB2,PBl,HA,NP和NA的测序,以阐明2007年至2008年上海地区H9N2亚型禽流感病毒分离株的遗传变异及分子特征。方法采集鸡气管和泄殖腔样品,将H9亚型荧光RT—PCR试剂盒检测的阳性样品处理后,经鸡胚尿囊腔接种分离病毒,HI进一步确定HA亚型,通过RT-PCR方法分别扩增了这11个毒株的PB2,PBl,HA,NP和NA并进行了序列测定。结果对HA基因进行遗传发生关系分析,这11株分离株均属于Ck／Bei／1／94系。这11个毒株的5个片段的组成有两种方式。结论上海活禽批发市场的1l株H9N2亚型AIV毒株中已包含了H5的片段,所以在今后的工作中加强H9N2亚型禽流感流行病学监测是非常必要的。     

Resistance of influenza A virus to amantadine and rimantadine: results of one decade of surveillance

All clinical isolates of influenza A viruses from patients in Huntington, West Virginia, during the decade 1978-1988 were tested, and 65 of 65 H1N1 and 176 of 181 H3N2 viruses were susceptible to the antiviral action of amantadine and rimantadine. The five resistant viruses were obtained from three members of a family undergoing therapy or prophylaxis with rimantadine. Resistant influenza emerged during treatment with rimantadine and spread to two family contacts, causing typical influenza with fever, myalgia, and cough of 5 days' or less duration. Genetic characterization of the resistant viruses when compared to the susceptible virus isolated on day 1 from the index case revealed a single amino acid change in the transmembrane portion of the M2 protein. In vitro studies showed that rimantadine was significantly more active than amantadine against both H1N1 and H3N2 viruses. Although this resistant influenza was transmitted and caused illness in one family, the absence of naturally occurring resistant viruses suggests that the emergence of new strains of influenza A each few years may prevent the widespread emergence of resistant influenza A virus.     

Serologic evidence of human influenza virus infections in swine populations,Cambodia

Background This study was conducted from 2006 to 2010 and investigated the seroprevalence of influenza A viruses in Cambodian pigs, including human H1N1, H3N2, 2009 pandemic H1N1 (A(H1N1)pdm09), and highly pathogenic avian H5N1 influenza A viruses. Methods A total of 1147 sera obtained from pigs in Cambodia were tested by haemagglutination inhibition (HI) assays for antibody to human influenza A viruses along with both HI and microneutralization (MN) tests to assess immunological responses to H5N1 virus. The results were compared by year, age, and province. Results Antibodies against a human influenza A virus were detected in 14·9% of samples. A(H1N1)pdm09 virus were dominant over the study period (23·1%), followed by those to human H1N1 (17·3%) and H3N2 subtypes (9·9%). No pigs were serologically positive for avian H5 influenza viruses. The seroprevalence of human H1N1 and H3N2 influenza viruses peaked in 2008, while that of A(H1N1)pdm09 reached a peak in 2010. No significant differences in seroprevalence to human influenza subtypes were observed in different age groups. Conclusions Cambodian pigs were exposed to human strains of influenza A viruses either prior to or during this study. The implications of these high prevalence rates imply human‐to‐swine influenza virus transmission in Cambodia. Although pigs are mostly raised in small non‐commercial farms, our preliminary results provide evidence of sustained human influenza virus circulation in pig populations in Cambodia.     

2009年广州地区季节性甲型流感病毒对烷胺类药物耐药性分析

目的 分析2009年1-10月份广州地区季节性甲型流感病毒对烷胺类药物的耐药情况,为临床预防和治疗季节性甲型流感提供参考依据.方法 选取2009年1-10月份广州地区6家医院分离的季节性甲型流感病毒株311株,其中H1亚型159株,H3亚型152株.对病毒的毒株基质蛋白(MP)基因进行序列测定,利用数据库和软件进行生物信息分析,并测定软件随机抽取的临床分离的H1和H3病毒株(各10株)对金刚烷胺的药物敏感度,分析广州地区2009年1-10月份季节性甲型流感病毒的耐药性和基因重组情况.结果 159株H1亚型流感病毒中148株对金刚烷胺耐药(93.1%);152株H3型流感病毒均对金刚烷胺耐药(100%);除1株H1亚型流感病毒发生V27A/S31N双重位点突变外,其余均为S31N单位点突变;159株H1亚型流感病毒中MP基因B型(人类)97株,F型(欧洲/澳洲鸟类)62株;152株H3亚型病毒的MP基因均为B型.结论 广州地区季节性甲型流感病毒对烷胺类药物的耐药比例高,且H1亚型流感病毒与欧洲/澳洲鸟类流感病毒可能存在MP基因交换.

Abstract：

Objective To study the prevalence of adamantane-resistance among influenza A viruses isolated from Guangzhou between January and October in 2009, and to provide more information for clinical usage of adamantine drugs. Methods Totally 311 influenza A strains isolated from 6 hospitals in Guangzhou between January and October in 2009 were selected, and the MP gene of all 311 strains ( 159 strains of H1subtype, 152 strains of H3 subtype ) was sequenced. The susceptibility of viruses to rimantadine was assayedby biological methods in cells. Result A hundred and forty-eight strains of influenza A ( H1 ) viruses( 93. 1%, 148/159 ) were resistant to the adamantanes, and all the 152 influenza A ( H3 ) viruses were resistant to the adamantanes. An amino acid substitution S31N was found in most of the strains except 1strain with double mutation V27A/S31N. Furthermore, the M gene of influenza A ( H1 ) viruses was divided into genotype B ( human ) ( 97/159 ) and genotype F ( European and Australian birds, 62/159 ), while the M gene of influenza A ( H3 ) viruses was genotype B ( human ) ( 152/152 ). Conclusion Resistance rate of seasonal influenza A viruses isolated from Guangzhou was high. The MP gene of influenza A ( H1 ) may be replaced by a gene from European and Australian birds through a reassortment event.     

Contemporary North American influenza H7 viruses possess human receptor specificity: Implications for virus transmissibility

Avian H7 influenza viruses from both the Eurasian and North American lineage have caused outbreaks in poultry since 2002, with confirmed human infection occurring during outbreaks in The Netherlands, British Columbia, and the United Kingdom. The majority of H7 infections have resulted in self-limiting conjunctivitis, whereas probable human-to-human transmission has been rare. Here, we used glycan microarray technology to determine the receptor-binding preference of Eurasian and North American lineage H7 influenza viruses and their transmissibility in the ferret model. We found that highly pathogenic H7N7 viruses from The Netherlands in 2003 maintained the classic avian-binding preference for α2–3-linked sialic acids (SA) and are not readily transmissible in ferrets, as observed previously for highly pathogenic H5N1 viruses. However, H7N3 viruses isolated from Canada in 2004 and H7N2 viruses from the northeastern United States isolated in 2002–2003 possessed an HA with increased affinity toward α2–6-linked SA, the linkage type found prominently on human tracheal epithelial cells. We identified a low pathogenic H7N2 virus isolated from a man in New York in 2003, A/NY/107/03, which replicated efficiently in the upper respiratory tract of ferrets and was capable of transmission in this species by direct contact. These results indicate that H7 influenza viruses from the North American lineage have acquired sialic acid-binding properties that more closely resemble those of human influenza viruses and have the potential to spread to naïve animals.