Locally Acquired Human Infection with Swine-Origin Influenza A(H3N2) Variant Virus, Australia, 2018.
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ABSTRACT:
SUBMITTER: Deng YM
PROVIDER: S-EPMC6924914 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Recent isolation of a novel swine-origin influenza A H3N2 variant virus [A(H3N2)v] from humans in the United States has raised concern over the pandemic potential of these viruses. Here, we analyzed the virulence, transmissibility, and receptor-binding preference of four A(H3N2)v influenza viruses isolated from humans in 2009, 2010, and 2011. High titers of infectious virus were detected in nasal turbinates and nasal wash samples of A(H3N2)v-inoculated ferrets. All four A(H3N2)v viruses possessed the capacity to spread efficiently between cohoused ferrets, and the 2010 and 2011 A(H3N2)v isolates transmitted efficiently to naïve ferrets by respiratory droplets. A dose-dependent glycan array analysis of A(H3N2)v showed a predominant binding to ?2-6-sialylated glycans, similar to human-adapted influenza A viruses. We further tested the viral replication efficiency of A(H3N2)v viruses in a relevant cell line, Calu-3, derived from human bronchial epithelium. The A(H3N2)v viruses replicated in Calu-3 cells to significantly higher titers compared with five common seasonal H3N2 influenza viruses. These findings suggest that A(H3N2)v viruses have the capacity for efficient replication and transmission in mammals and underscore the need for continued public health surveillance.
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Project description:Because swine influenza virus infection is seldom diagnosed in humans, its frequency might be underestimated. We report a immunocompromised hematologic patient with swine influenza A(H3N2) virus in 2014 in Italy. Local pigs were the source of this human infection.
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Project description:The full-genome sequence of A/swine/Henan/1/2010, a strain of influenza A virus isolated in central China, was determined. Phylogenetic analyses show that its eight genomic segments are human-like, and some of its segments have appeared in swine H1N2, swine H1N1, and human H1N2 influenza viruses.
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Project description:While several swine-origin influenza A H3N2 variant (H3N2v) viruses isolated from humans prior to 2011 have been previously characterized for their virulence and transmissibility in ferrets, the recent genetic and antigenic divergence of H3N2v viruses warrants an updated assessment of their pandemic potential. Here, four contemporary H3N2v viruses isolated during 2011 to 2016 were evaluated for their replicative ability in both in vitro and in vivo in mammalian models as well as their transmissibility among ferrets. We found that all four H3N2v viruses possessed similar or enhanced replication capacities in a human bronchial epithelium cell line (Calu-3) compared to a human seasonal influenza virus, suggestive of strong fitness in human respiratory tract cells. The majority of H3N2v viruses examined in our study were mildly virulent in mice and capable of replicating in mouse lungs with different degrees of efficiency. In ferrets, all four H3N2v viruses caused moderate morbidity and exhibited comparable titers in the upper respiratory tract, but only 2 of the 4 viruses replicated in the lower respiratory tract in this model. Furthermore, despite efficient transmission among cohoused ferrets, recently isolated H3N2v viruses displayed considerable variance in their ability to transmit by respiratory droplets. The lack of a full understanding of the molecular correlates of virulence and transmission underscores the need for close genotypic and phenotypic monitoring of H3N2v viruses and the importance of continued surveillance to improve pandemic preparedness.IMPORTANCE Swine-origin influenza viruses of the H3N2 subtype, with the hemagglutinin (HA) and neuraminidase (NA) derived from historic human seasonal influenza viruses, continue to cross species barriers and cause human infections, posing an indelible threat to public health. To help us better understand the potential risk associated with swine-origin H3N2v viruses that emerged in the United States during the 2011-2016 influenza seasons, we use both in vitro and in vivo models to characterize the abilities of these viruses to replicate, cause disease, and transmit in mammalian hosts. The efficient respiratory droplet transmission exhibited by some of the H3N2v viruses in the ferret model combined with the existing evidence of low immunity against such viruses in young children and older adults highlight their pandemic potential. Extensive surveillance and risk assessment of H3N2v viruses should continue to be an essential component of our pandemic preparedness strategy.
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Project description:BackgroundSwine origin A(H3N2) variant [A(H3N2)v] viruses continue to evolve and remain a public health threat. Recent outbreaks in humans in 2016-2018 were caused by a newly emerged A(H3N2)v cluster 2010.1, which are genetically and antigenically distinct from the previously predominant cluster IV. To address the public health risk, we evaluated the levels of heterologous cross-reactive antibodies to A(H3N2)v cluster 2010.1 viruses induced from an existing cluster IV A(H3N2)v vaccine and several seasonal inactivated influenza vaccines (IIVs) in adults, elderly individuals, and children.MethodsHuman vaccine sera and ferret antisera were analyzed by hemagglutination inhibition (HI) and neutralization assays against representative A(H3N2)v viruses from clusters IV and 2010.1 and seasonal A(H3N2) viruses.ResultsFerret antisera detected no or little cross-reactivity between the 2 A(H3N2)v clusters or between A(H3N2)v and seasonal A(H3N2) viruses. In humans, cluster IV A(H3N2)v vaccine induced antibodies cross-reactive to cluster 2010.1 viruses in approximately one-third of the 89 adult and elderly vaccinees. Seasonal IIVs did not induce seroprotective antibodies (≥40) to A(H3N2)v viruses in young children, but induced higher antibodies to A(H3N2)v viruses in cluster 2010.1 than those in cluster IV in adults.ConclusionsCluster IV A(H3N2)v vaccine did not provide sufficient heterologous antibody responses against the new 2010.1 cluster A(H3N2)v viruses. Seasonal IIV could not induce seroprotective antibodies to 2010.1 cluster A(H3N2)v viruses in young children, suggesting that young children are still at high risk to the newly emerged A(H3N2)v viruses. Continued surveillance on A(H3N2)v viruses is critical for risk assessment and pandemic preparedness.
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