Journal articles on the topic 'H3N2 virus'
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1
Haredy, Ahmad M., Hiroshi Yamada, Yoshihiro Sakoda, Masatoshi Okamatsu, Naoki Yamamoto, Takeshi Omasa, Yasuko Mori, et al. "Neuraminidase gene homology contributes to the protective activity of influenza vaccines prepared from the influenza virus library." Journal of General Virology 95, no. 11 (November 1, 2014): 2365–71. http://dx.doi.org/10.1099/vir.0.067488-0.
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Whole-virus (WV) vaccines from influenza A/duck/Hokkaido/77 (H3N2), and its reassortant strains H3N4, H3N5 and H3N7, which have the same haemagglutinin (HA) gene but different neuraminidase (NA) genes, were prepared from our influenza virus library. Mice were intranasally immunized with equivalent doses of each vaccine (1–0.01 µg per mouse). All of the mice that received the highest dose of each vaccine (1 µg per mouse) showed equivalent high HA-inhibiting (HI) antibody titres and survived the H3N2 challenge viruses. However, mice that received lower doses of vaccine (0.1 or 0.01 µg per mouse) containing a heterologous NA had lower survival rates than those given the H3N2-based vaccine. The lungs of mice challenged with H3N2 virus showed a significantly higher virus clearance rate when the vaccine contained the homologous NA (N2) versus a heterologous NA, suggesting that NA contributed to the protection, especially when the HI antibody level was low. These results suggested that, even if vaccines prepared for a possible upcoming pandemic do not induce sufficient HI antibodies, WV vaccines can still be effective through other matched proteins such as NA.
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Song, Daesub, Hyoung-Joon Moon, Dong-Jun An, Hye-Young Jeoung, Hyekwon Kim, Min-Joo Yeom, Minki Hong, et al. "A novel reassortant canine H3N1 influenza virus between pandemic H1N1 and canine H3N2 influenza viruses in Korea." Journal of General Virology 93, no. 3 (March 1, 2012): 551–54. http://dx.doi.org/10.1099/vir.0.037739-0.
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During recent canine influenza surveillance in South Korea, a novel H3N1 canine influenza virus (CIV) that is a putative reassortant between pandemic H1N1 2009 and H3N2 CIVs was isolated. Genetic analysis of eight genes of the influenza virus revealed that the novel H3N1 isolate presented high similarities (99.1–99.9 %) to pandemic influenza H1N1, except for in the haemagglutinin (HA) gene. The HA gene nucleotide sequence of the novel CIV H3N1 was similar (99.6 %) to that of CIV H3N2 isolated in Korea and China. Dogs infected with the novel H3N1 CIV did not show any notable symptoms, in contrast to dogs infected with H3N2 CIV. Despite no visible clinical signs of disease, nasal shedding of virus was detected and the infected dogs presented mild histopathological changes.
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Ma, Wenjun, Marie Gramer, Kurt Rossow, and Kyoung-Jin Yoon. "Isolation and Genetic Characterization of New Reassortant H3N1 Swine Influenza Virus from Pigs in the Midwestern United States." Journal of Virology 80, no. 10 (May 15, 2006): 5092–96. http://dx.doi.org/10.1128/jvi.80.10.5092-5096.2006.
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ABSTRACT Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998, H1N2 and H1N1 reassortant viruses have emerged from reassortment between classical H1N1 and H3N2 viruses. In 2004, a new reassortant H3N1 virus (A/Swine/Minnesota/00395/2004) was identified from coughing pigs. Phylogenetic analyses revealed a hemagglutinin segment similar to those of contemporary cluster III H3N2 SIVs and a neuraminidase sequence of contemporary H1N1 origin. The internal genes were of swine, human, and avian influenza virus origin, similar to those of contemporary U.S. cluster III H3N2 SIVs. The recovery of H3N1 is further evidence of reassortment among SIVs and justifies continuous surveillance.
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Kwasnik, Malgorzata, Marcin Smreczak, Jerzy Rola, Kinga Urbaniak, and Wojciech Rozek. "Serologic investigation of influenza A virus infection in dogs in Poland." Journal of Veterinary Diagnostic Investigation 32, no. 3 (March 24, 2020): 420–22. http://dx.doi.org/10.1177/1040638720913526.
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The 2 predominant circulating subtypes of influenza A virus in the dog population, equine-origin H3N8 and avian-origin H3N2, constitute a potential zoonotic risk. We determined the prevalence of influenza A antibodies in 496 dogs in Poland and found 2.21% of sera positive by commercial ELISA. Hemagglutination inhibition (HI) assays indicated 7.25% of sera positive using equine H3N8, swine H3N2, and pandemic H1N1 antigens, with the most frequently detected immune response being to H3N2. Considering interspecies transfer, reassortment ability, and close contact between dogs and humans, infections of dogs with influenza A virus should be monitored.
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Johansson, B. E., T. M. Moran, C. A. Bona, S. W. Popple, and E. D. Kilbourne. "Immunologic response to influenza virus neuraminidase is influenced by prior experience with the associated viral hemagglutinin. II. Sequential infection of mice simulates human experience." Journal of Immunology 139, no. 6 (September 15, 1987): 2010–14. http://dx.doi.org/10.4049/jimmunol.139.6.2010.
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Abstract In man, vaccination with neuraminidase (NA) in H7N2 virus hybrids elicits greater anti-NA response than does N2 NA in H3N2 conventional vaccine, presumably because humans are H3 hemagglutinin (HA) primed and anti-H3 anamnestic response depresses concomitant N2 responses by antigenic competition. In a laboratory model, BALB/c mice were primed by different schedules of infection with H3N1, H3N2, and H3N7 viruses and given H3N2 and H7N2 vaccines equivalent in NA immunogenicity. In schedules using sequential infections, but not after a single infection with any virus, anti-N2 booster response was fourfold greater with H7N2 vaccine and was reciprocal to the magnitude of anti-H3 response. Thus, HA-influenced suppression of immunologic response to viral NA requires adequate HA priming but is not unique to man and can be studied in the murine model. An incidental finding of this study was the sharing of cross-reactive determinants by N1, N2, and N7 NA.
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Nelson, Martha I., Amy L. Vincent, Pravina Kitikoon, Edward C. Holmes, and Marie R. Gramer. "Evolution of Novel Reassortant A/H3N2 Influenza Viruses in North American Swine and Humans, 2009–2011." Journal of Virology 86, no. 16 (June 13, 2012): 8872–78. http://dx.doi.org/10.1128/jvi.00259-12.
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Novel H3N2 influenza viruses (H3N2v) containing seven genome segments from swine lineage triple-reassortant H3N2 viruses and a 2009 pandemic H1N1 (H1N1pdm09) matrix protein segment (pM) were isolated from 12 humans in the United States between August and December 2011. To understand the evolution of these novel H3N2 viruses in swine and humans, we undertook a phylogenetic analysis of 674 M sequences and 388 HA and NA sequences from influenza viruses isolated from North American swine during 2009–2011, as well as HA, NA, and M sequences from eight H3N2v viruses isolated from humans. We identified 34 swine influenza viruses (termed rH3N2p) with the same combination of H3, N2, and pM segments as the H3N2v viruses isolated from humans. Notably, these rH3N2p viruses were generated in swine via reassortment events between H3N2 viruses and the pM segment approximately 4 to 10 times since 2009. The pM segment has also reassorted with multiple distinct lineages of H1 virus, especially H1δ viruses. Importantly, the N2 segment of all H3N2v viruses isolated from humans is derived from a genetically distinct N2 lineage that has circulated in swine since being acquired by reassortment with seasonal human H3N2 viruses in 2001–2002, rather than from the N2 that is associated with the 1998 H3N2 swine lineage. The identification of this N2 variant may have implications for influenza vaccine design and the potential pandemic threat of H3N2v to human age groups with differing levels of prior exposure and immunity.
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Rajão, Daniela S., Phillip C. Gauger, Tavis K. Anderson, Nicola S. Lewis, Eugenio J. Abente, Mary Lea Killian, Daniel R. Perez, Troy C. Sutton, Jianqiang Zhang, and Amy L. Vincent. "Novel Reassortant Human-Like H3N2 and H3N1 Influenza A Viruses Detected in Pigs Are Virulent and Antigenically Distinct from Swine Viruses Endemic to the United States." Journal of Virology 89, no. 22 (August 26, 2015): 11213–22. http://dx.doi.org/10.1128/jvi.01675-15.
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ABSTRACTHuman-like swine H3 influenza A viruses (IAV) were detected by the USDA surveillance system. We characterized two novel swine human-like H3N2 and H3N1 viruses with hemagglutinin (HA) genes similar to those in human seasonal H3 strains and internal genes closely related to those of 2009 H1N1 pandemic viruses. The H3N2 neuraminidase (NA) was of the contemporary human N2 lineage, while the H3N1 NA was of the classical swine N1 lineage. Both viruses were antigenically distant from swine H3 viruses that circulate in the United States and from swine vaccine strains and also showed antigenic drift from human seasonal H3N2 viruses. Their pathogenicity and transmission in pigs were compared to those of a human H3N2 virus with a common HA ancestry. Both swine human-like H3 viruses efficiently infected pigs and were transmitted to indirect contacts, whereas the human H3N2 virus did so much less efficiently. To evaluate the role of genes from the swine isolates in their pathogenesis, reverse genetics-generated reassortants between the swine human-like H3N1 virus and the seasonal human H3N2 virus were tested in pigs. The contribution of the gene segments to virulence was complex, with the swine HA and internal genes showing effectsin vivo. The experimental infections indicate that these novel H3 viruses are virulent and can sustain onward transmission in pigs, and the naturally occurring mutations in the HA were associated with antigenic divergence from H3 IAV from humans and swine. Consequently, these viruses could have a significant impact on the swine industry if they were to cause more widespread outbreaks, and the potential risk of these emerging swine IAV to humans should be considered.IMPORTANCEPigs are important hosts in the evolution of influenza A viruses (IAV). Human-to-swine transmissions of IAV have resulted in the circulation of reassortant viruses containing human-origin genes in pigs, greatly contributing to the diversity of IAV in swine worldwide. New human-like H3N2 and H3N1 viruses that contain a mix of human and swine gene segments were recently detected by the USDA surveillance system. The human-like viruses efficiently infected pigs and resulted in onward airborne transmission, likely due to the multiple changes identified between human and swine H3 viruses. The human-like swine viruses are distinct from contemporary U.S. H3 swine viruses and from the strains used in swine vaccines, which could have a significant impact on the swine industry due to a lack of population immunity. Additionally, public health experts should consider an appropriate assessment of the risk of these emerging swine H3 viruses for the human population.
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Ma, Jingjiao, Huigang Shen, Qinfang Liu, Bhupinder Bawa, Wenbao Qi, Michael Duff, Yuekun Lang, et al. "Pathogenicity and Transmissibility of Novel Reassortant H3N2 Influenza Viruses with 2009 Pandemic H1N1 Genes in Pigs." Journal of Virology 89, no. 5 (December 24, 2014): 2831–41. http://dx.doi.org/10.1128/jvi.03355-14.
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ABSTRACTAt least 10 different genotypes of novel reassortant H3N2 influenza viruses with 2009 pandemic H1N1 [A(H1N1)pdm09] gene(s) have been identified in U.S. pigs, including the H3N2 variant with a single A(H1N1)pdm09 M gene, which has infected more than 300 people. To date, only three genotypes of these viruses have been evaluated in animal models, and the pathogenicity and transmissibility of the other seven genotype viruses remain unknown. Here, we show that three H3N2 reassortant viruses that contain 3 (NP, M, and NS) or 5 (PA, PB2, NP, M, and NS) genes from A(H1N1)pdm09 were pathogenic in pigs, similar to the endemic H3N2 swine virus. However, the reassortant H3N2 virus with 3 A(H1N1)pdm09 genes and a recent human influenza virus N2 gene was transmitted most efficiently among pigs, whereas the reassortant H3N2 virus with 5 A(H1N1)pdm09 genes was transmitted less efficiently than the endemic H3N2 virus. Interestingly, the polymerase complex of reassortant H3N2 virus with 5 A(H1N1)pdm09 genes showed significantly higher polymerase activity than those of endemic and reassortant H3N2 viruses with 3 A(H1N1)pdm09 genes. Further studies showed that an avian-like glycine at position 228 at the hemagglutinin (HA) receptor binding site is responsible for inefficient transmission of the reassortant H3N2 virus with 5 A(H1N1)pdm09 genes. Taken together, our results provide insights into the pathogenicity and transmissibility of novel reassortant H3N2 viruses in pigs and suggest that a mammalian-like serine at position 228 in the HA is critical for the transmissibility of these reassortant H3N2 viruses.IMPORTANCESwine influenza is a highly contagious zoonotic disease that threatens animal and public health. Introduction of 2009 pandemic H1N1 virus [A(H1N1)pdm09] into swine herds has resulted in novel reassortant influenza viruses in swine, including H3N2 and H1N2 variants that have caused human infections in the United States. We showed that reassortant H3N2 influenza viruses with 3 or 5 genes from A(H1N1)pdm09 isolated from diseased pigs are pathogenic and transmissible in pigs, but the reassortant H3N2 virus with 5 A(H1N1)pdm09 genes displayed less efficient transmissibility than the endemic and reassortant H3N2 viruses with 3 A(H1N1)pdm09 genes. Further studies revealed that an avian-like glycine at the HA 228 receptor binding site of the reassortant H3N2 virus with 5 A(H1N1)pdm09 genes is responsible for less efficient transmissibility in pigs. Our results provide insights into viral pathogenesis and the transmission of novel reassortant H3N2 viruses that are circulating in U.S. swine herds and warrant future surveillance.
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Mancini, Dalva Assunção Portari, Rita Maria Zucatelli Mendonça, Aparecida Santo Pietro Pereira, Adélia Hiroko Nagamori Kawamoto, Camila Infantosi Vannucchi, José Ricardo Pinto, Enio Mori, and Jorge Mancini Filho. "Influenza viruses in adult dogs raised in rural and urban areas in the state of São Paulo, Brazil." Revista do Instituto de Medicina Tropical de São Paulo 54, no. 6 (December 2012): 311–14. http://dx.doi.org/10.1590/s0036-46652012000600004.
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In 1970, searching for the interspecies transmission of influenza viruses led to the first study on influenza viruses in domestic animals. Birds and mammals, including human beings, are their natural hosts; however, other animals may also play a role in the virus epidemiology. The objective was to investigate the incidence of influenza viruses in adult dogs raised in rural (9, 19.56%) and urban (37, 80.43%) areas in the state of São Paulo, Brazil. Dog serum samples were examined for antibodies to influenza viruses by the hemagglutination inhibition (HI) test using the corresponding antigens from the circulating viruses in Brazil. Dogs from rural areas presented antibodies to influenza A H3N2, and influenza A H7N7 and H3N8. In rural areas, dog sera displayed mean titers as 94.37, 227.88, 168.14, 189.62 HIU/25 µL for subtypes H1N1, H3N2, H7N7, H3N8, respectively. About 84% and 92% of dogs from urban areas exhibited antibodies to human influenza A H1N1 and H3N2, respectively, with statistical difference at p < 0.05 between the mean titers of antibodies to H1N1 and H3N2. About 92% and 100% were positive for H7N7 and H3N8, respectively. In dogs from urban areas, the mean titers of antibodies against influenza A H1N1, H3N2, H7N7 and H3N8, were 213.96, 179.42, 231.76, 231.35 HIU/25 µL respectively. The difference among them was not statistically significant at p > 0.05. In conclusion, these dogs were positive for both human and equine influenza viruses. The present study suggests the first evidence that influenza viruses circulate among dogs in Brazil.
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MOON, H., M. HONG, J. K. KIM, B. SEON, W. NA, S. J. PARK, D. J. AN, et al. "H3N2 canine influenza virus with the matrix gene from the pandemic A/H1N1 virus: infection dynamics in dogs and ferrets." Epidemiology and Infection 143, no. 4 (June 30, 2014): 772–80. http://dx.doi.org/10.1017/s0950268814001617.
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SUMMARYAfter an outbreak of pandemic influenza A/H1N1 (pH1N1) virus, we had previously reported the emergence of a recombinant canine influenza virus (CIV) between the pH1N1 virus and the classic H3N2 CIV. Our ongoing routine surveillance isolated another reassortant H3N2 CIV carrying the matrix gene of the pH1N1 virus from 2012. The infection dynamics of this H3N2 CIV variant (CIV/H3N2mv) were investigated in dogs and ferrets via experimental infection and transmission. The CIV/H3N2mv-infected dogs and ferrets produced typical symptoms of respiratory disease, virus shedding, seroconversion, and direct-contact transmissions. Although indirect exposure was not presented for ferrets, CIV/H3N2mv presented higher viral replication in MDCK cells and more efficient transmission was observed in ferrets compared to classic CIV H3N2. This study demonstrates the effect of reassortment of the M gene of pH1N1 in CIV H3N2.
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Riberdy, Janice M., Kirsten J. Flynn, Juergen Stech, Robert G. Webster, John D. Altman, and Peter C. Doherty. "Protection against a Lethal Avian Influenza A Virus in a Mammalian System." Journal of Virology 73, no. 2 (February 1, 1999): 1453–59. http://dx.doi.org/10.1128/jvi.73.2.1453-1459.1999.
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ABSTRACT The question of how best to protect the human population against a potential influenza pandemic has been raised by the recent outbreak caused by an avian H5N1 virus in Hong Kong. The likely strategy would be to vaccinate with a less virulent, laboratory-adapted H5N1 strain isolated previously from birds. Little attention has been given, however, to dissecting the consequences of sequential exposure to serologically related influenza A viruses using contemporary immunology techniques. Such experiments with the H5N1 viruses are limited by the potential risk to humans. An extremely virulent H3N8 avian influenza A virus has been used to infect both immunoglobulin-expressing (Ig+/+) and Ig−/− mice primed previously with a laboratory-adapted H3N2 virus. The cross-reactive antibody response was very protective, while the recall of CD8+ T-cell memory in the Ig−/− mice provided some small measure of resistance to a low-dose H3N8 challenge. The H3N8 virus also replicated in the respiratory tracts of the H3N2-primed Ig+/+ mice, generating secondary CD8+ and CD4+ T-cell responses that may contribute to recovery. The results indicate that the various components of immune memory operate together to provide optimal protection, and they support the idea that related viruses of nonhuman origin can be used as vaccines.
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Su, Wen, Reimi Kinoshita, Jane Gray, Yue Ji, Dan Yu, Joseph Sriyal Malik Peiris, and Hui-Ling Yen. "Seroprevalence of dogs in Hong Kong to human and canine influenza viruses." Veterinary Record Open 6, no. 1 (April 2019): e000327. http://dx.doi.org/10.1136/vetreco-2018-000327.
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As a unique mammalian host for influenza A viruses, dogs support the transmission of canine influenza viruses (CIVs) of H3N8 and H3N2 subtypes and are susceptible to infection by avian and human influenza viruses. A cross-sectional serological study was performed to assess the exposure history of dogs in Hong Kong to CIV and human influenza viruses. Among 555 companion dogs sampled in 2015–2017, 1.3 per cent and 9.5 per cent showed hemagglutination inhibition (HI) antibody titre to CIV of H3N8 or H3N2 subtypes and to A(H1N1)pdm09 human influenza viruses, respectively. Among 182 shelter dogs sampled in 2017–2018, none showed HI titre to CIV and 1.1 per cent reacted to H3N2 human influenza virus. There was a poor correlation between ELISA and HI test results. The higher seropositive rates to human influenza viruses suggests that the contact dynamics of dogs under urban settings may affect the exposure risk to human influenza viruses and CIVs.
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Omoniwa, D. O., C. N. Chinyere, E. R. Agusi, N. Mkpuma2, J. S. Oyetunde, O. E. Igah, J. Adole, A. M. Adidu-Omoniwa, and C. A. Meseko. "Serological and molecular investigation of canine influenza virus in Plateau State, Nigeria." Sokoto Journal of Veterinary Sciences 20, no. 3 (October 17, 2022): 212–15. http://dx.doi.org/10.4314/sokjvs.v20i3.8.
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Canine influenza is a highly contagious respiratory infection of dogs caused by the Influenza A Virus (IAV), characterized by cough, sneeze, nasal secretions, and inappetence. Infections can be mild, severe or fatal. Aquatic birds constitute a natural reservoir for IAV, which is transmitted to terrestrial birds, including poultry. IAV has also emerged in other mammalian species, including humans, swine, horses, and dogs. IAV epidemics in dogs are a recent development. Commonly detected Canine Influenza Virus (CIV) strains are A/H3N2 and A/H3N8 from avian and equine influenza, respectively. Nigeria’s agro-ecology witnessed widespread circulation of avian influenza since 2006, and recent outbreaks of equine influenza in 2018/2019 raise the possibility of inter-species transmission to dogs. To investigate canine Influenza in Plateau State, we collected 113 nasal swabs and 270 sera samples from dogs in clinics, live dog markets, and during dog vaccination campaigns. After extracting nucleic acid with the Qiagen kit, RT-PCR analysed swabs for the Influenza A matrix gene. Sera samples were screened by Enzyme-Linked Immunosorbent Assay before subtyping a cross-section for H3 antibody by Hemagglutination Inhibition. No matrix gene was amplified from extracted nucleic acid from the nasal swabs. Though few sera were reactive to influenza A nucleoprotein, none was positive for influenza A/H3. The H3N8 strain of equine influenza virus first caused an epidemic in dogs in 1999 in the United States. Subsequently, avian-origin H3N2 CIV emerged in dogs in China and South Korea in 2005. Past CIV epidemics arose from a single cross-species transmission of H3N8 subtype from a mammalian intermediate host and the H3N2 subtype from an avian reservoir. Even though this limited investigation did not detect CIV in Plateau State, the potential remains because of the persistent circulation of avian, swine, and equine Influenza in Nigeria, which requires more extensive virological and serological surveillance.
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Heinen, Paul P., Els A. de Boer-Luijtze, and Andre T. J. Bianchi. "Respiratory and systemic humoral and cellular immune responses of pigs to a heterosubtypic influenza A virus infection." Journal of General Virology 82, no. 11 (November 1, 2001): 2697–707. http://dx.doi.org/10.1099/0022-1317-82-11-2697.
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The level of heterosubtypic immunity (Het-I) and the immune mechanisms stimulated by a heterosubtypic influenza virus infection were investigated in pigs. Pigs are natural hosts for influenza virus and, like humans, they host both subtypes H1N1 and H3N2. Marked Het-I was observed when pigs were infected with H1N1 and subsequently challenged with H3N2. After challenge with H3N2, pigs infected earlier with H1N1 did not develop fever and showed reduced virus excretion compared with non-immune control pigs. In addition, virus transmission to unchallenged group-mates could be shown by virus isolation in the non-immune control group but not in the group infected previously with H1N1. Pigs infected previously with homologous H3N2 virus were protected completely. After challenge with H3N2, pigs infected previously with H1N1 showed a considerable increase in serum IgG titre to the conserved extracellular domain of M2 but not to the conserved nucleoprotein. These results suggest that antibodies against external conserved epitopes can have an important role in broad-spectrum immunity. After primary infection with both H1N1 and H3N2, a long-lived increase was observed in the percentage of CD8+ T cells in the lungs and in the lymphoproliferation response in the blood. Upon challenge with H3N2, pigs infected previously with H1N1 again showed an increase in the percentage of CD8+ T cells in the lungs, whereas pigs infected previously with H3N2 did not, suggesting that CD8+ T cells also have a role in Het-I. To confer broad-spectrum immunity, future vaccines should induce antibodies and CD8+ T cells against conserved antigens.
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Ursin, Rebecca L., Hsuan Liu, Harrison R. Powell, Jason W. Westerbeck, Kathryn Shaw-Saliba, Kristyn E. Sylvia, Katherine J. Fenstermacher, et al. "Differential Antibody Recognition of H3N2 Vaccine and Seasonal Influenza Virus Strains Based on Age, Vaccine Status, and Sex in the 2017–2018 Season." Journal of Infectious Diseases 222, no. 8 (June 4, 2020): 1371–82. http://dx.doi.org/10.1093/infdis/jiaa289.
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Abstract Background An antigenic mismatch between the vaccine and circulating H3N2 strains was hypothesized to contribute to the severity of the 2017–2018 season in North America. Methods Serum and nasal washes were collected from influenza positive and negative patients during the 2017–2018 season to determine neutralizing antibody (nAb) titers and for influenza virus sequencing, respectively. Results The circulating and vaccine H3N2 virus strains were different clades, with the vaccine strain being clade 3C.2a and the circulating viruses being 3C.2a2 or 3C.3a. At enrollment, both the H3N2 negative and positive patients had greater nAb titers to the egg-adapted vaccine virus compared to the cell-grown vaccine but the H3N2-negative population had significantly greater titers to the circulating 3C.2a2. Among H3N2-positive patients, vaccination, younger age, and female sex were associated with greater nAb responses to the egg-adapted vaccine H3N2 virus but not to the cell-grown vaccine or circulating viruses. Conclusions For the 2017–2018 circulating viruses, mutations introduced by egg adaptation decreased vaccine efficacy. No increased protection was afforded by vaccination, younger age, or female sex against 2017–2018 circulating H3N2 viruses.
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Hillaire, Marine L. B., Stella E. Vogelzang-van Trierum, Joost H. C. M. Kreijtz, Gerrie de Mutsert, Ron A. M. Fouchier, Albert D. M. E. Osterhaus, and Guus F. Rimmelzwaan. "Human T-cells directed to seasonal influenza A virus cross-react with 2009 pandemic influenza A (H1N1) and swine-origin triple-reassortant H3N2 influenza viruses." Journal of General Virology 94, no. 3 (March 1, 2013): 583–92. http://dx.doi.org/10.1099/vir.0.048652-0.
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Virus-specific CD8+ T-cells contribute to protective immunity against influenza A virus (IAV) infections. As the majority of these cells are directed to conserved viral proteins, they may afford protection against IAVs of various subtypes. The present study assessed the cross-reactivity of human CD8+ T-lymphocytes, induced by infection with seasonal A (H1N1) or A (H3N2) influenza virus, with 2009 pandemic influenza A (H1N1) virus [A(H1N1)pdm09] and swine-origin triple-reassortant A (H3N2) [A(H3N2)v] viruses that are currently causing an increasing number of human cases in the USA. It was demonstrated that CD8+ T-cells induced after seasonal IAV infections exerted lytic activity and produced gamma interferon upon in vitro restimulation with A(H1N1)pdm09 and A(H3N2)v influenza A viruses. Furthermore, CD8+ T-cells directed to A(H1N1)pdm09 virus displayed a high degree of cross-reactivity with A(H3N2)v viruses. It was concluded that cross-reacting T-cells had the potential to afford protective immunity against A(H1N1)pdm09 viruses during the pandemic and offer some degree of protection against infection with A(H3N2)v viruses.
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Santoso, Alvian Rendy, and Erick Sidarta. "Pengaruh evolusi virus H3N2 pada perubahan hemaglutinin, neuraminidase dan efeknya terhadap Major Histocompatibility Complex (MHC) kelas II di Indonesia pada tahun 2005-2019." Tarumanagara Medical Journal 3, no. 2 (November 1, 2021): 220–29. http://dx.doi.org/10.24912/tmj.v4i1.13712.
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Virus H3N2 merupakan salah satu virus yang dapat menyebabkan terjadinya epidemi dan pandemi di seluruh belahan dunia. Di Indonesia sendiri, virus ini merupakan penyebab 64,6% penyakit influenza. Virus H3N2 merupakan virus RNA yang dapat berevolusi dengan cepat sehingga dapat menyebabkan terjadinya kegagalan vaksinasi ataupun respon imun yang tidak sempurna dalam mengeliminasi virus. Molekul major histocompatibility complex (MHC) kelas II adalah komponen yang penting bagi respon imun dalam proses mengeliminasi virus. Pada proses ini, sel T helper akan teraktivasi dan menghasilkan sitokin yang menstimulasi sel imun lainnya. Tujuan studi ini adalah mengetahui pengaruh evolusi virus H3N2 Indonesia pada perubahan hemaglutinin, neuraminidase dan efeknya terhadap pengikatan MHC kelas II pada tahun 2005 - 2019. Data 133 gen HA dan 130 gen NA virus H3N2 di Indonesia tahun 2005 sampai 2019 diperoleh melalui bank data Global Initiative on Sharing All Influence Data (GISAID). Evaluasi dilakukan secara in silico berupa pembangunan pohon filogenetik melalui software MEGA X, uji pengikatan MHC kelas II melalui Immune Epitope Data Base (IEDB) dan uji antigenisitas melalui software Vaxijen 2.0. Pada pohon filogenetik menunjukkan kekerabatan antar sekuens dan terjadinya antigenic drift pada virus H3N2 di Indonesia. Hasil uji pengikatan MHC kelas II dan antigenisitas menunjukkan adanya perubahan skor akibat terbentuknya beberapa variasi epitop seperti pada pada predicted sites 151-165 dengan skor 0.7728 ? 0.4373. Pada studi ini didapatkan juga beberapa epitope sebagai prediksi pembuatan vaksin seperti predicted sites 441-455 gen HA. Evolusi virus H3N2 di Indonesia mengakibatkan terjadinya perubahan atau hilangnya prediksi pengikatan terhadap MHC kelas II dan HLA dominan.
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Liu, Feng, Vic Veguilla, Felicia Gross, Min Levine, Xiyan Xu, Terrence Tumpey, Jacqueline Katz, and Xiuhua Lu. "Age-related prevalence of serum hemagglutination-inhibition antibodies cross-reactive to 2012 and 2013 newly emerging swine-origin influenza A(H3N2) variant viruses (VIR5P.1134)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 148.2. http://dx.doi.org/10.4049/jimmunol.194.supp.148.2.
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Abstract Recent outbreaks of swine-origin influenza A(H3N2) variant virus (H3N2v) in the U.S., mainly among young children with swine exposure, have raised concerns. Previous studies demonstrated older children and young adults had the highest hemagglutination-inhibition (HI) antibodies (Ab) to 2011 H3N2v viruses. In 2013, newly emerging antigenic variants of H3N2v viruses, responsible for 18 human infections, acquired N145K/R mutations in hemagglutinin (HA). Here, human and postinfection ferret sera were tested in HI assays against 2012-13 H3N2v viruses possessing 145N, K or R HA mutations, together with nine historical seasonal H3N2 (sH3N2) viruses circulating since 1968. We found the H3N2v viruses were antigenically distinct but retained a low degree of serologic cross-reactivity (CR) (with ferret antisera) to sH3N2 viruses that circulated in 1990s. Across all age groups (6-80+ years), approximately half were seropositive (HI titer≥40) to the H3N2v viruses. The age related seroprevalence among children were likely associated with primary exposure to sH3N2 viruses in 1990s. We observed a single substitution at 145 in HA was sufficient to change an individual’s seropositivity to the virus and significantly influenced the seroprevalence in certain age groups. The susceptibility to 2012-13 H3N2v viruses remains high in young children, and low in older children and young adults. Improved knowledge of age-related CR Ab is critical for influenza risk assessment and pandemic preparedness.
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Xie, Lixiang, Guanlong Xu, Lingxiang Xin, Zhaofei Wang, Rujuan Wu, Mingqing Wu, Yuqiang Cheng, et al. "Eurasian Avian-like M1 Plays More Important Role than M2 in Pathogenicity of 2009 Pandemic H1N1 Influenza Virus in Mice." Viruses 13, no. 12 (November 23, 2021): 2335. http://dx.doi.org/10.3390/v13122335.
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Reassortant variant viruses generated between 2009 H1N1 pandemic influenza virus [A(H1N1)pdm09] and endemic swine influenza viruses posed a potential risk to humans. Surprisingly, genetic analysis showed that almost all of these variant viruses contained the M segment from A(H1N1)pdm09, which originated from Eurasian avian-like swine influenza viruses. Studies have shown that the A(H1N1)pdm09 M gene is critical for the transmissibility and pathogenicity of the variant viruses. However, the M gene encodes two proteins, M1 and M2, and which of those plays a more important role in virus pathogenicity remains unknown. In this study, the M1 and M2 genes of A(H1N1)pdm09 were replaced with those of endemic H3N2 swine influenza virus, respectively. The chimeric viruses were rescued and evaluated in vitro and in mice. Both M1 and M2 of H3N2 affected the virus replication in vitro. In mice, the introduction of H3N2 M1 attenuated the chimeric virus, where all the mice survived from the infection, compared with the wild type virus that caused 100 % mortality. However, the chimeric virus containing H3N2 M2 was still virulent to mice, and caused 16.6% mortality, as well as similar body weight loss to the wild type virus infected group. Compared with the wild type virus, the chimeric virus containing H3N2 M1 induced lower levels of inflammatory cytokines and higher levels of anti-inflammatory cytokines, whereas the chimeric virus containing H3N2 M2 induced substantial pro-inflammatory responses, but higher levels of anti-inflammatory cytokines. The study demonstrated that Eurasian avian-like M1 played a more important role than M2 in the pathogenicity of A(H1N1)pdm09 in mice.
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Zost, Seth J., Kaela Parkhouse, Megan E. Gumina, Kangchon Kim, Sebastian Diaz Perez, Patrick C. Wilson, John J. Treanor, Andrea J. Sant, Sarah Cobey, and Scott E. Hensley. "Contemporary H3N2 influenza viruses have a glycosylation site that alters binding of antibodies elicited by egg-adapted vaccine strains." Proceedings of the National Academy of Sciences 114, no. 47 (November 6, 2017): 12578–83. http://dx.doi.org/10.1073/pnas.1712377114.
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H3N2 viruses continuously acquire mutations in the hemagglutinin (HA) glycoprotein that abrogate binding of human antibodies. During the 2014–2015 influenza season, clade 3C.2a H3N2 viruses possessing a new predicted glycosylation site in antigenic site B of HA emerged, and these viruses remain prevalent today. The 2016–2017 seasonal influenza vaccine was updated to include a clade 3C.2a H3N2 strain; however, the egg-adapted version of this viral strain lacks the new putative glycosylation site. Here, we biochemically demonstrate that the HA antigenic site B of circulating clade 3C.2a viruses is glycosylated. We show that antibodies elicited in ferrets and humans exposed to the egg-adapted 2016–2017 H3N2 vaccine strain poorly neutralize a glycosylated clade 3C.2a H3N2 virus. Importantly, antibodies elicited in ferrets infected with the current circulating H3N2 viral strain (that possesses the glycosylation site) and humans vaccinated with baculovirus-expressed H3 antigens (that possess the glycosylation site motif) were able to efficiently recognize a glycosylated clade 3C.2a H3N2 virus. We propose that differences in glycosylation between H3N2 egg-adapted vaccines and circulating strains likely contributed to reduced vaccine effectiveness during the 2016–2017 influenza season. Furthermore, our data suggest that influenza virus antigens prepared via systems not reliant on egg adaptations are more likely to elicit protective antibody responses that are not affected by glycosylation of antigenic site B of H3N2 HA.
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Wang, Lin, Qinghua Cui, Xiujuan Zhao, Ping Li, Yanyan Wang, Lijun Rong, and Ruikun Du. "Generation of a Reassortant Influenza A Subtype H3N2 Virus Expressing Gaussia Luciferase." Viruses 11, no. 7 (July 20, 2019): 665. http://dx.doi.org/10.3390/v11070665.
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Reporter influenza A viruses (IAVs) carrying fluorescent or luminescent genes provide a powerful tool for both basic and translational research. Most reporter IAVs are based on the backbone of either subtype H1N1 viruses, A/Puerto Rico/8/1934 (PR8) or A/WSN/1933, but no reporter subtype H3N2 virus is currently available to our knowledge. Since the IAV subtype H3N2 co-circulates with H1N1 among humans causing annual epidemics, a reporter influenza A subtype H3N2 virus would be highly valuable. In this study, the segments of A/Wyoming/3/03 (NY, H3N2) virus encoding hemagglutinin and neuraminidase, respectively, were reassorted with the six internal genes of PR8 where the NS gene was fused with a Gaussia luciferase (Gluc) gene. Using reverse genetics, NY-r19-Gluc, a replication competent reassortant influenza A subtype H3N2 virus expressing reporter Gluc was successfully generated. This reporter virus is stable during replication in Madin-Darby canine kidney (MDCK) cells, and preliminary studies demonstrated it as a useful tool to evaluate antivirals. In addition, NY-r19-Gluc virus will be a powerful tool in other studies including the application of diagnostic and therapeutic antibodies as well as the evaluation of novel vaccines.
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Song, D. S., D. J. An, H. J. Moon, M. J. Yeom, H. Y. Jeong, W. S. Jeong, S. J. Park, et al. "Interspecies transmission of the canine influenza H3N2 virus to domestic cats in South Korea, 2010." Journal of General Virology 92, no. 10 (October 1, 2011): 2350–55. http://dx.doi.org/10.1099/vir.0.033522-0.
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In the past 4 years, incidences of endemic or epidemic respiratory diseases associated with canine influenza H3N2 virus in Asian dogs have been reported in countries such as South Korea and China. Canine species were considered to be the new natural hosts for this virus. However, at the beginning of 2010, influenza-like respiratory signs, such as dyspnoea, were also observed among cats as well as in dogs in an animal shelter located in Seoul, South Korea. The affected cats showed 100 % morbidity and 40 % mortality. We were able to isolate a virus from a lung specimen of a dead cat, which had suffered from the respiratory disease, in embryonated-chicken eggs. The eight viral genes isolated were almost identical to those of the canine influenza H3N2 virus, suggesting interspecies transmission of canine influenza H3N2 virus to the cat. Moreover, three domestic cats infected with intranasal canine/Korea/GCVP01/07 (H3N2) all showed elevated rectal temperatures, nasal virus shedding and severe pulmonary lesions, such as suppurative bronchopneumonia. Our study shows, for the first time, that cats are susceptible to canine influenza H3N2 infection, suggesting that cats may play an intermediate host role in transmitting the H3N2 virus among feline and canine species, which could lead to the endemic establishment of the virus in companion animals. Such a scenario raises a public health concern, as the possibility of the emergence of new recombinant feline or canine influenza viruses in companion animals with the potential to act as a zoonotic infection cannot be excluded.
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Kitikoon, Pravina, Martha I. Nelson, Mary Lea Killian, Tavis K. Anderson, Leo Koster, Marie R. Culhane, and Amy L. Vincent. "Genotype patterns of contemporary reassorted H3N2 virus in US swine." Journal of General Virology 94, no. 6 (June 1, 2013): 1236–41. http://dx.doi.org/10.1099/vir.0.051839-0.
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To understand the evolution of swine-origin H3N2v influenza viruses that have infected 320 humans in the USA since August 2011, we performed a phylogenetic analysis at a whole genome scale of North American swine influenza viruses (n = 200). All viral isolates evolved from the prototypical North American H3 cluster 4 (c4), with evidence for further diversification into subclusters. At least ten distinct reassorted H3N2/pandemic H1N1 (rH3N2p) genotypes were identified in swine. Genotype 1 (G1) was most frequently detected in swine and all human H3N2v viruses clustered within a single G1 clade. These data suggest that the genetic requirements for transmission to humans may be restricted to a specific subset of swine viruses. Mutations at putative antigenic sites as well as reduced serological cross-reactivity among the H3 subclusters suggest antigenic drift of these contemporary viruses.
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DE DONNO, A., A. IDOLO, M. QUATTROCCHI, A. ZIZZA, G. GABUTTI, A. ROMANO, P. GRIMA, I. DONATELLI, and M. GUIDO. "Surveillance of human influenza A(H3N2) virus from 1999 to 2009 in southern Italy." Epidemiology and Infection 142, no. 5 (August 22, 2013): 933–39. http://dx.doi.org/10.1017/s095026881300201x.
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SUMMARYThe aim of this study was to evaluate the presence of influenza virus co-infections in humans and changes in the genetic variability of A(H3N2) virus strains in southern Italy from 1999 to 2009. A partial sequence of the haemagglutinin (HA) gene by human influenza H3N2 strains identified in oropharyngeal swabs from patients with influenza-like illness was analysed by DNA sequencing and a phylogenetic analysis was performed. During the seasons 1999–2000, 2002–2003, 2004–2005 and 2008–2009, the influenza viruses circulating belonged to subtype H3N2. However, A(H1N1) subtype virus and B type were respectively prevalent during the 2000–2001, 2006–2007, 2007–2008 and 2001–2002, 2003–2004, 2005–2006 seasons. The HA sequences appeared to be closely related to the sequence of the influenza A vaccine strain. Only the 2002–2003 season was characterized by co-circulation of two viral lineages: A/New York/55/01(H3N2)-like virus of the previous season and A/Fujian/411/02(H3N2)-like virus, a new H3 variant. In this study, over the decade analysed, no significant change was seen in the sequences of the HA gene of H3 viruses isolated.
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Pan, Keyao, and Michael W. Deem. "Quantifying selection and diversity in viruses by entropy methods, with application to the haemagglutinin of H3N2 influenza." Journal of The Royal Society Interface 8, no. 64 (May 4, 2011): 1644–53. http://dx.doi.org/10.1098/rsif.2011.0105.
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Many viruses evolve rapidly. For example, haemagglutinin (HA) of the H3N2 influenza A virus evolves to escape antibody binding. This evolution of the H3N2 virus means that people who have previously been exposed to an influenza strain may be infected by a newly emerged virus. In this paper, we use Shannon entropy and relative entropy to measure the diversity and selection pressure by an antibody in each amino acid site of H3 HA between the 1992–1993 season and the 2009–2010 season. Shannon entropy and relative entropy are two independent state variables that we use to characterize H3N2 evolution. The entropy method estimates future H3N2 evolution and migration using currently available H3 HA sequences. First, we show that the rate of evolution increases with the virus diversity in the current season. The Shannon entropy of the sequence in the current season predicts relative entropy between sequences in the current season and those in the next season. Second, a global migration pattern of H3N2 is assembled by comparing the relative entropy flows of sequences sampled in China, Japan, the USA and Europe. We verify this entropy method by describing two aspects of historical H3N2 evolution. First, we identify 54 amino acid sites in HA that have evolved in the past to evade the immune system. Second, the entropy method shows that epitopes A and B on the top of HA evolve most vigorously to escape antibody binding. Our work provides a novel entropy-based method to predict and quantify future H3N2 evolution and to describe the evolutionary history of H3N2.
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Zhao, Jin, Wanting He, Meng Lu, Haijian He, and Alexander Lai. "Emergence and Characterization of a Novel Reassortant Canine Influenza Virus Isolated from Cats." Pathogens 10, no. 10 (October 14, 2021): 1320. http://dx.doi.org/10.3390/pathogens10101320.
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Cats are susceptible to a wide range of influenza A viruses (IAV). Furthermore, cats can serve as an intermediate host, and transfer avian influenza virus (AIV) H7N2 to a veterinarian. In this report, a novel reassortant influenza virus, designated A/feline/Jiangsu/HWT/2017 (H3N2), and abbreviated as FIV-HWT-2017, was isolated from nasal swab of a symptomatic cat in Jiangsu province, China. Sequence analysis indicated that, whilst the other seven genes were most similar to the avian-origin canine influenza viruses (CIV H3N2) isolated in China, the NS gene was more closely related to the circulating human influenza virus (H3N2) in the region. Therefore, FIV-HWT-2017 is a reassortant virus. In addition, some mutations were identified, and they were similar to a distinctive CIV H3N2 clade. Whether these cats were infected with the reassortant virus was unknown, however, this random isolation of a reassortant virus indicated that domestic or stray cats were “mixing vessel” for IAV cannot be ruled out. An enhanced surveillance for novel influenza virus should include pet and stray cats.
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Lee, Yu-Na, Dong-Hun Lee, Jae-Keun Park, Seong-Su Yuk, Jung-Hoon Kwon, Sang-Soep Nahm, Joong-Bok Lee, Seung-Yong Park, In-Soo Choi, and Chang-Seon Song. "Experimental infection and natural contact exposure of ferrets with canine influenza virus (H3N2)." Journal of General Virology 94, no. 2 (February 1, 2013): 293–97. http://dx.doi.org/10.1099/vir.0.042473-0.
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Epidemics of H3N2 canine influenza virus (CIV) among dogs in South Korea and southern China have raised concern over the potential for zoonotic transmission of these viruses. Here, we analysed the pathogenesis and transmissibility of H3N2 CIV in ferret. H3N2 CIV replicated efficiently in the respiratory system of inoculated ferrets and caused acute necrotizing bronchioalveolitis and non-suppurative encephalitis. Transmission of H3N2 CIV was detected in three of six ferrets co-housed with inoculated ferrets, but no viruses were detected in second-contact ferrets. These findings show that H3N2 CIV has the capacity to replicate in and transmit partially among co-housed ferrets and underscore the need for continued public health surveillance.
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Fediakina, I. T., M. V. Konopleva, E. S. Proshina, E. V. Linnik, and N. I. Nikitina. "ANTIVIRAL EFFECT OF «KAGOCEL» SUBSTANCE IN VITRO ON INFLUENZA VIRUSES H1N1, H1N1PDM09 AND H3N2." Problems of Virology, Russian journal 64, no. 3 (June 20, 2019): 125–31. http://dx.doi.org/10.18821/0507-4088-2019-64-3-125-131.
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Introduction. Active circulation of pandemic influenza and new variants of influenza H3N2 strains requires monitoring of antiviral efficacy of drugs permitted for influenza therapy in the Russian Federation. Purpose. Assessment of antiviral efficacy of «Kagocel» substance against influenza viruses H1N1, H1N1pdm09 and H3N2 in vitro. Material and methods. Cytotoxic effect of «Kagocel» substance on MDCK cells had been determined by stained with MTS. Antiviral efficacy of «Kagocel» substance against influenza infection has been studied in vitro in the culture of MDCK cells infected with influenza virus strains: A/Puerto Rico/8/34 (H1N1), А/California/7/2009 (H1N1)pdm09, А/Hong Kong/1/68 (H3N2) and А/Hong Kong/4801/2014 (H3N2). The antiviral activity of «Kagocel» substance was tested by its effect on the infectious titer of the influenza viruses and on its impact on the expression level of viral antigens in the enzyme immunoassay test system. Results. «Kagocel» substance had low toxicity for MDCK cells. «Kagocel» inhibited the infection titer of influenza virus strains A/Puerto Rico/8/34 (H1N1), А/California/7/2009 (H1N1)pdm09, А/Hong Kong/1/68 (H3N2) and А/ Hong Kong /4801/2014 (H3N2) in the MDCK cell culture with equal efficacy. Study of the impact of «Kagocel» substance on the expression level of viral antigens by ELISA also revealed its antiviral efficacy for all tested strains. Dose dependence was observed from concentration of substance and from infective dose of virus. Discussion. Effective suppression of the reproduction of influenza virus strains A(H1N1), A(Н1N1)pdm09 and A(H3N2) in the different sublines of MDCK cells with «Kagocel» was shown by the different methods. These results give the possibility to suggest that along with the ability to induce interferons, «Kagocel» can impact on the reproduction of influenza virus, but the further research is needed. Conclusion. «Kagocel» substance effectively inhibits the reproduction of influenza virus strains A(H1N1), A(Н1N1)pdm09 and A(H3N2) in vitro. At the same time, the selectivity index is quite high.
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Le Sage, Valerie, Jennifer E. Jones, Karen A. Kormuth, William J. Fitzsimmons, Eric Nturibi, Gabriella H. Padovani, Claudia P. Arevalo, et al. "Pre-existing heterosubtypic immunity provides a barrier to airborne transmission of influenza viruses." PLOS Pathogens 17, no. 2 (February 18, 2021): e1009273. http://dx.doi.org/10.1371/journal.ppat.1009273.
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Human-to-human transmission of influenza viruses is a serious public health threat, yet the precise role of immunity from previous infections on the susceptibility to airborne infection is still unknown. Using the ferret model, we examined the roles of exposure duration and heterosubtypic immunity on influenza transmission. We demonstrate that a 48 hour exposure is sufficient for efficient transmission of H1N1 and H3N2 viruses. To test pre-existing immunity, a gap of 8–12 weeks between primary and secondary infections was imposed to reduce innate responses and ensure robust infection of donor animals with heterosubtypic viruses. We found that pre-existing H3N2 immunity did not significantly block transmission of the 2009 H1N1pandemic (H1N1pdm09) virus to immune animals. Surprisingly, airborne transmission of seasonal H3N2 influenza strains was abrogated in recipient animals with H1N1pdm09 pre-existing immunity. This protection from natural infection with H3N2 virus was independent of neutralizing antibodies. Pre-existing immunity with influenza B virus did not block H3N2 virus transmission, indicating that the protection was likely driven by the adaptive immune response. We demonstrate that pre-existing immunity can impact susceptibility to heterologous influenza virus strains, and implicate a novel correlate of protection that can limit the spread of respiratory pathogens through the air.
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Liu, Yongping, Jiming Tong, Ying Tong, Ping Li, Xiaolan Cui, and Hongbao Cao. "In vitro anti-influenza virus effect of total flavonoid from Trollius ledebouri Reichb." Journal of International Medical Research 46, no. 4 (February 14, 2018): 1380–90. http://dx.doi.org/10.1177/0300060517750284.
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Objective To investigate the in vitro antivirus effect of total flavonoid from Trollius ledebouri Reichb (TFTLR). Methods Madin-Darby canine kidney (MDCK) and Human epithelial type 2 (HEp-2) cell lines were used to test the antivirus effect of TFTLR on nine virus subtypes: four H1N1, one H3N2, and four other subtypes prevalent in North China. Tamiflu, Ribavirin and Lianhua Qingwen were used as active comparators. Comprehensive molecular pathway analyses of TFTLR-H1N1 and TFTLR-H3N2 relationships were also conducted. Results TFTLR inhibited MDCK cell lesions induced by H1N1 subtypes (A/FM1/1/47, A/Puerto Rico/8/1934 H1N1, A1/Tianjin Jinnan/15/2009, and A/Brisbane/59/2007) and by the H3N2 Brisbane/10/2009 strain. TFTLR inhibitory concentration (IC)50 values against these viruses were 0.13, 0.07, 0.06, 0.14, and 0.07 mg/ml, respectively; and therapeutic index (TI) values were 8.62, 16.0, 18.67, 8.0, and 16.0, respectively. TFTLR showed no effect on parainfluenza virus type 1, herpes simplex virus type 1, respiratory syncytial virus, and coxsackie group B virus type 4. Pathway analysis revealed possible functional therapeutic mechanisms for TFTLR against H1N1 and H3N2 infections. Conclusion TFTLR may represent a potential therapeutic agent against influenza A subtypes H1N1 and H3N2 that are prevalent in North China, and should be investigated further.
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de Jong, J. C., D. J. Smith, A. S. Lapedes, I. Donatelli, L. Campitelli, G. Barigazzi, K. Van Reeth, et al. "Antigenic and Genetic Evolution of Swine Influenza A (H3N2) Viruses in Europe." Journal of Virology 81, no. 8 (February 7, 2007): 4315–22. http://dx.doi.org/10.1128/jvi.02458-06.
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ABSTRACT In the early 1970s, a human influenza A/Port Chalmers/1/73 (H3N2)-like virus colonized the European swine population. Analyses of swine influenza A (H3N2) viruses isolated in The Netherlands and Belgium revealed that in the early 1990s, antigenic drift had occurred, away from A/Port Chalmers/1/73, the strain commonly used in influenza vaccines for pigs. Here we show that Italian swine influenza A (H3N2) viruses displayed antigenic and genetic changes similar to those observed in Northern European viruses in the same period. We used antigenic cartography methods for quantitative analyses of the antigenic evolution of European swine H3N2 viruses and observed a clustered virus evolution as seen for human viruses. Although the antigenic drift of swine and human H3N2 viruses has followed distinct evolutionary paths, potential cluster-differentiating amino acid substitutions in the influenza virus surface protein hemagglutinin (HA) were in part the same. The antigenic evolution of swine viruses occurred at a rate approximately six times slower than the rate in human viruses, even though the rates of genetic evolution of the HA at the nucleotide and amino acid level were similar for human and swine H3N2 viruses. Continuous monitoring of antigenic changes is recommended to give a first indication as to whether vaccine strains may need updating. Our data suggest that humoral immunity in the population plays a smaller role in the evolutionary selection processes of swine H3N2 viruses than in human H3N2 viruses.
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Pando, Rakefet, Shahar Stern, Ital Nemet, Aharona Glatman-Freedman, Hanna Sefty, Neta S. Zuckerman, Yaron Drori, et al. "Diversity in the Circulation of Influenza A(H3N2) Viruses in the Northern Hemisphere in the 2018–19 Season." Vaccines 9, no. 4 (April 13, 2021): 375. http://dx.doi.org/10.3390/vaccines9040375.
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While vaccination is considered the most effective means to prevent influenza infection, its seasonal effectiveness varies, depending on the circulating influenza strains. Here, we characterized the circulation of influenza strains in October-2018 and March-2019 around the world. For this, we used nasopharyngeal samples collected from outpatient and hospitalized patients in Israel and data reported in ECDC, CDC, and WHO databases. Influenza A(H3N2) was dominant in Israel, while in Europe, Asia, and USA, A(H1N1)pdm09 virus circulated first, and then the A(H3N2) virus also appeared. Phylogenetic analysis indicated that A(H3N2) viruses circulating in Israel belonged to clade-3C.3a, while in Europe, Asia, and USA, A(H3N2) viruses belonged to subclade-3C.2a1, but were later replaced by clade-3C.3a viruses in USA. The vaccine A(H3N2) components of that year, A/Singapore/INFIMH-16-0019/2016-(H3N2)-like-viruses, belonged to clade-3C.2a1. The circulation of different influenza subtypes and clades of A(H3N2) viruses in a single season highlights the need for universal influenza vaccines.
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Kühn, Nora, Silke Bergmann, Nadine Kösterke, Ruth L. O. Lambertz, Anna Keppner, Judith M. A. van den Brand, Stefan Pöhlmann, et al. "The Proteolytic Activation of (H3N2) Influenza A Virus Hemagglutinin Is Facilitated by Different Type II Transmembrane Serine Proteases." Journal of Virology 90, no. 9 (February 17, 2016): 4298–307. http://dx.doi.org/10.1128/jvi.02693-15.
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ABSTRACTCleavage of influenza virus hemagglutinin (HA) by host cell proteases is necessary for viral activation and infectivity. In humans and mice, members of the type II transmembrane protease family (TTSP), e.g., TMPRSS2, TMPRSS4, and TMPRSS11d (HAT), have been shown to cleave influenza virus HA for viral activation and infectivityin vitro. Recently, we reported that inactivation of a single HA-activating protease gene,Tmprss2, in knockout mice inhibits the spread of H1N1 influenza viruses. However, after infection ofTmprss2knockout mice with an H3N2 influenza virus, only a slight increase in survival was observed, and mice still lost body weight. In this study, we investigated an additional trypsin-like protease, TMPRSS4. Both TMPRSS2 and TMPRSS4 are expressed in the same cell types of the mouse lung. Deletion ofTmprss4alone in knockout mice does not protect them from body weight loss and death upon infection with H3N2 influenza virus. In contrast,Tmprss2−/−Tmprss4−/−double-knockout mice showed a remarkably reduced virus spread and lung pathology, in addition to reduced body weight loss and mortality. Thus, our results identified TMPRSS4 as a second host cell protease that, in addition to TMPRSS2, is able to activate the HA of H3N2 influenza virusin vivo.IMPORTANCEInfluenza epidemics and recurring pandemics are responsible for significant global morbidity and mortality. Due to high variability of the virus genome, resistance to available antiviral drugs is frequently observed, and new targets for treatment of influenza are needed. Host cell factors essential for processing of the virus hemagglutinin represent very suitable drug targets because the virus is dependent on these host factors for replication. We reported previously thatTmprss2-deficient mice are protected against H1N1 virus infections, but only marginal protection against H3N2 virus infections was observed. Here we show that deletion of two host protease genes,Tmprss2andTmprss4, strongly reduced viral spread as well as lung pathology and resulted in increased survival after H3N2 virus infection. Thus, TMPRSS4 represents another host cell factor that is involved in cleavage activation of H3N2 influenza virusesin vivo.
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Li, Yuanguo, Xinghai Zhang, Yuxiu Liu, Ye Feng, Tiecheng Wang, Ye Ge, Yunyi Kong, et al. "Characterization of Canine Influenza Virus A (H3N2) Circulating in Dogs in China from 2016 to 2018." Viruses 13, no. 11 (November 15, 2021): 2279. http://dx.doi.org/10.3390/v13112279.
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Avian H3N2 influenza virus follows cross-host transmission and has spread among dogs in Asia since 2005. After 2015–2016, a new H3N2 subtype canine influenza epidemic occurred in dogs in North America and Asia. The disease prevalence was assessed by virological and serological surveillance in dogs in China. Herein, five H3N2 canine influenza virus (CIV) strains were isolated from 1185 Chinese canine respiratory disease samples in 2017–2018; these strains were on the evolutionary branch of the North American CIVs after 2016 and genetically far from the classical canine H3N2 strain discovered in China before 2016. Serological surveillance showed an HI antibody positive rate of 6.68%. H3N2 was prevalent in the coastal areas and northeastern regions of China. In 2018, it became the primary epidemic strain in the country. The QK01 strain of H3N2 showed high efficiency in transmission among dogs through respiratory droplets. Nevertheless, the virus only replicated in the upper respiratory tract and exhibited low pathogenicity in mice. Furthermore, highly efficient transmission by direct contact other than respiratory droplet transmission was found in a guinea pig model. The low-level replication in avian species other than ducks could not facilitate contact and airborne transmission in chickens. The current results indicated that a novel H3N2 virus has become a predominant epidemic strain in dogs in China since 2016 and acquired highly efficient transmissibility but could not be replicated in avian species. Thus, further monitoring is required for designing optimal immunoprophylactic tools for dogs and estimating the zoonotic risk of CIV in China.
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Glatman-Freedman, Aharona, Rakefet Pando, Hanna Sefty, Itay Omer, Alina Rosenberg, Yaron Drori, Ital Nemet, Ella Mendelson, Lital Keinan-Boker, and Michal Mandelboim. "Predominance of a Drifted Influenza A (H3N2) Clade and Its Association with Age-Specific Influenza Vaccine Effectiveness Variations, Influenza Season 2018–2019." Vaccines 8, no. 1 (February 9, 2020): 78. http://dx.doi.org/10.3390/vaccines8010078.
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Background: Influenza A (H3N2) clade 3C.3a was the predominant influenza virus in Israel throughout the 2018-2019 season, constituting a drift from the influenza A (H3N2) vaccine. We estimated the end-of season vaccine effectiveness (VE) by age, among community patients with influenza-like illness (ILI), considering the hemagglutinin (HA) gene mutations and amino acid substitutions of influenza A (H3N2) viruses detected. Methods: Nose-throat samples were analyzed for the presence of influenza virus, type/subtype, and HA gene sequence. HA gene sequences and amino acid substitutions were compared to the influenza A/Singapore/INFIMH-16-0019/2016 (H3N2)-like 2018-2019 vaccine virus, and a phylogenetic tree was generated. Influenza VE against influenza A (H3N2) was estimated using the test-negative design. VE was estimated by age group and by 15 year moving age intervals. Results: In total, 90% of the influenza A (H3N2) viruses belonged to the 3C.3a clade, constituting a unique situation in the northern hemisphere. Adjusted all-age influenza A (H3N2) VE was −3.5% (95% CI: −51.2 to 29.1). Although adjusted VEs were very low among infants, children, and young adults, a VE of 45% (95% CI: −19.2 to 74.6) was estimated among adults aged ≥45 years old. Conclusions: The higher VE point estimates among older adults may be related to previous exposure to similar influenza viruses.
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Webby, Richard J., Sabrina L. Swenson, Scott L. Krauss, Philip J. Gerrish, Sagar M. Goyal, and Robert G. Webster. "Evolution of Swine H3N2 Influenza Viruses in the United States." Journal of Virology 74, no. 18 (September 15, 2000): 8243–51. http://dx.doi.org/10.1128/jvi.74.18.8243-8251.2000.
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ABSTRACT During 1998, severe outbreaks of influenza were observed in four swine herds in the United States. This event was unique because the causative agents, H3N2 influenza viruses, are infrequently isolated from swine in North America. Two antigenically distinct reassortant viruses (H3N2) were isolated from infected animals: a double-reassortant virus containing genes similar to those of human and swine viruses, and a triple-reassortant virus containing genes similar to those of human, swine, and avian influenza viruses (N. N. Zhou, D. A. Senne, J. S. Landgraf, S. L. Swenson, G. Erickson, K. Rossow, L. Liu, K.-J. Yoon, S. Krauss, and R. G. Webster, J. Virol. 73:8851–8856, 1999). Because the U.S. pig population was essentially naive in regard to H3N2 viruses, it was important to determine the extent of viral spread. Hemagglutination inhibition (HI) assays of 4,382 serum samples from swine in 23 states indicated that 28.3% of these animals had been exposed to classical swine-like H1N1 viruses and 20.5% had been exposed to the triple-reassortant-like H3N2 viruses. The HI data suggested that viruses antigenically related to the double-reassortant H3N2 virus have not become widespread in the U.S. swine population. The seroreactivity levels in swine serum samples and the nucleotide sequences of six additional 1999 isolates, all of which were of the triple-reassortant genotype, suggested that H3N2 viruses containing avian PA and PB2 genes had spread throughout much of the country. These avian-like genes cluster with genes from North American avian viruses. The worldwide predominance of swine viruses containing an avian-like internal gene component suggests that these genes may confer a selective advantage in pigs. Analysis of the 1999 swine H3N2 isolates showed that the internal gene complex of the triple-reassortant viruses was associated with three recent phylogenetically distinct human-like hemagglutinin (HA) molecules. Acquisition of HA genes from the human virus reservoir will significantly affect the efficacy of the current swine H3N2 vaccines. This finding supports continued surveillance of U.S. swine populations for influenza virus activity.
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Greenbaum, Adena H., K. Wong, D. Nguyen, E. Smith, L. Torso, G. Chen, M. Wise, et al. "Assessment for Possible Healthcare-Associated Transmission of a New Variant Influenza Virus—Pennsylvania, August 2011." Infection Control & Hospital Epidemiology 34, no. 12 (December 2013): 1306–9. http://dx.doi.org/10.1086/673980.
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In August 2011, one of the earliest cases of influenza A(H3N2) variant [A(H3N2)v] virus infection was hospitalized with severe illness. To investigate the potential for healthcare-associated transmission of influenza A(H3N2)v, we evaluated both healthcare providers and patient contacts of the case. We found that healthcare-associated transmission was unlikely.
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Hara, Koyu, Yoko Nakazono, Takahito Kashiwagi, Nobuyuki Hamada, and Hiroshi Watanabe. "Co-incorporation of the PB2 and PA polymerase subunits from human H3N2 influenza virus is a critical determinant of the replication of reassortant ribonucleoprotein complexes." Journal of General Virology 94, no. 11 (November 1, 2013): 2406–16. http://dx.doi.org/10.1099/vir.0.053959-0.
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The influenza virus RNA polymerase, composed of the PB1, PB2 and PA subunits, has a potential role in influencing genetic reassortment. Recent studies on the reassortment of human H3N2 strains suggest that the co-incorporation of PB2 and PA from the same H3N2 strain appears to be important for efficient virus replication; however, the underlying mechanism remains unclear. Here, we reconstituted reassortant ribonucleoprotein (RNP) complexes and demonstrated that the RNP activity was severely impaired when the PA subunit of H3N2 strain A/NT/60/1968 (NT PA) was introduced into H1N1 or H5N1 polymerase. The NT PA did not affect the correct assembly of the polymerase trimeric complex, but it significantly reduced replication-initiation activity when provided with a vRNA promoter and severely impaired the accumulation of RNP, which led to the loss of RNP activity. Mutational analysis demonstrated that PA residues 184N and 383N were the major determinants of the inhibitory effect of NT PA and 184N/383N sequences were unique to human H3N2 strains. Significantly, NT PB2 specifically relieved the inhibitory effect of NT PA, and the PB2 residue 627K played a key role. Our results suggest that PB2 from the same H3N2 strain might be required for overcoming the inhibitory effect of H3N2 PA in the genetic reassortment of influenza virus.
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Nakajima, S., F. Nishikawa, K. Nakamura, and K. Nakajima. "Analysis of influenza A virus reinfection in children in Japan during 1983–91." Epidemiology and Infection 115, no. 3 (December 1995): 591–601. http://dx.doi.org/10.1017/s0950268800058751.
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SummaryThe epidemiology of influenza A in Japan was studied during 1979–91 and viruses isolated from reinfections during 1983–91 were analysed, Of 2963 influenza viruses isolated during this period, 922 and 1006 were influenza A(H1N1) and A(H3N2) viruses respectively; the others were influenza B viruses. Influenza A(H1N1) and A(H3N2) caused 5 and 6 epidemics respectively, most accompanied by antigenic drift. Seventeen reinfections with H1N1 and 17 with H3N2 were detected during our study. The primary and reinfection strains isolated from 7 H1N1 and 10 H3N2 cases were studied by haemagglutination-inhibition, and amino acid and nucleotide sequences of the HA1 region of the haemagglutinin. Most of the primary and reinfection strains were antigenically and genetically similar to the epidemic viruses circulating at that time. However, in 4 out of 10 cases of reinfection with influenza H3N2 virus, reinfection strains were genetically different from the epidemic viruses.
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Zhang, Jun, Xiao Ling Yu, Lei Xu, Fang Zhi Li, and Yong Gang Li. "Sequence Characterization of matrix protein (M1) in influenza A viruses (H1, H3 and H5)." Microbiology Research 2, no. 1 (October 7, 2011): 16. http://dx.doi.org/10.4081/mr.2011.e16.
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<p><strong> </strong>This study brings the analysis of amino acid sequences of matrix protein (M1) from the influenza virus A (H1N1, H3N2 and H5N1) during 2007-2208. 741 sequences of M1 were compared, of them, H1N1 388; H3N2 251 and H5N1 102. Even though, the M1 is relatively conserved among the influenza A viruses, we found some variations in the M1 among the viruses, H1N1, H3N2 and H5N1. The nuclear localization signal at amino acid 101 to 105 is RKLKR for H1N1 and H3N2, but for H5N1 is KKLKR. All differences of amino acid in M1 of H1, H3 and H5 were listed. 80 sequences of M1 of H1N1 H3N2 and H5N1 were used for phylogenetic analysis. There is no reasontantment found in the M1 among these subtypes. Further study is needed to study the differences of the function of M1 among H1N1, H3N2 and H5N1. The M1 of H5N1 may contribute to the high pathogenesis to this virus.</p>
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Liu, Tengfei, Yuhao Huang, Shumin Xie, Lingyu Xu, Junhong Chen, Wenbao Qi, Ming Liao, and Weixin Jia. "A Characterization and an Evolutionary and a Pathogenicity Analysis of Reassortment H3N2 Avian Influenza Virus in South China in 2019–2020." Viruses 14, no. 11 (November 21, 2022): 2574. http://dx.doi.org/10.3390/v14112574.
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Seasonal H3N2 influenza virus has always been a potential threat to public health. The reassortment of the human and avian H3N2 influenza viruses has resulted in major influenza outbreaks, which have seriously damaged human life and health. To assess the possible threat of the H3N2 avian influenza virus to human health, we performed whole-genome sequencing and genetic evolution analyses on 10 H3N2 field strains isolated from different hosts and regions in 2019–2020 and selected representative strains for pathogenicity tests on mice. According to the results, the internal gene cassettes of nine strains had not only undergone reassortment with the H1, H2, H4, H6, and H7 subtypes, which circulate in poultry and mammals, but also with H10N8, which circulates in wild birds in the natural environment. Three reassorted strains were found to be pathogenic to mice, of these one strain harboring MP from H10N8 showed a stronger virulence in mice. This study indicates that reassorted H3N2 AIVs may cross the host barrier to infect mammals and humans, thereby, necessitating persistent surveillance of H3N2 AIVs.
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Malchikov, I. A., A. V. Slobodenyuk, I. V. Vyalykh, A. Yu Markaran, Yu V. Grigorieva, Yu Yu Burtseva, and I. P. Malchikova. "Population immunity for influenza in population of Sverdlovsk Region in epidemic season of 2018–2019." Medical alphabet, no. 18 (September 24, 2020): 26–28. http://dx.doi.org/10.33667/2078-5631-2020-18-26-28.
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Donor blood serum was tested to detect antibodies against circulating influenza viruses. The titer of specific antibodies was determined in the hemagglutination inhibition test (RTGA) against influenza viruses A/California/07/09(H1N1) pdm09, A/HongKong/4801/14(H3N2) and B/Brisben/46/15. In the pre-epidemic period 2018–2019, the immune layer of people with conditionally protective titers of antiviral antibodies was detected in terms of the lowest to A(H3N2) virus (50.0 %), the highest to influenza B (85.4 %). In the post-epidemic season of 2018–2019, the immune layer to influenza A(H1N1) pdm09 virus did not change significantly, which could indicate the preservation of the activity of this virus in the adult population; an increase in the immune layer of individuals with protective titers of antibodies to influenza A(H3N2) – 67.4 % and a decrease in influenza B virus – 49.2 %. A comparison of the results of laboratory data carried out in the pre- and post-epidemic seasons revealed significant differences in the number of people with average antibody titers against influenza A(H3N2) and B viruses (p < 0.05).
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Miller, Darren S., John Finnie, Timothy R. Bowden, Anita C. Scholz, Sawyin Oh, Tuckweng Kok, Christopher J. Burrell, Lee Trinidad, David B. Boyle, and Peng Li. "Preclinical efficacy studies of influenza A haemagglutinin precursor cleavage loop peptides as a potential vaccine." Journal of General Virology 92, no. 5 (May 1, 2011): 1152–61. http://dx.doi.org/10.1099/vir.0.028985-0.
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A universal influenza vaccine that does not require annual reformulation would have clear advantages over the currently approved seasonal vaccine. In this study, we combined the mucosal adjuvant alpha-galactosylceramide (αGalCer) and peptides designed across the highly conserved influenza precursor haemagglutinin (HA0) cleavage loop as a vaccine. Peptides designed across the HA0 of influenza A/H3N2 viruses, delivered to mice via the intranasal route with αGalCer as an adjuvant, provided 100 % protection following H3N2 virus challenge. Similarly, intranasal inoculation of peptides across the HA0 of influenza A/H5N1 with αGalCer completely protected mice against heterotypic challenge with H3N2 virus. Our data suggest that these peptide vaccines effectively inhibited subsequent influenza A/H3N2 virus replication. In contrast, only 20 % of mice vaccinated with αGalCer-adjuvanted peptides spanning the HA0 of H5N1 survived homologous viral challenge, possibly because the HA0 of this virus subtype is cleaved by intracellular furin-like enzymes. Results of these studies demonstrated that HA0 peptides adjuvanted with αGalCer have the potential to form the basis of a synthetic, intranasal influenza vaccine.
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Schrauwen, Eefje J. A., Theo M. Bestebroer, Vincent J. Munster, Emmie de Wit, Sander Herfst, Guus F. Rimmelzwaan, Albert D. M. E. Osterhaus, and Ron A. M. Fouchier. "Insertion of a multibasic cleavage site in the haemagglutinin of human influenza H3N2 virus does not increase pathogenicity in ferrets." Journal of General Virology 92, no. 6 (June 1, 2011): 1410–15. http://dx.doi.org/10.1099/vir.0.030379-0.
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A multibasic cleavage site (MBCS) in the haemagglutinin (HA) protein of influenza A virus is a key determinant of pathogenicity in chickens, and distinguishes highly pathogenic avian influenza (HPAI) viruses from low pathogenic avian influenza viruses (LPAI). An MBCS has only been detected in viruses of the H5 and H7 subtypes. Here we investigated the phenotype of a human H3N2 virus with an MBCS in HA. Insertion of an MBCS in the H3N2 virus resulted in cleavage of HA and efficient replication in Madin–Darby canine kidney cells in the absence of exogenous trypsin in vitro, similar to HPAI H5N1 virus. However, studies in ferrets demonstrated that insertion of the MBCS into HA did not result in increased virus shedding, cellular host range, systemic replication or pathogenicity, as compared with wild-type virus. This study indicates that acquisition of an MBCS alone is insufficient to increase pathogenicity of a prototypical seasonal human H3N2 virus.
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Okuya, Kosuke, Ahmed Magdy Khalil, Mana Esaki, Isshu Kojima, Natsuko Nishi, Donna Koyamada, Tsutomu Matsui, Yuuhei Yoshida, and Makoto Ozawa. "Genetic Characterization of Avian Influenza Viruses Isolated from the Izumi Plain, Japan in 2019/20 Winter Season." Pathogens 11, no. 9 (September 5, 2022): 1013. http://dx.doi.org/10.3390/pathogens11091013.
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The Izumi plain in the Kagoshima Prefecture, Japan, is known as an overwintering site for more than 30,000 migratory waterfowl, including endangered crane species. We previously reported that environmental water samples, from artificial wet paddies created as crane roost sites on the Izumi plain, are useful for avian influenza virus (AIV) surveillance. During the 2019/20 winter season, we collected 238 water samples from the crane roost sites and isolated 22 AIVs of six subtypes: one H1N1, one H3N2, seven H3N8, four H4N6, nine H6N6, and one H11N2 subtypes. Genetic analyses revealed that AIVs of the same subtype isolated from the Izumi plain during a single winter season exhibited multiple genetic constellations. Furthermore, phylogenetic analyses suggested that our H3N2 isolate may be a genetic reassortant between close relatives to our H3N8 and H11N2 isolates. Our study highlighted the importance of monitoring AIV circulation to better understand AIV ecology in migratory waterfowl populations.
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Magiri, Royford Bundi, Ken John Lai, George Kiremu Mutwiri, and Heather Lynne Wilson. "Experimental PCEP-Adjuvanted Swine Influenza H1N1 Vaccine Induced Strong Immune Responses but Did Not Protect Piglets against Heterologous H3N2 Virus Challenge." Vaccines 8, no. 2 (May 18, 2020): 235. http://dx.doi.org/10.3390/vaccines8020235.
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Vaccination is the most efficient method of protection against influenza infections. However, the rapidly mutating viruses and development of new strains make it necessary to develop new influenza vaccines annually. Hence, vaccines that stimulate cross-protection against multiple influenza subtypes are highly sought. Recent evidence suggests that adjuvants such as PCEP that promote Th1-type T cell and Th2-type T cell immune responses and broad-spectrum immune responses may confer cross-protection against heterologous influenza strains. In this study, we evaluated whether the immunogenic and protective potential of PCEP-adjuvanted inactivated swine influenza virus H1N1 vaccine can protect pigs immunized against live H3N2 virus. Piglets were vaccinated via the intradermal route with PCEP-adjuvanted inactivated swine influenza virus (SIV) H1N1 vaccine, boosted at day 21 with the same vaccines then challenged with infectious SIV H3N2 virus at day 35 via the tracheobronchial route. The pigs showed significant anti-H1N1 SIV specific antibody titres and H1N1 SIV neutralizing antibody titres, and these serum titres remained after the challenge with the H3N2 virus. In contrast, vaccination with anti-H1N1 SIV did not trigger anti-H3N2 SIV antibody titres or neutralizing antibody titres and these titres remained low until pigs were challenged with H3N2 SIV. At necropsy (six days after challenge), we collected prescapular lymph nodes and tracheobronchial draining the vaccination sites and challenge site, respectively. ELISPOTs from lymph node cells restimulated ex vivo with inactivated SIV H1N1 showed significant production of IFN-γ in the tracheobronchial cells, but not the prescapular lymph nodes. In contrast, lymph node cells restimulated ex vivo with inactivated SIV H1N1 showed significantly higher IL-13 and IL-17A in the prescapular lymph nodes draining the vaccination sites relative to unchallenged animals. Lung lesion scores show that intradermal vaccination with H1N1 SIV plus PCEP did not prevent lesions when the animals were challenged with H3N2. These results confirm previous findings that PCEP is effective as a vaccine adjuvant in that it induces strong immune responses and protects against homologous swine influenza H1N1 virus, but the experimental H1N1 vaccine failed to cross-protect against heterologous H3N2 virus.
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Jang, Eun-Hee, Do-Yun Hah, Dong-Yeop Park, Kuk-Cheon Lee, and Jung-Ho Heo. "Seroprevalence survey of swine influenza virus (H1N1, H3N2) in pigs in Gyeongnam area." Korean Journal of Veterinary Service 34, no. 3 (September 30, 2011): 195–200. http://dx.doi.org/10.7853/kjvs.2011.34.3.195.
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Paget, W. J., T. J. Meerhoff, and A. Meijer. "Epidemiological and virological assessment of influenza activity in Europe during the 2003-2004 season." Eurosurveillance 10, no. 4 (April 1, 2005): 1–2. http://dx.doi.org/10.2807/esm.10.04.00529-en.
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The 2003-2004 influenza season in Europe was dominated by the spread of the new drift variant A/Fujian/411/2002 (H3N2)-like virus which was not perfectly matched with the A(H3N2) component of the influenza vaccine. Sporadic cases of this virus were detected in Europe at the end of the 2002-2003 season and influenza activity associated with this virus began relatively early during the 2003-2004 season. Generally, influenza activity first occurred in the west of Europe (Ireland, the United Kingdom and the Iberian Peninsula) in October/November and gradually moved east across Europe, affecting Latvia, Lithuania and Poland during the months of January and February 2004. In general, the intensity of clinical activity was higher than during the 2002-2003 season (in 13 out of 20 networks) and, in countries reporting age specific data, the highest consultation incidences were observed among children aged 0-14. However, despite the emergence of the A(H3N2) drift variant, clinical incidences were not especially high compared with historical data. The composition of the 2004-2005 influenza vaccine has been modified compared with the 2003-2004 season and includes an A/Fujian/411/2002 (H3N2)-like virus strain and a new B virus strain (a B/Shanghai/361/2002-like virus).
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Cappuccio, Javier A., Lindomar Pena, Marina Dibárbora, Agustina Rimondi, Pablo Piñeyro, Lucas Insarralde, María A. Quiroga, et al. "Outbreak of swine influenza in Argentina reveals a non-contemporary human H3N2 virus highly transmissible among pigs." Journal of General Virology 92, no. 12 (December 1, 2011): 2871–78. http://dx.doi.org/10.1099/vir.0.036590-0.
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Sporadic outbreaks of human H3N2 influenza A virus (IAV) infections in swine populations have been reported in Asia, Europe and North America since 1970. In South America, serological surveys in pigs indicate that IAVs of the H3 and H1 subtypes are currently in circulation; however, neither virus isolation nor characterization has been reported. In November 2008, an outbreak of respiratory disease in pigs consistent with swine influenza virus (SIV) infection was detected in Argentina. The current study describes the clinical epidemiology, pathology, and molecular and biological characteristics of the virus. Phylogenetic analysis revealed that the virus isolate shared nucleotide identities of 96–98 % with H3N2 IAVs that circulated in humans from 2000 to 2003. Antigenically, sera from experimentally inoculated animals cross-reacted mainly with non-contemporary human-origin H3N2 influenza viruses. In an experimental infection in a commercial swine breed, the virus was of low virulence but was transmitted efficiently to contact pigs and caused severe disease when an infected animal acquired a secondary bacterial infection. This is the first report of a wholly human H3N2 IAV associated with clinical disease in pigs in South America. These studies highlight the importance of two-way transmission of IAVs and SIVs between pigs and humans, and call for enhanced influenza surveillance in the pig population worldwide.
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WONG, J. Y., P. WU, E. GOLDSTEIN, E. H. Y. LAU, D. K. M. IP, J. T. WU, and B. J. COWLING. "Analysis of potential changes in seriousness of influenza A and B viruses in Hong Kong from 2001 to 2011." Epidemiology and Infection 143, no. 4 (June 17, 2014): 766–71. http://dx.doi.org/10.1017/s0950268814001472.
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SUMMARYContinued monitoring of the seriousness of influenza viruses is a public health priority. We applied time-series regression models to data on cardio-respiratory mortality rates in Hong Kong from 2001 to 2011. We used surveillance data on outpatient consultations for influenza-like illness, and laboratory detections of influenza types/subtypes to construct proxy measures of influenza activity. In the model we allowed the regression coefficients for influenza to drift over time, and adjusted for temperature and humidity. The regression coefficient for influenza A(H3N2) increased significantly in 2005. The regression coefficients for influenza A(H1N1) and B were relatively stable over the period. Our model suggested an increase in seriousness of A(H3N2) in 2005, the year after the appearance of the A/Fujian/411/2002(H3N2)-like virus when the drifted A/California/7/2004(H3N2)-like virus appeared. Ongoing monitoring of mortality and influenza activity could permit identification of future changes in seriousness of influenza virus infections.