No announcement yet.

list of reassortment studies

  • Filter
  • Time
  • Show
Clear All
new posts

  • list of reassortment studies

    who helps with that pubmed reassortment meta-study ?
    making a list of the viruses,species,(lab),reassorted segments,dates, from the studies

    motivation is, of course, to get a feeling for what we can expect with H7N9,
    when we can see first experiments and results

    I managed to create and attach a file with the 725 abstracts to this post !

    pubmed reassortment influenza 725 hits

    pubmed reassortment influenza ferret(s) 37(36) hits

    pubmed reassortment influenza mouse(mice) 83(81) hits

    pubmed reassortment influenza guinea 7 hits

    pubmed reassortment influenza pig(s)[swine] 225(238)[216] hits

    pubmed reassortment influenza horse(s) 14(14) hits

    pubmed reassortment influenza cell culture(s) 16(10) hits

    pubmed reassortment influenza chicken(s) 119(86) hits

    pubmed reassortment influenza mallard(s) 12(9) hits

    pubmed reassortment influenza duck(s) 106(78) hits

    reassortment studies with ******:

    Mar.2011 cell culture,WI
    Feb.2011 ferrets,NL, H1N2
    July 2011 ferrets,MD, H9N2
    Mar 2013 ferrets,MD,H1N2
    July 2011 mice,Korea,H3N2,H5N1
    July 2011 mice,Beijin,guinea pigs,triple
    Sept.2011 mice,TW,H1N1(PA!)
    May 2012 mice,UK,H3N2,PR34
    Feb.2013 mice,JP,Mex


    threads in this subforum (not so easy to make it clickable)

    VJ: Experimental infection with a Thai reassortant swine influenza virus of pandemic     H1N1 origin induced disease     tetano March 16th, 2013
    Characterization of influenza virus reassortants based on new donor strain   A/HK/1/68/162/35(H3N2)    tetano March 16th, 2013
    A comprehensive analysis of reassortment in influenza A virus    tetano March 10th, 2013
    Reassortment Complements Spontaneous Mutation in Influenza A Virus NP and    M1 genes to Accelerate Adaptation to a New Host    tetano February 2nd, 2013
    In vivo selection of H1N2 influenza virus reassortants in the ferret model    tetano January 12th, 2013
    New approaches for unravelling reassortment pathways      tetano January 5th, 2013
    Possible outcomes of reassortment in vivo between wild type and live attenuated   influenza vaccine strains   tetano October 17th, 2012
    Pathogenicity and transmissibility of reassortant H9 influenza viruses with genes   from pandemic H1N1 virus   tetano August 11th, 2012
    Viral reassortment as an information exchange between viral segments    tetano Feb 18th, 2012
    An influenza reassortant with polymerase of pH1N1 and NS gene of H3N2 influenza A virus   is attenuated in vivo     February 11th, 2012  by tetano
    Polymerase activity of hybrid ribonucleoprotein complexes generated from reassortment    between 2009 pandemic H1N1 and seasonal H3N2 influenza A viruses   tetano Dec 12th, 2011
    A Novel Reassortant Canine H3N1 Influenza Virus between Pandemic H1N1 and   Canine H3N2 Influenza Viruses in Korea   tetano December 5th, 2011
    Palindromes drive the re-assortment in Influenza A    tetano December 4th, 2011
    Reassortment and mutation of the avian influenza polymerase PA subunit overcomes   species barriers  tetano November 18th, 2011
    Novel genetic reassortants in H9N2 influenza A viruses and their diverse pathogenicity   to mice    tetano November 4th, 2011
    Reassortant H9N2 Influenza Viruses Containing H5N1-Like PB1 Genes Isolated from    Black-Billed Magpies in Southern China    tetano October 10th, 2011
    H9N2 avian influenza viruses and pH1N1 virus can reassort and generate novel    viruses with respiratory transmission potential in mammals  Gert van der Hoek Sep 18th, 2011
    Increased pathogenicity of a reassortant 2009 pandemic H1N1 influenza virus containing   an H5N1 hemagglutinin   tetano September 16th, 2011
    Altered Pathogenicity for Seasonal Influenza Virus by Single Reassortment of the RNP   Genes Derived From the 2009 Pandemic Influenza Virus   tetano August 20th, 2011
    When Flu Strains 'Hook Up,' Dangerous Progeny Can Result    tetano July 14th, 2011
    Reassortment between seasonal H1N1 and pandemic (H1N1) 2009 influenza viruses   is restricted by limited compatibility among polymerase subunits   tetano June 22nd, 2011
    ProMed: H3N2/H1N1 REASSORTANT ex PATIENT    Tonka June 9th, 2011 06:52 PM
    reassortment database    gsgs May 29th, 2011
    Reassortant Pandemic (H1N1) 2009 Virus in Pigs, United Kingdom    tetano May 25th, 2011 08:35 PM
    Virulence and genetic compatibility of polymerase reassortant viruses derived from the pandemic (H1N1) 2009 virus and circulating influenza A viruses   tetano April 23rd, 2011
    N-Glycans from Porcine Trachea and Lung: Predominant NeuAc╬▒2-6Gal Could Be a Selective Pressure for Influenza Variants in Favor of Human-Type Receptor   tetano February 26th, 2011
    germany/ reassortant H1N1 in pigs   Anne February 12th, 2011
    Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment   tetano February 5th, 2011
    The nonadaptive nature of the H1N1 2009 Swine Flu pandemic contrasts with the adaptive facilitation of transmission to a new host   tetano January 8th, 2011
    Reassortment between seasonal and swine-origin H1N1 influenza viruses generates viruses with enhanced growth capability in cell culture   tetano January 5th, 2011
    Reassortment of Ancient Neuraminidase and Recent Hemagglutinin in Pandemic (H1N1) 2009 Virus,   tetano September 30th, 2010
    Genetic characterization of 2008 reassortant influenza A virus (H5N1), Thailand   tetano September 16th, 2010
    Scientists prove humans can have two flus at once   tetano September 16th, 2010
    Reassortant between Human-Like H3N2 and Avian H5 Subtype Influenza A Viruses in Pigs: A Potential Public Health Risk   tetano September 15th, 2010
    Reassortment of pandemic H1N1/2009 influenza A virus in swine   tetano August 10th, 2010
    Kawaoka: hybridization of H1N1 and H5N1   tetano August 5th, 2010
    Evidence Obtained from anova to Reason Cross-species Infection and Cross-subtype Mutation in Neuraminidases of Influenza A Viruses   tetano June 17th, 2010
    A phylogenetic approach to detecting reassortments in viruses with segmented genomes   tetano June 17th, 2010
    Viral reassortment and transmission after coinfection of pigs with classical H1N1 and triple reassortant H3N2 swine influenza viruses   tetano May 21st, 2010
    Chinese study: a case of H1N1-H3N2 (seasonal) hybrid virus   tetano May 13th, 2010
    graphics of evolution of PB1 since 1968   gsgs December 16th, 2009
    will newflu reassort with oldflu ?   gsgs August 26th, 2009
    Reassortment Patterns in Swine Influenza Viruses  sharon sanders August 22nd, 2009
    seasonal H1N1, 2006/7  gsgs August 22nd, 2009
    Reassortment of the Influenza Virus Genome    Chuck July 7th, 2009
    Reassortment between avian H5N1 and human H3N2 influenza viruses in ferrets   Anne June 6th, 2009
    what reassortments can we expect in pandemic flu now ?   gsgs June 1st, 2009
    reassortments in swine  gsgs June 1st, 2009
    5% have 2 viruses   gsgs May 30th, 2009
    H1N1 Related to Virus Born on Hog Factories in 1998   Veg May 3rd, 2009
    |A STUDY: Deviation from the random distribution pattern of influenza A virus...|_   Giuseppe Michieli April 19th, 2008
    Reassortant Avian Influenza Virus (H5N1) in Poultry, Nigeria, 2007  sharon sanders March 26th, 2008
    Bird flu genes found in new swine flu  Coleman December 22nd, 2007
    similarity of the 16 HAs   gsgs August 29th, 2007
    H3N2, 1976   gsgs April 2nd, 2007
    The use of the word, "reassortment".  GaudiaRay November 9th, 2006
    New data show how bird flu quickly spreads  Harriet August 19th, 2006
    Tests suggest bird flu hybrids not big threat  Snowy Owl August 1st, 2006
    Attached Files
    Last edited by gsgs; July 21, 2013, 10:20 AM. Reason: transmission added
    I'm interested in expert panflu damage estimates
    my current links: ILI-charts:

  • #2
    Re: list of reassortment studies

    counts of seroptypes mentioned in that file of 725 abstracts:

    I'm interested in expert panflu damage estimates
    my current links: ILI-charts:


    • #3
      Re: list of reassortment studies

      hey, I didn't know that you can easily download all the abstracts from pubmed !
      72002 influenza abstracts in 88MB

      779524 hits for "virus" , that could be~ 1GB
      21286702 hits for "journal"

      eassort : 1537
      eassort,H7 : 96
      eassort,H9 : 136
      eassort,N9 : 17
      eassort,N2 : 662 (presumably because of H3N2)

      I attach the 3 smaller files
      Attached Files
      I'm interested in expert panflu damage estimates
      my current links: ILI-charts:


      • #4
        Re: list of reassortment studies

        Reassortment between Avian H5N1 and Human Influenza Viruses
        Is Mainly Restricted to the Matrix and Neuraminidase Gene Segments
        H1N1, H3N2 and pandemic H1N1
        human NA and MP were preferentially selected by H5
        these H5 reassortants did not show a marked increase in replication
        in MDCK cells and human bronchial epithelial cells.
        In ferrets, inoculation with a mixture of H5N1-pandemic H1N1 reassortant
        viruses resulted in outgrowth of (aaaaahha) viruses
        This virus was not transmitted via aerosols or respiratory droplets
        to naïve recipient ferrets.

        Compatibility of H9N2 avian influenza surface genes and 2009 pandemic H1N1 internal
        genes for transmission in the ferret model
        (33393933) could gain efficient respiratory droplet transmission ferrets
        1P10:111p11111 (best)
        2P10:111p1p111 ok
        1wf10:111w1111 no
        2wf10:111w1w111 a bit
        1:A/NL/602/09(H1N1),p:A/ferret/MD/P10-UMD/08(H9N2),w:A/guinea fowl/HK/WF10/00(H9N2)

        Both H9N2 avian influenza and 2009 pandemic H1N1 viruses (pH1N1) are able to infect humans and swine, which has raised concerns that novel reassortant H9 viruses with pH1N1 genes might be generated in these hosts by reassortment. Although previous studies have demonstrated that reassortant H9 viruse …

        99999999 (G1) bad in pigs
        11111111 good in pigs
        11191111 good in pigs
        11191911 good in pigs
        I'm interested in expert panflu damage estimates
        my current links: ILI-charts:


        • #5
          Re: list of reassortment studies

          (1:H1N1pdn,2009 , 5:H5N1,1997)
          increased replication of 11151111 in epithelial cells ,(others 7+1 reduced) , 100% lethal to mice
          Serial passage of 11111111 or 11151111 in cells increased pathogenicity
          Serial passage of 55555555 attenuated

          Coinfection of MDCK cells with 1 and 5 gave singlegene reassortants in vitro
          single-gene reassortment is common among H1N1 and H3N2 i.e. with HA

          tested in MDCK cells ,human A549 cells ,normal human bronchial epithelial cells (NHBE)

          11111111 was mild in mice with <10% weightloss , also 51111111,15111111,11511111,11115111,11111115
          11151111 and 55555555 100% lethal
          11111511 and 11111151 : no weithloss

          serially passaged 3 times in differentiated NHBE cells cultured at the air-liquid interface
          11111111 and 11151111 replicated to high titers , 55555555 attenuated after passage 2
          11151111 100 fold of 11111111

          11111111(p3,3 passages) 11151111(p3) more weight loss than p0.
          11111111 transmits in ferrets 11151111 and 55555555 not
          Octaviani et al. found that 15555555,51555555,11555555 had enhanced growth in A549-M2 cells
          transmissibility is a multigenic trait, involving the PB2

          Experimental adaptation of an influenza H5 HA
          confers respiratory droplet transmission to a
          reassortant H5 HA/H1N1 virus in ferrets

          11151111 + --> droplet in ferrets

          avian H3 Q226L
          avian H5 Q226L not
          Q226L and G228S, increased
          Q226L and N224K yes (2,6)


          Dec.2009,guinea pigs,701(PB2),158-160(HA)
          I'm interested in expert panflu damage estimates
          my current links: ILI-charts:


          • #6
            Re: list of reassortment studies


            Compatibility of H9N2 avian influenza surface genes and 2009 pandemic H1N1
            internal genes for transmission in the ferret model

            reassortant virus composed of wild-type avian H9N2 surface genes in a
            seasonal human H3N2 backbone could gain efficient respiratory droplet
            transmission in the ferret model.

            Experimentally, H9N2 surface genes reassorted with
            seasonalH3N2internalgeneshaveshownefficienttransmi ssionin
            a ferret model only after adaptation by serial passage and in-
            corporation of amino acid changes on the surface and internal
            genes (15)

            All four viruses were made with the pH1N1 internal
            genes (PB2, PB1, PA, NP, M, and NS) from A/Netherlands/602/
            2009 (H1N1) (20). The surface genes came from either A/guinea
            fowl/Hong Kong/WF10/1999 (H9N2) or from A/ferret/Mary-
            land/P10_UMD/2008 (H9N2), herein referred to as WF10 and
            P10, respectively (15, 21).

            The P10 virus is the result of 10 serial passages in
            ferrets of an avian-human H9N2:H3N2 reassortant containing
            the WF10 surface on a seasonal H3N2 (A/Memphis/14/1998)
            backbone (15).

            (T189A in HA1 and G192R in HA2) and one in the NA (I28V)
            compared with the WF10

            These amino acid changes were shown
            to be crucial for efficient and reproducible respiratory droplet
            transmission in ferrets (15). The four viruses generated in this
            report had P10 HA and NA (2P10), P10 HA and pH1N1 NA
            (1P10), WF10 HA and NA, (2WF10) or WF10 HA and pH1N1
            NA (1WF10) (Fig. 1A).


            Sorrell EM, Wan H, Araya Y, Song H, Perez DR (2009) Minimal molecular constraints
            for respiratory droplet transmission of an avian-human H9N2 influenza A virus. Proc
            Natl Acad Sci USA 106:7565–7570


            . Sun Y, et al. (2011) High genetic compatiblity and increased pathologenicity of
            reassortants derived from avian H9N2 and pandemic H1N1/2009 influenza viruses.
            Proc Natl Acad Sci USA 108:4164–4169.

            people in China, ranging from 13.7&#37; to 37.2%, might have ev-
            idence of prior infections of the H9N2 virus (11, 12).

            A/chicken/Hebei/LC/2008, HB08) and a pan-
            demic H1N1 influenza virus (A/Beijing/16/2009, BJ09)

            the virus is very poultry-adapted
            in the inner segments. As was the 1997
            Hong Kong virus, a reassortant from chickens.
            It was not in wild birds and they could wipe
            it out. The ~2002 recurrent H5N1 was not so
            much a poultry virus (#amino acid mutations in segment 8 etc.), it was in wild birds and did
            spread and still persists. I think chances are good that they can wipe out this H7N9.
            Testing must be increased since it's LP, but they can do that.
            I'm interested in expert panflu damage estimates
            my current links: ILI-charts:


            • #7
              Re: list of reassortment studies

              not really about reassortment, but related, since it deals with H7-viruses,
              even H7N9 ones, although from the American lineage.

              > Several high and low pathogenicity H7N3 and H7N9 viruses replicated
              > efficiently in the respiratory tract of mice without prior adaptation following
              > intranasal inoculation, but only MX/7218 virus caused lethal disease in this
              > species. H7N3 and H7N9 viruses were also detected in the mouse eye
              > following ocular inoculation. Virus from both H7N3 and H7N9 subtypes
              > replicated efficiently in the upper and lower respiratory tract of ferrets,
              > however, only MX/7218 virus infection caused clinical signs and symptoms
              > and was capable of transmission to na&#239;ve ferrets in a direct contact model.
              > Similar to other highly pathogenic H7 viruses, MX/7218 replicated to high
              > titers in human bronchial epithelial cells, yet downregulated numerous
              > genes related to NF-κB-mediated signaling transduction.


              we have quantitatively characterized the glycan receptor-binding specificity of HAs from representative
              strains of Eurasian (H7N7) and North American (H7N2) lineages that have caused human infection.
              Furthermore, we have demonstrated for the first time that two specific mutations; Gln226→Leu and
              Gly228→Ser in glycan receptor-binding site of H7 HA substantially increase its binding affinity to human

              Introducing the double Gln226→Leu/Gly228→Ser mutations on FC (mFC:LS) and CC (mCC:LS) resulted in
              binding to both avian and human receptors
              The FC, CC and NY/107 strains were also previously analyzed for their ability to transmit in the ferret
              animal model NY/107 and the highly pathogenic CC strain showed some transmission via direct
              contact, however the other highly pathogenic strain isolated from fatal case did not show any transmission.
              None of the viruses transmitted via respiratory droplets.
              We previously demonstrated that the human receptor-binding specificity and affinity correlates with
              respiratory droplet transmissibility in ferrets.
              We demonstrated that the double Gln226→Leu/Gly228→Ser mutation (hallmark changes for
              human adaptation of H3 and H2 HA) dramatically increased human receptor-binding affinity
              of FC and CC HA
              (A/Netherlands/230/03 referred to henceforth as CC
              A/Netherlands/219/03 henceforth referred to as FC


              copy of post 4 from the other thread:
              2 other papers about h9n2 evolution

              Samples of chicken, duck, quail, and pigeon were collected from Jiangsu, Anhui, and Hebei in 2009-2011, and sixteen H9N2 subtype isolates of avian influenza virus (AIV) were identified. The eight full-length genes of 16 AIV isolates were amplified by RT-PCR and sequenced. Genome sequence analysis sh …

              Samples of chicken, duck, quail, and pigeon were collected from Jiangsu, Anhui,
              and Hebei in 2009-2011
              amino acid motif of cleavage sites in the HA gene was P-S-R/K-S-S-R
              Leucine (L) at the amino acid position 226 in the HA
              AIVs originated from F98-like virus as backbone and formed two new genotypes through
              reassortment with HA gene of Y280-like virus and PB2 and M genes of G1-like virus


              there is variable homology among the various NA subtype sequences, especially
              in the N1 and N2 subtypes with the deletion of 4~30 amino acids in the stalk domain [23,1993]
              Meanwhile, the factors that influence NA include deletion of the stalk domain,
              the mutations drug-resistance, as well as the changing of antigen sites or glycosites
              and the variation of the topology of N-glycan structures [28,2011].
              The pattern of stalk domain deletion in N2 NA is distinctive in different combinations of IVs.
              The representative NA sequences in each available N2 subtypes are aligned in the stalk domain.
              As can be observed, the number of deletions varies from 4 to 24 residues,
              causing the loss of one or two potential glycosites.
              9 NA subtypes are concentrated into two evolutionary groups: one group was represented by
              N2 and contains N3, N6, N7, and N9; and another group contains N1, N4, N5, and N8.

              deletion of 3 residues and one corresponding glycosite with the pattern “E-R-61N-3-64T-V-H”
              (meaning 3 residues missing between 61N and 64T, e.g., A/chicken/Zhejiang/611/2011 (H9N2)),
              appeared in most of the NA subtypes of the H9N2 virus.

              Last edited by gsgs; April 22, 2013, 01:31 AM. Reason: link to full paper now
              I'm interested in expert panflu damage estimates
              my current links: ILI-charts:


              • #8
                Re: list of reassortment studies

                Avian influenza subtypes such as H5, H7 and H9 are yet to adapt to the human host so as to establish airborne transmission between humans. However, lab-generated reassorted viruses possessing hemagglutinin (HA) and neuraminidase (NA) genes from an avian H9 isolate and other genes from a human-adapted (H3 or H1) subtype acquired two amino acid changes in HA and a single amino acid change in NA that confer respiratory droplet transmission in ferrets. We previously demonstrated for human-adapted H1, H2 and H3 subtypes that quantitative binding affinity of their HA to α2→6 sialylated glycan receptors correlates with respiratory droplet transmissibility of the virus in ferrets. Such a relationship remains to be established for H9 HA. In this study, we performed a quantitative biochemical characterization of glycan receptor binding properties of wild-type and mutant forms of representative H9 HAs that were previously used in context of reassorted viruses in ferret transmission studies. We demonstrate here that distinct molecular interactions in the glycan receptor-binding site of different H9 HAs affect the glycan-binding specificity and affinity. Further we show that α2→6 glycan receptor-binding affinity of a mutant H9 HA carrying Thr-189→Ala amino acid change correlates with the respiratory droplet transmission in ferrets conferred by this change. Our findings contribute to a framework for monitoring the evolution of H9 HA by understanding effects of molecular changes in HA on glycan receptor-binding properties.

                Although the Kd' ~300 pM for WF10 HA binding to human receptor is 5 fold higher
                than that of 2009 H1N1 HA [7], a reassorted virus with HA and NA from WF10 and
                other internal genes from a human-adapted H3N2 virus did not show respiratory droplet
                transmission in ferrets [15].

                Repeated passaging of this reassorted virus in ferrets led to a strain (RCP10) that had
                additional mutations in HA and NA and transmitted via respiratory droplets in ferrets.
                One of the mutations Thr-189→Ala is in the RBS of H9 HA while the other mutation
                is in HA2 close to the transmembrane region (unlikely to impact RBS features and
                hence receptor binding). It was demonstrated that both these mutations are needed
                for conferring respiratory droplet transmission.
                Thr-189→Ala mutation is needed
                H9 HA a single mutation Q226L might be sufficient
                Leu-226 in context of His-156 and Lys-137 in the Qa88 RBS provides a more optimal
                environment than Leu-226 in the context of Gln-156 and Arg-137 in WF10 RBS for
                achieving a higher quantitative human receptor affinity
                While H9N2 subtype is yet to adapt to the human host, reassorted strains with H9 HA
                and NA have acquired as few as 2 amino acid changes in HA and a single Ile-28→Val
                change in NA to confer respiratory droplet transmission in ferrets
                Such an outcome has not been possible with HAs from other avian subtypes
                I'm interested in expert panflu damage estimates
                my current links: ILI-charts:


                • #9
                  Re: list of reassortment studies

                  both PA and NS of H1N1 made H5N1
                  transmissible by droplet in guinea pigs, without death

                  could spread through the air between guinea pigs in adjacent cages, as long as they carried
                  either or both of two genes from H1N1 called PA and NS

                  but in 293T cells 6,7,8 were selected from H1N1p , 67 from H3N2, 6,7 from H1N1s
                  in MDCK cells few differences , NA alone was worse
                  in wdNHBE cells wt was best
                  in ferrets 6,7(1) were selected from the mix

                  Reassortment between Avian H5N1 and Human Influenza Viruses
                  Is Mainly Restricted to the Matrix and Neuraminidase Gene Segments
                  H1N1, H3N2 and pandemic H1N1 , post 4 above
                  I'm interested in expert panflu damage estimates
                  my current links: ILI-charts:


                  • #10
                    Re: reassortment studies

                    Exploring the reassortment ability of the 2009 pandemic H1N1 (A/H1N1pdm09) influenza virus with other circulating human or avian influenza viruses is the main concern related to the generation of more virulent or new variants having implications for public health. After different coinfection experim …

                    > Conversely, HA and each of the three polymerase segments, alone or in combination,
                    > of the avian influenza viruses mainly reassorted in the A/H1N1pdm09 virus backbone.

                    I'm not sure, what that means. 55551111 reassorts or 71771111 or 11191111 ?

                    > Of note, A/H1N1pdm09 viruses that reassorted with HA of H1N1 seasonal human or
                    > H11N6 avian viruses or carried different combination of avian origin polymerase segments,
                    > exerted a higher replication effectiveness than that of the parental viruses.

                    111s1111 , 111e1111 , 55511111 , 71711111 all replicate better than 11111111

                    > These results confirm that reassortment of the A/H1N1pdm09 with circulating low pathogenic
                    > avian influenza viruses should not be misjudged in the prediction of the next pandemic.

                    nothing should be misjudged in any prediction

                    Exploring the reassortment ability of the 2009 pandemic H1N1 (A/H1N1pdm09) influenza virus with other circulating human or avian influenza viruses is the main concern related to the generation of more virulent or new variants having implications for public health. After different coinfection experim …

                    well working reassortments in A549 cells are:

                    111s1111 (?)

                    a1111111,1a111111,11a11111,aa111111,1aa11111,a1a11 111,aaa11111

                    1:H1N1pdm,a:avian,e:H11N6,s:old seasonal H1N1,x:{H1N1,H3N2,H11,H10,H9,H7,H1av}

                    I'm interested in expert panflu damage estimates
                    my current links: ILI-charts:


                    • #11
                      Re: list of reassortment studies

                      Josh P. • 4 hours ago

                      ..I agree with your Vincent, this is quality science and much more relevant than the gain of function
                      experiments done last year in ferrets. I will tell you this, the PA segment of H1N1 is a nasty ******.
                      I find this segment increases the replication fitness within seven segments of H3N2 swine over the
                      parent strain in both human and swine cells when I make reassortments. The more alarming scenario
                      that isn't mentioned is that multiple genome segments of pH1N1 are circulating in the swine population
                      right now..including pH1N1 PA. However there is a little surveillance data on internal influenza genes
                      as mostly just sequencing is done with NA, HA and sometimes M. I hypothesize based on my co-infection
                      reassortment studies in swine (Hopefully some upcoming animal data) and data in the influenza online
                      database (although limited) that the PA gene segment of pH1N1 will be an issue for years to come.
                      I bet if you took H7N9 and replaced the PA gene with pH1N1 you would get a very nasty virus...this
                      could very well happen in pigs. 50 million pigs in the H7N9-infected region, knowing how reassortments
                      behave is VERY important.
                      I'm interested in expert panflu damage estimates
                      my current links: ILI-charts:


                      • #12
                        Re: list of reassortment studies


                        e=A/swine/Fujian/204/2007 (H1N1)
                        t=A/swine/Guangdong/1222/2006 (H1N2)

                        rH1N1 in mice had higher replicability and pathogenicity than sH1N1,eH1N1
                        but similar to the pH1N1 and tH1N2
                        in guinea pigs rH1N1 was not transmissible, but p2009 was
                        HA and NS contributed to the transmission of pH1N1.
                        HA+NA of pH1N1 gave good contact transmission among guinea pigs.
                        [A/Swine/Korea/1204/2009; Sw/1204 (H1N2)] was virulent in ferrets, causing death within
                        10 d of inoculation, and was efficiently transmitted to naive contact ferrets via respiratory droplets
                        the TRS viruses were moderately pathogenic in ferrets and grew efficiently in both the upper and
                        lower respiratory tracts. All North American TRS viruses studied were transmitted between ferrets
                        via direct contact. However, their transmissibility by respiratory droplets was related to their HA
                        and NA lineages: TRS viruses with human-like HA and NA were transmitted most efficiently, those
                        with swine-like HA and NA were transmitted minimally or not transmitted, and those with swine-like
                        HA and human-like NA (N2) showed intermediate transmissibility.
                        We previously reported that A/swine/Korea/1204/2009(H1N2) virus was virulent and transmissible in ferrets in which the respiratory droplet'transmissible virus (CT-Sw/1204) had acquired simultaneous HAD225G and NAS315N mutations. Incorporating these mutations into the non-pathogenic A/swine/Korea/1130/2009(H1N2, Sw/1130) virus consequently altered pathogenicity and growth in animal models but could not establish efficient transmission or remarkable disease. We, therefore, exploited various reassortants of these two viruses to better understand and identify other viral factors responsible for pathogenicity, transmissibility, or both. We found that possession of the CT-Sw/1204 tripartite viral polymerase enhanced replicative ability and pathogenicity in mice more significantly than did individual expression of polymerase subunit proteins. In ferrets, homologous expression of viral RNA polymerase complex genes in the context of the mutant Sw/1130 carrying the HA225G and NA315N modifications induced optimal replication in the upper nasal and lower respiratory tracts and also promoted efficient aerosol transmission to respiratory droplet'contact ferrets. These data show that the synergistic function of the tripartite polymerase gene complex of CT-Sw/1204 is critically important for virulence and transmission independent of the surface glycoproteins. Sequence comparison results reveal putative differences that are likely to be responsible for variation in disease. Our findings may help elucidate previously undefined viral factors that could expand the host range and disease severity induced by triple-reassortant swine viruses, including the A(H1N1)pdm09 virus, and therefore further justify the ongoing development of novel antiviral drugs targeting the viral polymerase complex subunits.

                        CT-Sw/1204 (=A/Sw/Korea/1204/2009(H1N2)+D225G(4)+S315N(6)
                        is virulent and transmissible in ferrets
                        segments 1,2,3 are responsible for enhanced replication and pathogenicity in mice
                        1,2,3 from Sw/1204 and 4,5,6,7,8 from A/Sw/Korea/1130/2009(H1N2) and D225G(4) and S315N(6)
                        was transmissible in ferrets
                        1130 and 1204 are triple reass.

                        2005-2009 : H5N1(THA05+H3N2(WY05) , ferrets attenuated, not transmissible
                        I'm interested in expert panflu damage estimates
                        my current links: ILI-charts:


                        • #13
                          Re: list of reassortment studies

                          Kash, Taubenberger,2012

                          x=1918flu, a="avian consensus A/green-winged teal/Ohio/175/1986(H2N1) plus HA from Ohio/265

                          xaxxxxxx,xxaxxxxx,xxxaxxxx,xxxxaxxx,xxxxxaxx,xxxxx xax,xxxxxxxa
                          inintranasally infected mice. replicated and caused disease equivalent to p1918.
                          axxxxxxx also, when E627K(1) was added
                          I'm interested in expert panflu damage estimates
                          my current links: ILI-charts:


                          • #14
                            Re: list of reassortment studies

                            The viruses isolated from birds were nonpathogenic in chickens, ducks, and mice;
                            however, the viruses isolated from humans caused up to 30&#37; body weight loss in mice.
                            Most importantly, one virus isolated from humans was highly transmissible in ferrets by
                            respiratory droplets.

                            Three human viruses (SH/1, SH/2, and AH/1)

                            and even though their HA and NA proteins were genetically quite similar, at least one H7N9
                            isolate transmitted readily via respiratory droplets among ferrets.

                            four of the five viruses tested could be transmitted between ferrets in direct contact with
                            each other, and one transmitted with high efficiency via respiratory droplets.

                            H7N9 in one ferret exposed to those infected with one of the bird strains and two human
                            strains isolated from some of the first patients in Shanghai

                            virus in all three ferrets exposed to animals with AH/1

                            mouse study: SH/1, SH/2, AH/1, CK/S1053, PG/S1069, PG/S1421

                            ferret transmission study: SH/1, SH/2, AH/1 ,CK/S1053 , PG/S1421

                            For the respiratory droplet transmission studies, groups of three ferrets were
                            inoculated i.n. with 106 EID50

                            amino-acid differences from the index:

                            nucleotide-differences from the index:
                            I'm interested in expert panflu damage estimates
                            my current links: ILI-charts:


                            • #15
                              Re: list of reassortment studies

                     , July 2012
                              virulent mouse-adapted H9N2 (147L,627K) , 8 lung passages-->M147L(1),V250G,E627K,L226Q(4),R210K(7)
                              in A/chicken/Shandong/16/05(H9N2) [that virus is not at genbank,
                              Shandong however is in NE-China, so presumably quite different from the H9N2
                              that led to H7N9 (as are other H9N2 from Shandong)]
                              more details and keywords:

                              Increased virulence was detectable after 8 sequential lung passages in mice.
                              Five amino acid substitutions were found in the genome of SD16-MA compared
                              with SD16 virus: PB2 (M147L, V250G and E627K), HA (L226Q) and M1 (R210K).
                              [none of the avian viruses at genbank have L at 147 in PB2 : I=7410,M=82,T=966,V=236]

                              Assessments of replication in mice showed that all of the SD16-MA PB2, HA and M1
                              genome segments increased virus replication; however, only the mouse-adapted PB2
                              significantly increased virulence. Although the PB2 E627K amino acid substitution
                              enhanced viral polymerase activity and replication, none of the single mutations of
                              mouse adapted PB2 could confer increased virulence on the SD16 backbone.
                              The combination of M147L and E627K significantly enhanced viral replication ability
                              and virulence in mice. Thus, our results show that the combination of PB2 amino
                              acids at position 147 and 627 is critical for the increased pathogenicity of H9N2
                              influenza virus in mammalian host.

                              A/Chicken/Hebei/4/2008 virus caused acute respiratory distress syndrome (ARDS) in mice,

                              A mouse-adapted H9N2 virus, generated by serial lung-to-lung passage, gained improved
                              growth characteristics on mammalian cells, extended tissue tropism in mice, and was lethal for mice [17].

                              Isoleucine residue at position 97 in PA protein plays a key role in enhanced virulence in mice and is
                              implicated in the adaptation of avian influenza viruses to mammalian hosts [27].

                              H9N2 influenza viruses with an A316S substitution in hemagglutinin (HA) and a
                              shorter neuraminidase (NA) stalk have become predominant in China. The A316S
                              was shown to increase HA cleavage efficiency when combining with short stalk NA,
                              and the short stalk NA improved NA enzyme activity and release of virus from
                              erythrocytes. Single or combination of these mutations strengthened the virulence of
                              H9N2 virus in chickens and mice.
                              BJ/94-like lineage
                              1994–2004, 79.8–95.4&#37; of Chinese H9N2 influenza viruses
                              possessed the PARSSR/GL amino acid sequence motif in the HA cleavage site

                              20. Sun, Y., J. Pu, Z. Jiang, T. Guan, Y. Xia, Q. Xu, L. Liu, B. Ma, F. Tian, E.
                              G. Brown, and J. Liu. 2010. Genotypic evolution and antigenic drift of H9N2
                              influenza viruses in China from 1994 to 2008. Vet Microbiol 146:215-225.
                              five series (BJ/94-, G1-, BG-, F/98- and Aq-series
                              BJ/94,F/98 in N and S China, others in S-China
                              BJ/94 <2000,F/98 since 2004
                              26. Xu, K. M., G. J. Smith, J. Bahl, L. Duan, H. Tai, D. Vijaykrishna, J. Wang,
                              J. X. Zhang, K. S. Li, X. H. Fan, R. G. Webster, H. Chen, J. S. Peiris, and
                              Y. Guan. 2007. The genesis and evolution of H9N2 influenza viruses in
                              poultry from southern China, 2000 to 2005. J Virol 81:10389-10401.

                              Chicken/Beijing/1/94 (Ck/Bei-like) and Quail/Hong Kong/G1/97 (G1-like)
                              Duck/Hong Kong/Y439/97 (Y439-like or Korean-like)
                              Qa/HK/G1/97, Dk/HK/Y280/97, and Ck/HK/G9/97,
                              A total of 89 H9N2 viruses were isolated from 49,150 duck samples
                              I'm interested in expert panflu damage estimates
                              my current links: ILI-charts: