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      The matrix segment of the “Spanish flu” virus originated from intragenic recombination between avian and human influenza A viruses

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          Abstract

          The 1918 Spanish flu virus has claimed more than 50 million lives. However, the mechanism of its high pathogenicity remains elusive; and the origin of the virus is controversial. The matrix (M) segment regulates the replication of influenza A virus, thereby affecting its virulence and pathogenicity. This study found that the M segment of the Spanish flu virus is a recombinant chimera originating from avian influenza virus and human influenza virus. The unique mosaic M segment might confer the virus high replication capacity, showing that the recombination might play an important role in inducing high pathogenicity of the virus. In addition, this study also suggested that the NA and NS segments of the virus were generated by reassortment between mammalian and avian viruses. Direct phylogenetic evidence was also provided for its avian origin.

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          Full-length human immunodeficiency virus type 1 genomes from subtype C-infected seroconverters in India, with evidence of intersubtype recombination.

          K Lole, R Bollinger, R S Paranjape … (1999)
          The development of an effective human immunodeficiency virus type 1 (HIV-1) vaccine is likely to depend on knowledge of circulating variants of genes other than the commonly sequenced gag and env genes. In addition, full-genome data are particularly limited for HIV-1 subtype C, currently the most commonly transmitted subtype in India and worldwide. Likewise, little is known about sequence variation of HIV-1 in India, the country facing the largest burden of HIV worldwide. Therefore, the objective of this study was to clone and characterize the complete genome of HIV-1 from seroconverters infected with subtype C variants in India. Cocultured HIV-1 isolates were obtained from six seroincident individuals from Pune, India, and virtually full-length HIV-1 genomes were amplified, cloned, and sequenced from each. Sequence analysis revealed that five of the six genomes were of subtype C, while one was a mosaic of subtypes A and C, with multiple breakpoints in env, nef, and the 3' long terminal repeat as determined by both maximal chi2 analysis and phylogenetic bootstrapping. Sequences were compared for preservation of known cytotoxic T lymphocyte (CTL) epitopes. Compared with those of the HIV-1LAI sequence, 38% of well-defined CTL epitopes were identical. The proportion of nonconservative substitutions for Env, at 61%, was higher (P < 0.001) than those for Gag (24%), Pol (18%), and Nef (32%). Therefore, characterized CTL epitopes demonstrated substantial differences from subtype B laboratory strains, which were most pronounced in Env. Because these clones were obtained from Indian seroconverters, they are likely to facilitate vaccine-related efforts in India by providing potential antigens for vaccine candidates as well as for assays of vaccine responsiveness.
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            1918 Influenza: the Mother of All Pandemics

            Jeffery K Taubenberger, David M. Morens (2006)
            The "Spanish" influenza pandemic of 1918–1919, which caused ≈50 million deaths worldwide, remains an ominous warning to public health. Many questions about its origins, its unusual epidemiologic features, and the basis of its pathogenicity remain unanswered. The public health implications of the pandemic therefore remain in doubt even as we now grapple with the feared emergence of a pandemic caused by H5N1 or other virus. However, new information about the 1918 virus is emerging, for example, sequencing of the entire genome from archival autopsy tissues. But, the viral genome alone is unlikely to provide answers to some critical questions. Understanding the 1918 pandemic and its implications for future pandemics requires careful experimentation and in-depth historical analysis.
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              Characterization of the 1918 influenza virus polymerase genes.

              Jeffery K Taubenberger, Ann Reid, Raina M. Lourens … (2005)
              The influenza A viral heterotrimeric polymerase complex (PA, PB1, PB2) is known to be involved in many aspects of viral replication and to interact with host factors, thereby having a role in host specificity. The polymerase protein sequences from the 1918 human influenza virus differ from avian consensus sequences at only a small number of amino acids, consistent with the hypothesis that they were derived from an avian source shortly before the pandemic. However, when compared to avian sequences, the nucleotide sequences of the 1918 polymerase genes have more synonymous differences than expected, suggesting evolutionary distance from known avian strains. Here we present sequence and phylogenetic analyses of the complete genome of the 1918 influenza virus, and propose that the 1918 virus was not a reassortant virus (like those of the 1957 and 1968 pandemics), but more likely an entirely avian-like virus that adapted to humans. These data support prior phylogenetic studies suggesting that the 1918 virus was derived from an avian source. A total of ten amino acid changes in the polymerase proteins consistently differentiate the 1918 and subsequent human influenza virus sequences from avian virus sequences. Notably, a number of the same changes have been found in recently circulating, highly pathogenic H5N1 viruses that have caused illness and death in humans and are feared to be the precursors of a new influenza pandemic. The sequence changes identified here may be important in the adaptation of influenza viruses to humans.
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                Author and article information

                Contributors
                Nai‐Zheng Ding:
                ORCID: https://orcid.org/0000-0001-9795-0616
                nzding@sdnu.edu.cn
                Journal
                Journal ID (nlm-ta): Transbound Emerg Dis
                Journal ID (iso-abbrev): Transbound Emerg Dis
                Journal ID (doi): 10.1111/(ISSN)1865-1682
                Journal ID (publisher-id): TBED
                Title: Transboundary and Emerging Diseases
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1865-1674
                ISSN (Electronic): 1865-1682
                Publication date (Electronic): 15 July 2019
                Publication date (Print): September 2019
                Volume: 66
                Issue: 5 ( doiID: 10.1111/tbed.v66.5 )
                Pages: 2188-2195
                Affiliations
                [ 1 ] The Key Laboratory of Animal Resistant Biology of Shandong, College of Life Science Shandong Normal University Jinan China
                Author notes
                [*] [* ] Correspondence

                Nai‐Zheng Ding, The Key Laboratory of Animal Resistant Biology of Shandong, College of Life Science, Shandong Normal University, Shandong Province 250014, China.

                Email: nzding@ 123456sdnu.edu.cn

                Author information
                https://orcid.org/0000-0001-9795-0616
                Article
                Publisher ID: TBED13282
                DOI: 10.1111/tbed.13282
                PMC ID: 7168540
                PubMed ID: 31241237
                SO-VID: 766ac070-e408-4851-8cfb-f91d0a856d7e
                Copyright statement: © 2019 Blackwell Verlag GmbH
                License:

                This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.

                History
                Date received : 23 April 2019
                Date revision received : 30 May 2019
                Date accepted : 19 June 2019
                Page count
                Figures: 4, Tables: 0, Pages: 8, Words: 6057
                Product
                Funding
                Funded by: Key R & D project of Shandong Province
                Award ID: 2017GNC10125
                Categories
                Subject: Short Communication
                Subject: Short Communications
                Custom metadata
                source-schema-version-number 2.0
                cover-date September 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.0 mode:remove_FC converted:15.04.2020

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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