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      Evolutionary ecology of virus emergence

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          Abstract

          The cross‐species transmission of viruses into new host populations, termed virus emergence, is a significant issue in public health, agriculture, wildlife management, and related fields. Virus emergence requires overlap between host populations, alterations in virus genetics to permit infection of new hosts, and adaptation to novel hosts such that between‐host transmission is sustainable, all of which are the purview of the fields of ecology and evolution. A firm understanding of the ecology of viruses and how they evolve is required for understanding how and why viruses emerge. In this paper, I address the evolutionary mechanisms of virus emergence and how they relate to virus ecology. I argue that, while virus acquisition of the ability to infect new hosts is not difficult, limited evolutionary trajectories to sustained virus between‐host transmission and the combined effects of mutational meltdown, bottlenecking, demographic stochasticity, density dependence, and genetic erosion in ecological sinks limit most emergence events to dead‐end spillover infections. Despite the relative rarity of pandemic emerging viruses, the potential of viruses to search evolutionary space and find means to spread epidemically and the consequences of pandemic viruses that do emerge necessitate sustained attention to virus research, surveillance, prophylaxis, and treatment.

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          Most cited references175

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          Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China.

          Y Guan (2003)
          A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS). SCoV-like viruses were isolated from Himalayan palm civets found in a live-animal market in Guangdong, China. Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market. All the animal isolates retain a 29-nucleotide sequence that is not found in most human isolates. The detection of SCoV-like viruses in small, live wild mammals in a retail market indicates a route of interspecies transmission, although the natural reservoir is not known.
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            Early alterations of the receptor-binding properties of H1, H2, and H3 avian influenza virus hemagglutinins after their introduction into mammals.

            Interspecies transmission of influenza A viruses circulating in wild aquatic birds occasionally results in influenza outbreaks in mammals, including humans. To identify early changes in the receptor binding properties of the avian virus hemagglutinin (HA) after interspecies transmission and to determine the amino acid substitutions responsible for these alterations, we studied the HAs of the initial isolates from the human pandemics of 1957 (H2N2) and 1968 (H3N2), the European swine epizootic of 1979 (H1N1), and the seal epizootic of 1992 (H3N3), all of which were caused by the introduction of avian virus HAs into these species. The viruses were assayed for their ability to bind the synthetic sialylglycopolymers 3'SL-PAA and 6'SLN-PAA, which contained, respectively, 3'-sialyllactose (the receptor determinant preferentially recognized by avian influenza viruses) and 6'-sialyl(N-acetyllactosamine) (the receptor determinant for human viruses). Avian and seal viruses bound 6'SLN-PAA very weakly, whereas the earliest available human and swine epidemic viruses bound this polymer with a higher affinity. For the H2 and H3 strains, a single mutation, 226Q-->L, increased binding to 6'SLN-PAA, while among H1 swine viruses, the 190E-->D and 225G-->E mutations in the HA appeared important for the increased affinity of the viruses for 6'SLN-PAA. Amino acid substitutions at positions 190 and 225 with respect to the avian virus consensus sequence are also present in H1 human viruses, including those that circulated in 1918, suggesting that substitutions at these positions are important for the generation of H1 human pandemic strains. These results show that the receptor-binding specificity of the HA is altered early after the transmission of an avian virus to humans and pigs and, therefore, may be a prerequisite for the highly effective replication and spread which characterize epidemic strains.
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              Why do RNA viruses recombine?

              Key Points RNA viruses are able to undergo two forms of recombination: RNA recombination, which (in principle) can occur in any type of RNA virus, and reassortment, which is restricted to those viruses with segmented genomes. Rates of RNA recombination vary markedly among RNA viruses. Some viruses, particularly those with negative-sense single-stranded genomes, exhibit such low rates of recombination that they are effectively clonal. By contrast, some positive-sense single-stranded RNA viruses and some retroviruses such as HIV exhibit high rates of recombination that can exceed the rates of mutation when measured per nucleotide. Although recombination is often argued to represent a form of sexual reproduction, there is little evidence that recombination in RNA viruses evolved as a way of creating advantageous genotypes or removing deleterious mutations. In particular, there is no association between recombination frequency and the burden of a deleterious mutation. Similarly, there is little evidence that recombination could have been selected as a form of genetic repair. The strongest association for rates of recombination in RNA viruses is with genome structure. Hence, negative-sense single-stranded RNA viruses may recombine at low rates because of the restrictive association of genomic RNA in a ribonucleoprotein complex, as well as a lack of substrates for template switching, whereas some retroviruses recombine rapidly because their virions contain two genome copies and template switching between these copies is an inevitable part of the viral replication cycle. We therefore hypothesize that recombination in RNA viruses is a mechanistic by-product of the processivity of the viral polymerase that is used in replication, and that it varies with genome structure.
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                Author and article information

                Contributors
                john.dennehy@qc.cuny.edu
                Journal
                Ann N Y Acad Sci
                Ann. N. Y. Acad. Sci
                10.1111/(ISSN)1749-6632
                NYAS
                Annals of the New York Academy of Sciences
                John Wiley and Sons Inc. (Hoboken )
                0077-8923
                1749-6632
                30 December 2016
                February 2017
                : 1389
                : 1 , The Year in Evolutionary Biology ( doiID: 10.1111/nyas.2017.1389.issue-1 )
                : 124-146
                Affiliations
                [ 1 ] Biology Department Queens College of the City University of New York, Queens, New York and The Graduate Center of the City University of New York New York New York
                Author notes
                [*] [* ]Address for correspondence: John J. Dennehy, Biology Department, Queens College of the City University of New York, 65‐30 Kissena Blvd., Queens, NY 11367. john.dennehy@ 123456qc.cuny.edu
                Article
                NYAS13304
                10.1111/nyas.13304
                7167663
                28036113
                c3ee5416-2ae0-428b-887c-d5f17b74fe61
                © 2016 New York Academy of Sciences.

                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
                : 08 June 2016
                : 24 October 2016
                : 09 November 2016
                Page count
                Figures: 5, Tables: 1, Pages: 23, Words: 14851
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                February 2017
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.0 mode:remove_FC converted:15.04.2020

                Uncategorized
                host range expansion,host shift,virus evolution,virus ecology,emerging infectious diseases

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