bioshock.bib

@incollection{childs2004zoonotic,
  title={Zoonotic viruses of wildlife: hither from yon},
  author={Childs, JE},
  booktitle={Emergence and Control of Zoonotic Viral Encephalitides},
  pages={1--11},
  year={2004},
  publisher={Springer}
}
@article{rulli2017nexus,
  title={The nexus between forest fragmentation in Africa and Ebola virus disease outbreaks},
  author={Rulli, Maria Cristina and Santini, Monia and Hayman, David TS and D’Odorico, Paolo},
  journal={Scientific reports},
  volume={7},
  pages={41613},
  year={2017},
  publisher={Nature Publishing Group}
}
@article{chua2002anthropogenic,
  title={Anthropogenic deforestation, El Niiio and the emergence of Nipah virus in Malaysia},
  author={Chua, Kaw Bing and Chua, Beng Hui and Wang, Chew Wen},
  journal={Malaysian Journal of Pathology},
  volume={24},
  number={1},
  pages={15--21},
  year={2002},
  publisher={Academic of Medicine Malaysia. College of Pathology}
}
@article{fair2019viral,
  title={Viral Forecasting, Pathogen Cataloging, and Disease Ecosystem Mapping: Measuring Returns on Investments},
  author={Fair, Jeanne and Fair, Joseph},
  year={2019},
  publisher={Springer}
}

\@techreport{hannenhalli1995transforming,
  title={Transforming cabbage into turnip.(polynomial algorithm for sorting signed permutations by reversals). Dept. of Computer Science and Engineering, Penn State University},
  author={Hannenhalli, S and Pevzner, PA},
  year={1995},
  institution={Technical Report CSE-95-004}
}
@article{jean2007genome,
  title={Genome rearrangements: a correct algorithm for optimal capping},
  author={Jean, G{\'e}raldine and Nikolski, Macha},
  journal={Information Processing Letters},
  volume={104},
  number={1},
  pages={14--20},
  year={2007},
  publisher={Elsevier}
}
@article{ozery2003two,
  title={Two notes on genome rearrangement},
  author={Ozery-Flato, Michal and Shamir, Ron},
  journal={Journal of Bioinformatics and Computational Biology},
  volume={1},
  number={01},
  pages={71--94},
  year={2003},
  publisher={World Scientific}
}
@article{tesler2002efficient,
  title={Efficient algorithms for multichromosomal genome rearrangements},
  author={Tesler, Glenn},
  journal={Journal of Computer and System Sciences},
  volume={65},
  number={3},
  pages={587--609},
  year={2002},
  publisher={Elsevier}
}
@article{shao2012approximating,
  title={Approximating the edit distance for genomes with duplicate genes under DCJ, insertion and deletion},
  author={Shao, Mingfu and Lin, Yu},
  journal={BMC bioinformatics},
  volume={13},
  number={19},
  pages={S13},
  year={2012},
  publisher={BioMed Central}
}
@ARTICLE{Hothorn06unbiasedrecursive,
    author = {Torsten Hothorn and Kurt Hornik and Achim Zeileis},
    title = {Unbiased recursive partitioning: A conditional inference framework},
    journal = {JOURNAL OF COMPUTATIONAL AND GRAPHICAL STATISTICS},
    year = {2006},
    volume = {15},
    number = {3},
    pages = {651--674}
}
% 11516376 
@Article{pmid11516376,
   Author="Taylor, L. H.  and Latham, S. M.  and Woolhouse, M. E. ",
   Title="{{R}isk factors for human disease emergence}",
   Journal="Philos. Trans. R. Soc. Lond., B, Biol. Sci.",
   Year="2001",
   Volume="356",
   Number="1411",
   Pages="983--989",
   Month="Jul"
}
% 11516377 
@Article{pmid11516377,
   Author="Cleaveland, S.  and Laurenson, M. K.  and Taylor, L. H. ",
   Title="{{D}iseases of humans and their domestic mammals: pathogen characteristics, host range and the risk of emergence}",
   Journal="Philos. Trans. R. Soc. Lond., B, Biol. Sci.",
   Year="2001",
   Volume="356",
   Number="1411",
   Pages="991--999",
   Month="Jul"
}
% 19787654 
@Article{pmid19787654,
   Author="Childs, J. E.  and Gordon, E. R. ",
   Title="{{S}urveillance and control of zoonotic agents prior to disease detection in humans}",
   Journal="Mt. Sinai J. Med.",
   Year="2009",
   Volume="76",
   Number="5",
   Pages="421--428",
   Month="Oct"
}

% 16485465 
@Article{pmid16485465,
   Author="Wolfe, N. D.  and Daszak, P.  and Kilpatrick, A. M.  and Burke, D. S. ",
   Title="{{B}ushmeat hunting, deforestation, and prediction of zoonoses emergence}",
   Journal="Emerging Infect. Dis.",
   Year="2005",
   Volume="11",
   Number="12",
   Pages="1822--1827",
   Month="Dec"
}
% 17848060 
@Article{pmid17848060,
   Author="Holmes, E. C.  and Drummond, A. J. ",
   Title="{{T}he evolutionary genetics of viral emergence}",
   Journal="Curr. Top. Microbiol. Immunol.",
   Year="2007",
   Volume="315",
   Pages="51--66"
}
% 18772285 
@Article{pmid18772285,
   Author="Parrish, C. R.  and Holmes, E. C.  and Morens, D. M.  and Park, E. C.  and Burke, D. S.  and Calisher, C. H.  and Laughlin, C. A.  and Saif, L. J.  and Daszak, P. ",
   Title="{{C}ross-species virus transmission and the emergence of new epidemic diseases}",
   Journal="Microbiol. Mol. Biol. Rev.",
   Year="2008",
   Volume="72",
   Number="3",
   Pages="457--470",
   Month="Sep"
}
% 19281304 
@Article{pmid19281304,
   Author="Pulliam, J. R.  and Dushoff, J. ",
   Title="{{A}bility to replicate in the cytoplasm predicts zoonotic transmission of livestock viruses}",
   Journal="J. Infect. Dis.",
   Year="2009",
   Volume="199",
   Number="4",
   Pages="565--568",
   Month="Feb"
}
% 20938453 
@Article{pmid20938453,
   Author="Pepin, K. M.  and Lass, S.  and Pulliam, J. R.  and Read, A. F.  and Lloyd-Smith, J. O. ",
   Title="{{I}dentifying genetic markers of adaptation for surveillance of viral host jumps}",
   Journal="Nat. Rev. Microbiol.",
   Year="2010",
   Volume="8",
   Number="11",
   Pages="802--813",
   Month="Nov"
}

@article{Doms1986,
abstract = {Hemagglutinin (HA), a trimeric spike glycoprotein of influenza virus, mediates fusion between the viral envelope and the membrane of an endosome during virus entry. Fusion is triggered by low pH, which induces an irreversible conformational change in the protein. Several studies have indicated that intersubunit contacts along the trimer interfaces may be broken during this alteration. To determine whether HA dissociates into individual subunits as a consequence of the conformational change, we used velocity gradient sedimentation in the presence of Triton X-100. We also determined the resistance of acid-treated HA to dissociation by sodium dodecyl sulfate, a property of the HA trimer. At pH 7.0, isolated HA sedimented as a 9S trimer and gave the characteristic trimer pattern after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. After acidification the HA remained trimeric irrespective of whether it was exposed to acid in intact virus particles or in solubilized form. Only when very low concentrations of HA were acidified did a fraction dissociate to dimers and monomers. In contrast, the water-soluble ectodomain fragment of HA (BHA) readily dissociated under a variety of conditions. Negative-stain electron microscopy supported the notion that HA molecules in virus particles do not dissociate upon acidification and may form larger oligomeric structures in the plane of the viral membrane. Taken together, the results suggested that it is the trimeric HA, or higher-order structures thereof, that are active in the acid-induced fusion reaction. Further, the results emphasized the role of the transmembrane anchors of HA in preventing dissociation of the trimer.},
author = {Doms, R W and Helenius, a},
file = {:home/ishanu/Documents/Mendeley Desktop/Doms, Helenius/JOURNAL OF VIROLOGY/Doms, Helenius - 1986 - Quaternary Structure of Influenza Virus Hemagglutinin after Acid Treatment.pdf:pdf},
issn = {0022-538X},
journal = {Journal of virology},
number = {3},
pages = {833--839},
pmid = {3783818},
title = {{Quaternary structure of influenza virus hemagglutinin after acid treatment.}},
volume = {60},
year = {1986}
}
@article{Yoon2015,
abstract = {The virologic factors that limit the transmission of swine influenza viruses between humans are unresolved. While it has been shown that acquisition of the neuraminidase (NA) and matrix (M) gene segments from a Eurasian-lineage swine virus was required for airborne transmission of the 2009 pandemic H1N1 virus (H1N1pdm09), we show here that an arginine to lysine change in the hemagglutinin (HA) was also necessary. This change at position 149 was distal to the receptor binding site but affected virus-receptor affinity and HA dynamics, allowing the virus to replicate more efficiently in nasal turbinate epithelium and subsequently transmit between ferrets. Receptor affinity should be considered as a factor limiting swine virus spread in humans.},
author = {Yoon, S W and Chen, N and Ducatez, M F and McBride, R and Barman, S and Fabrizio, T P and Webster, R G and Haliloglu, T and Paulson, J C and Russell, C J and Hertz, T and Ben-Tal, N and Webby, R J},
doi = {10.1038/srep12828},
file = {:home/ishanu/Documents/Mendeley Desktop/Yoon et al/Nature Publishing Group/Yoon et al. - 2015 - Changes to the dynamic nature of hemagglutinin and the emergence of the 2009 pandemic H1N1 influenza virus.pdf:pdf},
isbn = {2045-2322},
issn = {2045-2322},
journal = {Sci Rep},
pages = {12828},
pmid = {26269288},
title = {{Changes to the dynamic nature of hemagglutinin and the emergence of the 2009 pandemic H1N1 influenza virus}},
volume = {5},
year = {2015}
}
@article{Doms1986a,
abstract = {Hemagglutinin (HA), a trimeric spike glycoprotein of influenza virus, mediates fusion between the viral envelope and the membrane of an endosome during virus entry. Fusion is triggered by low pH, which induces an irreversible conformational change in the protein. Several studies have indicated that intersubunit contacts along the trimer interfaces may be broken during this alteration. To determine whether HA dissociates into individual subunits as a consequence of the conformational change, we used velocity gradient sedimentation in the presence of Triton X-100. We also determined the resistance of acid-treated HA to dissociation by sodium dodecyl sulfate, a property of the HA trimer. At pH 7.0, isolated HA sedimented as a 9S trimer and gave the characteristic trimer pattern after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. After acidification the HA remained trimeric irrespective of whether it was exposed to acid in intact virus particles or in solubilized form. Only when very low concentrations of HA were acidified did a fraction dissociate to dimers and monomers. In contrast, the water-soluble ectodomain fragment of HA (BHA) readily dissociated under a variety of conditions. Negative-stain electron microscopy supported the notion that HA molecules in virus particles do not dissociate upon acidification and may form larger oligomeric structures in the plane of the viral membrane. Taken together, the results suggested that it is the trimeric HA, or higher-order structures thereof, that are active in the acid-induced fusion reaction. Further, the results emphasized the role of the transmembrane anchors of HA in preventing dissociation of the trimer.},
author = {Doms, R W and Helenius, a},
file = {:home/ishanu/Documents/Mendeley Desktop/Doms, Helenius/Journal of virology/Doms, Helenius - 1986 - Quaternary structure of influenza virus hemagglutinin after acid treatment.pdf:pdf},
issn = {0022-538X},
journal = {Journal of virology},
month = {dec},
number = {3},
pages = {833--839},
pmid = {3783818},
publisher = {American Society for Microbiology},
title = {{Quaternary structure of influenza virus hemagglutinin after acid treatment.}},
volume = {60},
year = {1986}
}
@article{Hill2015,
abstract = {The scientific understanding of the driving factors behind zoonotic and pandemic influenzas is hampered by complex interactions between viruses, animal hosts and humans. This complexity makes identifying influenza viruses of high zoonotic or pandemic risk, before they emerge from animal populations, extremely difficult and uncertain. As a first step towards assessing zoonotic risk of influenza, we demonstrate a risk assessment framework to assess the relative likelihood of influenza A viruses, circulating in animal populations, making the species jump into humans. The intention is that such a risk assessment framework could assist decision-makers to compare multiple influenza viruses for zoonotic potential and hence to develop appropriate strain-specific control measures. It also provides a first step towards showing proof of principle for an eventual pandemic risk model. We show that the spatial and temporal epidemiology is as important in assessing the risk of an influenza A species jump as understanding the innate molecular capability of the virus. We also demonstrate data deficiencies that need to be addressed in order to consistently combine both epidemiological and molecular virology data into a risk assessment framework.},
author = {Hill, A A and Dew{\'{e}}, T and Kosmider, R and {Von Dobschuetz}, S and Munoz, O and Hanna, A and Fusaro, A and {De Nardi}, M and Howard, W and Stevens, K and Kelly, L and Havelaar, A and St{\"{a}}rk, K},
doi = {10.1098/rsos.150173},
file = {:home/ishanu/Documents/Mendeley Desktop/Hill et al/Royal Society open science/Hill et al. - 2015 - Modelling the species jump towards assessing the risk of human infection from novel avian influenzas.pdf:pdf},
issn = {2054-5703},
journal = {Royal Society open science},
keywords = {avian influenza,risk assessment,zoonoses},
month = {sep},
number = {9},
pages = {150173},
pmid = {26473042},
publisher = {The Royal Society},
title = {{Modelling the species jump: towards assessing the risk of human infection from novel avian influenzas.}},
volume = {2},
year = {2015}
}
@article{Flanagan2012,
abstract = {Zoonotic disease surveillance is typically triggered after animal pathogens have already infected humans. Are there ways to identify high-risk viruses before they emerge in humans? If so, then how and where can identifications be made and by what methods? These were the fundamental questions driving a workshop to examine the future of predictive surveillance for viruses that might jump from animals to infect humans. Virologists, ecologists and computational biologists from academia, federal government and non-governmental organizations discussed opportunities as well as obstacles to the prediction of species jumps using genetic and ecological data from viruses and their hosts, vectors and reservoirs. This workshop marked an important first step towards envisioning both scientific and organizational frameworks for this future capability. Canine parvoviruses as well as seasonal H3N2 and pandemic H1N1 influenza viruses are discussed as exemplars that suggest what to look for in anticipating species jumps. To answer the question of where to look, prospects for discovering emerging viruses among wildlife, bats, rodents, arthropod vectors and occupationally exposed humans are discussed. Finally, opportunities and obstacles are identified and accompanied by suggestions for how to look for species jumps. Taken together, these findings constitute the beginnings of a conceptual framework for achieving a virus surveillance capability that could predict future species jumps.},
archivePrefix = {arXiv},
arxivId = {15334406},
author = {Flanagan, M. L. and Parrish, C. R. and Cobey, S. and Glass, G. E. and Bush, R. M. and Leighton, T. J.},
doi = {10.1111/j.1863-2378.2011.01439.x},
eprint = {15334406},
file = {:home/ishanu/Documents/Mendeley Desktop/Flanagan et al/Zoonoses Public Health/Flanagan et al. - 2012 - Anticipating the Species Jump Surveillance for Emerging Viral Threats HHS Public Access.pdf:pdf},
isbn = {1863-2378 (Electronic) 1863-1959 (Linking)},
issn = {18631959},
journal = {Zoonoses and Public Health},
keywords = {Disease reservoirs/virology,Host-pathogen interactions,Infectious disease surveillance,Predictive virus surveillance,Science policy/biology,Species jump},
number = {3},
pages = {155--163},
pmid = {21914152},
title = {{Anticipating the Species Jump: Surveillance for Emerging Viral Threats}},
volume = {59},
year = {2012}
}
@article{Brierley,
abstract = {Emerging infectious diseases (EIDs), particularly zoonoses, represent a significant threat to global health. Emergence is often driven by anthropogenic activity (e.g., travel, land use change). Although disease emergence frameworks suggest multiple steps from initial zoonotic transmission to human-to-human spread, there have been few attempts to empirically model specific steps. We create a process-based framework to separate out components of individual emergence steps. We focus on early emergence and expand the first step, zoonotic transmission, into processes of generation of pathogen richness, transmission opportunity, and establishment, each with its own hypothesized drivers. Using this structure, we build a spatial empirical model of these drivers, taking bat viruses shared with humans as a case study. We show that drivers of both viral richness (host diversity and climatic variability) and transmission opportunity (human population density, bushmeat hunting, and livestock production) are associated with virus sharing between humans and bats. We also show spatial heterogeneity between the global patterns of these two processes, suggesting that high-priority locations for pathogen discovery and surveillance in wildlife may not necessarily coincide with those for public health intervention. Finally, we offer direction for future studies of zoonotic EIDs by highlighting the importance of the processes underlying their emergence.},
author = {Brierley, Liam and Vonhof, Maarten J. and Olival, Kevin J. and Daszak, Peter and Jones, Kate E.},
doi = {10.1086/684391},
file = {:home/ishanu/Documents/Mendeley Desktop/Brierley et al/Unknown/Brierley et al. - Unknown - Quantifying Global Drivers of Zoonotic Bat Viruses A Process-Based Perspective.pdf:pdf},
isbn = {0003-0147},
issn = {0003-0147},
journal = {The American Naturalist},
keywords = {bats,emerging infectious diseases,hotspots,land use,viral richness,zoonoses},
number = {2},
pages = {E53--E64},
pmid = {26807755},
title = {{Quantifying Global Drivers of Zoonotic Bat Viruses: A Process-Based Perspective}},
volume = {187},
year = {2016}
}
@article{Olival2017,
abstract = {The majority of human emerging infectious diseases are zoonotic, with viruses that originate in wild mammals of particular concern (for example, HIV, Ebola and SARS). Understanding patterns of viral diversity in wildlife and determinants of successful cross-species transmission, or spillover, are therefore key goals for pandemic surveillance programs. However, few analytical tools exist to identify which host species are likely to harbour the next human virus, or which viruses can cross species boundaries. Here we conduct a comprehensive analysis of mammalian host–virus relationships and show that both the total number of viruses that infect a given species and the proportion likely to be zoonotic are predictable. After controlling for research effort, the proportion of zoonotic viruses per species is predicted by phylogenetic relatedness to humans, host taxonomy and human population within a species range—which may reflect human–wildlife contact. We demonstrate that bats harbour a significantly higher proportion of zoonotic viruses than all other mammalian orders. We also identify the taxa and geographic regions with the largest estimated number of 'missing viruses' and 'missing zoonoses' and therefore of highest value for future surveillance. We then show that phylogenetic host breadth and other viral traits are significant predictors of zoonotic potential, providing a novel framework to assess if a newly discovered mammalian virus could infect people.},
author = {Olival, Kevin J. and Hosseini, Parviez R. and Zambrana-Torrelio, Carlos and Ross, Noam and Bogich, Tiffany L. and Daszak, Peter},
doi = {10.1038/nature22975},
file = {:home/ishanu/Documents/Mendeley Desktop/Olival et al/Unknown/Olival et al. - 2017 - Host and viral traits predict zoonotic spillover from mammals.pdf:pdf},
isbn = {0028-0836},
issn = {0028-0836},
journal = {Nature},
number = {7660},
pages = {646--650},
pmid = {28636590},
title = {{Host and viral traits predict zoonotic spillover from mammals}},
volume = {546},
year = {2017}
}
@misc{Joseph2017,
abstract = {Since 2013, there have been several alarming influenza-related events; the spread of highly pathogenic avian influenza H5 viruses into North America, the detection of H10N8 and H5N6 zoonotic infections, the ongoing H7N9 infections in China and the continued zoonosis of H5N1 viruses in parts of Asia and the Middle East. The risk of a new influenza pandemic increases with the repeated interspecies transmission events that facilitate reassortment between animal influenza strains; thus, it is of utmost importance to understand the factors involved that promote or become a barrier to cross-species transmission of Influenza A viruses (IAVs). Here, we provide an overview of the ecology and evolutionary adaptations of IAVs, with a focus on a review of the molecular factors that enable interspecies transmission of the various virus gene segments.},
author = {Joseph, Udayan and Su, Yvonne C.F. and Vijaykrishna, Dhanasekaran and Smith, Gavin J.D.},
booktitle = {Influenza and other Respiratory Viruses},
doi = {10.1111/irv.12412},
file = {:home/ishanu/Documents/Mendeley Desktop/Unknown/Unknown/Unknown - 2016 - The ecology and adaptive evolution of influenza A interspecies transmission.pdf:pdf},
isbn = {1750-2659 (Electronic)
1750-2640 (Linking)},
issn = {17502659},
keywords = {adaptation,pandemic,zoonotic},
mendeley-groups = {bioshock},
pmid = {27426214},
title = {{The ecology and adaptive evolution of influenza A interspecies transmission}},
year = {2017}
}

@misc{WHO,
  author = {World Health Organization (WHO)},
  title = {{Avian and other zoonotic influenza}},
  howpublished = "\url{http://www.who.int/influenza/human_animal_interface/2017_10_30_tableH5N1.pdf?ua=1}",
  year = {2017}
  }
@misc{IRD,
  author = {NIH},
  title = {{Influenza Research Database (IRD)}},
  howpublished = "\url{https://www.ncbi.nlm.nih.gov/genomes/FLU/Database/}",
  year = {2017}
  }