Phylogenetic Analysis One approach to resolving the question of human-to-human transmission is analysis of nucleotide sequence data, sometimes referred to as forensic phylogenetics. Figure 4. Conclusions Our survey of the capacity of RNA and DNA virus infections to be transmitted, directly or indirectly, between humans leads to several conclusions and practical suggestions for improving surveillance of emerging infectious diseases and targeting efforts to identify future public health threats.
Technical Appendix: Literature search protocol used to obtain information on pyramid level for assessing the epidemic potential of RNA and DNA viruses. Click here to view. References 1. Risk factors for human disease emergence. Global trends in emerging infectious diseases. Prediction and prevention of the next pandemic zoonosis. Virus taxonomy: ninth report of the International Committee on Taxonomy of Viruses.
Amsterdam: Elsevier; Emerging pathogens: the epidemiology and evolution of species jumps. Trends Ecol Evol. Infectious diseases of humans: dynamics and control. New York: Oxford University Press; Global mapping of infectious disease. Woolhouse ME. Population biology of emerging and re-emerging pathogens. Trends Microbiol. Origins of major human infectious diseases. RNA viruses: a case study of the biology of emerging infectious diseases.
Microbiol Spectr. Woolhouse ME, Adair K. The diversity of human RNA viruses. Future Virol. Host species barriers to influenza virus infections.
Phylogeny and geography predict pathogen community similarity in wild primates and humans. Proc Biol Sci. Cooper N, Nunn CL.
Evol Med Public Health. Brief report: infection of a laboratory worker with simian immunodeficiency virus. N Engl J Med. Cold Spring Harb Perspect Med. The basic reproductive number of Ebola and the effects of public health measures: the cases of Congo and Uganda.
J Theor Biol. Schwartz O, Albert ML. Biology and pathogenesis of chikungunya virus. Nat Rev Microbiol. Zika virus in the Americas: yet another arbovirus threat. Inference of R 0 and transmission heterogeneity from the size distribution of stuttering chains. PLoS Comput Biol. Aggregation and distribution of strains in microparasites. How do pathogen evolution and host heterogeneity interact in disease emergence?
Measles outbreaks in a population with declining vaccine uptake. Woolhouse ME, Gaunt E. Ecological origins of novel human pathogens. Interhuman transmissibility of Middle East respiratory syndrome coronavirus: estimation of pandemic risk. The transmission potential of monkeypox virus in human populations. Int J Epidemiol. Centers for Disease Control and Prevention. Outbreaks chronology: Ebola virus disease [cited Feb 1]. Woolhouse M, Antia R. Emergence of new infectious diseases.
Evolution in health and disease. The quasispecies extremely heterogeneous nature of viral RNA genome populations: biological relevance—a review. Evolution and emergence of novel human infections. Spread, circulation, and evolution of the Middle East respiratory syndrome coronavirus. Genomic surveillance elucidates Ebola virus origin and transmission during the outbreak. Bayesian reconstruction of disease outbreaks by combining epidemiologic and genomic data. Phylodynamics of infectious disease epidemics.
Human infection with a novel avian-origin influenza A H7N9 virus. Europe PMC requires Javascript to function effectively. Recent Activity. Search life-sciences literature Over 39 million articles, preprints and more Search Advanced search. This website requires cookies, and the limited processing of your personal data in order to function.
By using the site you are agreeing to this as outlined in our privacy notice and cookie policy. Abstract Read article for free, via Unpaywall a legal, open copy of the full text. Domingo-Calap P ,. Affiliations All authors 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Based on their extremely high mutation rates, RNA viruses have been traditionally considered as the fastest evolving entities in nature.
However, recent work has revealed that, despite their greater replication fidelity, single-stranded ss DNA viruses can evolve fast in a similar way. Our results indicate that ssRNA phages evolve faster than ssDNA phages under strong selective pressure, and that their extremely high mutation rates appear to be optimal for this kind of scenario. However, their performance becomes similar to that of ssDNA phages over the longer term or when the population is moderately well-adapted.
Interestingly, the roughly fold difference between the mutation rates of ssRNA and ssDNA phages yields less than a fivefold difference in adaptation and nucleotide substitution rates. The results are therefore consistent with the observation that, despite their lower mutation rates, ssDNA viruses can sometimes match the evolvability of RNA viruses.
References Articles referenced by this article 40 The pleiotropic cost of host-specialization in Tobacco etch potyvirus. Exceptional convergent evolution in a virus. Genome properties and the limits of adaptation in bacteriophages. Distribution of fitness and virulence effects caused by single-nucleotide substitutions in Tobacco Etch virus.
Evolutionary reversals during viral adaptation to alternating hosts. Molecular basis of adaptive convergence in experimental populations of RNA viruses. Point mutation rate of bacteriophage PhiX Parallel molecular evolution of deletions and nonsense mutations in bacteriophage T7.
On the other hand, RNA virus proteins cannot exhibit such homologies with their eukaryotic counterparts, but still can communicate with host cells through complex networks of PHIs. RNA viruses have probably evolved a different strategy, i.
Consequently, it can be stated that, DNA and RNA viruses have developed some distinct infection strategies to cause generally chronic and acute infections, respectively. Nevertheless, the aforementioned systems view of viral infection mechanisms through PHIs is still lacking 2 , The general focus of computational analysis of PHI data is on the common and specific behaviors of bacterial and viral pathogens during infections, by comparing their protein interactions with human 3 , Pichlmair et al.
However the results drawn from this analysis should be interpreted with caution since PHI data for lots of virus families are still scarce. Pathogen—host interaction search tool phisto was developed by our group due to the lack of a comprehensive PHI database in the Web Ongoing studies on phisto are for covering experimental PHI data belonging also to other mammalian species as host organism.
Retroviruses were excluded from the RNA families since they replicate through reverse transcription. Similarly, Hepadnaviruses were excluded from the DNA viruses. Virus—human PHI networks obtained from phisto. Red nodes are viral proteins and blue nodes are human proteins.
A Human herpesvirus 4 Epstein—Barr virus — human protein—protein interaction network. On the other hand, to obtain the common infection strategies of viral pathogens, sets of human proteins targeted by all viruses, i.
The significance level was set to 0. In the enrichment process, kobas platform uses hypergeometric test and Benjamini and Hochberg correction method. The visualization of virus—human networks Fig. In a PHI network, few proteins may serve as hub nodes. These are human proteins targeted by lots of pathogen proteins; and pathogen proteins targeting lots of human proteins. On the other hand, in RNA viruses, very few viral proteins have roles in PHI networks because of their very small genomes.
All of these RNA virus proteins usually have lots of interactions with human proteins Fig. In fact, the degree distribution of the virus—human protein interaction networks could not be fitted to any model yet, mostly because of their incompleteness 21 , despite some preliminary attempts to model the graph properties of PHI networks A considerable amount of human proteins are targeted by both DNA and RNA viruses, constituting the common viral targets.
Human proteins that are highly targeted by viruses, i. The list includes 21 such human proteins with corresponding targeting viral families. All enriched GO process, function and component terms for each human protein set are available in Data S4. Special attention should be given to the results of sets of human proteins interacting with only DNA virus proteins and only RNA virus proteins Table 5 to retrieve specific attack strategies of these two different virus types.
On the other hand, the results of human proteins interacting with both DNA and RNA viruses Table 7 are also important to highlight common infection mechanisms shared by the two types of viruses.
Enriched pathway terms for five specific human protein sets are listed in Tables 8 , 9 , 10 , presenting the certain characteristics of DNA and RNA viruses attack strategies. Most of the current antiviral therapeutics act for inhibiting specific viral proteins, e. Unfortunately, this approach has been ineffective because of drug resistance developed by viruses, especially in the case of RNA viruses which can mutate very rapidly. If these host factors are indispensable for pathogens, but not essential for host cells, their silencing may effectively inhibit infections without developing drug resistance rapidly 1 , 21 , Another alternative approach is to inhibit the interactions between these host factors and pathogen proteins, instead of targeting the proteins This study of computational analysis of virus—human interactomes aims to provide initial insights on the infection mechanisms of DNA and RNA viruses, comparatively, through the observation of the characteristics of human proteins interacting with viral proteins.
As the main viral infection strategy, all viruses manipulate cellular processes to proliferate within the host. Therefore, viral proteins highly interact with human proteins functioning in cell cycle, human transcription factors to promote viral genetic material transcription, nuclear membrane proteins for transporting viral genetic material across the nuclear membrane, and also regulatory proteins for translation and apoptosis 3 , 15 , 25 , We identified human proteins that are highly interacting with viral proteins, sequentially based on the total number of targeting virus families Table 4.
The list includes the top viral targets which interact with multiple viral families, within the most comprehensive PHI data. Some of these human proteins were previously reported as targets for multiple viruses, i. Specifically, they take role in the export of mRNA from the nucleus to the cytoplasm. Being targeted by multiple viruses, HNRPU was reported as a hotspot of viral infection, and proposed as a potential antiviral human protein 4. Moreover, our analyses also reflected that proteins functioning in transport and localization related processes within the cell are targeted highly by both DNA and RNA viruses, i.
Interacting with IMA1 enables viruses to enter the nucleus and consequently to use the host's transcriptional machinery. Figure 4. Phylogenetic trees for simulated emerging infectious disease outbreaks caused by RNA and DNA viruses in a mixed population of 1, human and 5, nonhuman hosts. Trees were constructed by using a We provide some example phylogenetic trees generated from simulated epidemics Figure 4.
In an epidemic in an animal reservoir with occasional transmission to humans Figure 4 , panel A , for each human sequence, the most closely related next sequence is of animal origin. Clusters of closely related human sequences are shown, and the distribution of the expected cluster sizes is a function of R 0 Figure 4 , panels B, C In an outbreak, it might be difficult to find and sample the putative source animal cases. However, estimating the time to most recent common ancestor TMRCA of the human cases will indicate how long the infection has been spreading.
For sporadic zoonoses Figure 4 , panel A , most transmission has occurred unobserved in the animal reservoir, and the TMRCA of pairs of human cases will be long because these sequences are not closely related. For outbreaks involving human-to-human transmission Figure 4 , panels B, C , the TMRCA of the cluster of human cases will be closer to the date of the first human infection whether sampled or not and provides the estimated date of the zoonotic event.
Use of sequence data to distinguish between multiple instances of human infection from a common animal source and human-to-human transmission in the early stages of an outbreak is extremely challenging because of short timescales, and involvement of few mutations. However, genetic differences and phylogenetic evidence show that at least 2 of the first 3 reported cases of influenza A H7N9 virus infection in humans were believed to originate from distinct domestic avian sources Similarly, detection of genetically distant lineages of MERS-CoV, which persisted for only a few months each, suggest multiple introductions from an animal reservoir and only limited human-to-human transmission to date In contrast, the influenza A H1N1 pandemic in and the EVD epidemic in West Africa in were believed to be the results of single zoonotic events, followed by sustained human-to-human transmission 33 , as shown by a single rapidly expanding lineage.
Our survey of the capacity of RNA and DNA virus infections to be transmitted, directly or indirectly, between humans leads to several conclusions and practical suggestions for improving surveillance of emerging infectious diseases and targeting efforts to identify future public health threats. In support of these conclusions, the World Health Organization recently published list of priority emerging infectious diseases and corresponding viruses 38 included 6 of the viruses in Table 2.
A major observation is that the taxonomic diversity of viruses that are possible threats to public health is wide, but bounded. Most human infective viruses are closely related to viruses of other mammals and some to viruses of birds. There are no indications that humans acquire new viruses from any other source.
However, diversification within human populations occurs and is a prominent feature of some DNA virus taxa e. In general, however, our knowledge of origins of human viruses is still incomplete.
Although the origins of HIV-1 have been extensively investigated 16 , for most other viruses, even level 4 viruses, little or no research has occurred. An origins initiative 9 would help establish the routes into human populations that have been used by other viruses. Transmissibility within human populations is a key determinant of epidemic potential. Many viruses that can infect humans are not capable of being transmitted by humans; most human transmissible viruses that emerge already have that capability at first human infection or acquire it relatively rapidly.
If transmission from humans would require a change in a phylogenetically conserved trait, such as tissue tropism or transmission route 4 , then such viral paradigm shifts will probably be extremely rare However, because changes in virus traits or host population characteristics can influence R 0 , level 3 viruses Table 2 are of special interest from a public health perspective, and of special concern when, like MERS-CoV, they also cause severe illness.
Demonstrating human transmissibility is often difficult, but essential. The best evidence is likely to come from virus genome sequencing studies. These studies should be a public health priority We currently have few clues to help us predict which mammalian or avian viruses might pose a threat to humans and, especially, which might be transmissible between humans.
One argument in favor of experimental studies of these traits, including controversial gain of function experiments 30 , is that they could help guide molecular surveillance for high-risk virus lineages in nonhuman reservoirs.
The first line of defense against emerging viruses is effective surveillance A better understanding of which kinds of viruses in which circumstances pose the greatest risk to human health would enable evidence-based targeting of surveillance efforts, which would reduce costs and increase probable effectiveness of this endeavor. His primary research interests are pathogen emergence and antimicrobial drug resistance.
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Table 1 Table 2. Article Metrics. Abstract Many new and emerging RNA and DNA viruses are zoonotic or have zoonotic origins in an animal reservoir that is usually mammalian and sometimes avian. Figure 1 Figure 1. Data and Analysis. Identifying and Characterizing Level 3 and 4 Viruses We updated our previous systematic literature review 10 of the capacity of virus species to transmit between humans i.
Level 1 to Levels 3 and 4 Virus species of mammalian and, more rarely, avian origin are sometimes observed to be transmissible between humans when first found in humans, which constitutes a jump from level 1 straight to level 3 or 4 Figure 1 , and events of this kind have been reported regularly. Level 2 to Levels 3 and 4 The possibility that level 2 viruses might acquire the capacity to be transmitted between humans i.
Level 3 to Level 4 Level 3 viruses can also become level 4 viruses. Epidemiologic Patterns The preceding sections illustrate that identifying transitions of viruses between level 2 and level 3 or between level 3 and level 4 is not always straightforward. Figure 2 Figure 2. Figure 3 Figure 3. Evolution Changes in pyramid level might be mediated by virus evolution or changes in virus ecology
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