How viruses shape the tree of life - Future Medicine

PERSPECTIVE

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How viruses shape the tree of life Luis P Villarreal University of California, Center for Virus Research, 3232 McGaugh Hall, Irvine, CA 92697, USA Tel.: +1 949 824 6074; Fax: +1 949 824 9437; [email protected]

Keywords: emergence, evolution, persistence, species specificity, virus evolution, virus–host co-evolution

Consideration of virus evolution only from a disease perspective has provided a limited view of virus–host evolution. Such views assume all viruses fit predator/prey models for replication, but fail to explain the origin of disease or how viruses might make significant contributions to host evolution. On a long evolutionary time scale, the ability of a virus to persist in an individual host is a much more prevalent life strategy. Persistence can explain both origins of most viral disease and virus–host evolutionary stability. However, persistence (both genomic and epigenomic) is a much more complex and demanding virus–host relationship that is difficult to study. We must change our attitudes towards persistence if we are to understand how viruses shape the tree of life.

Readers of virus evolution literature are most likely to be interested in understanding viral disease and its origins. How can we understand the seemingly endless reports of new or re-emerging viral threats to human and animal health? How do these agents evolve, where do they come from, and how does this affect host evolution? Serious disease demands serious attention, so we have focused our efforts to understand the relevant relationships. Progress has been good and, although Darwinian concepts clearly apply to viruses, additional concepts such as clonal generation of quasispecies and error catastrophe, have expanded our understanding of virus evolution and led us to believe that no virus genomes exist as a single nucleotide sequence as they spread rapidly into a mutant spectra. Population selection, population memory, mutant clouds, Shannon entropy and Hamming distance are all concepts that appear to be consistent with the experimental study of viral disease, especially to RNA and retroviruses, such as hepatitis C virus and HIV [1]. But how does this relate to the tree of life? A prevalent concept is that viruses are just an overlay to the tree, rapidly evolving and constantly exploring sequence space as they seek new hosts for replication and disease. Thus, viruses can be considered to resemble ‘mistletoe on the tree of life’, an epibiont, although sometimes harmful, that decorates the branches, but does not actually connect to them [2]. Such a perspective has long dominated virology and appears central to our current understanding of virus evolution. But is it correct? Such decoration is not a position of high respect, but more of a biological afterthought. However, it has been asserted that viruses belong as prominent elements on the tree of life [3]. Disease-based concepts do not explain the long-term

10.2217/17460794.1.5.587 © 2006 Future Medicine Ltd ISSN 1746-0794

evolution of viruses and their hosts; and thus, can we account for, or justify the inclusion of, viruses in the tree of life? I have argued that this disease perspective, crucial as it may be, does not properly or fully inform us concerning the relationship of viruses to the tree of life [4]. Nor does it explain why some viral threats persist whereas others do not. To determine this, we must understand a virus–host relationship that is not usually disease associated and has received much less experimental and theoretical attention: persistence. Persistence: putting the cart first

The central premise I am asserting is that, on an evolutionary time scale, persistence is the predominant successful life-strategy used by viruses. Acute replication and disease are much less conserved from the perspective of long-term evolution and are mainly employed to explore new host possibilities. Previously, persistence was defined as the ability of a virus to be maintained or induced by an individual host [5]. I suggest that such a relationship deserves much more attention and respect than it has previously received. Persistence is neither a trivial nor easily attained relationship [6]. A persisting virus is not simply a reservoir for acute disease; it is a central and successful life strategy. It requires a highly intimate coordination between the virus and the innate and adaptive immune systems of the host. It demands precise gene function, and hence, evolution of the persisting virus, and operates in most host population structures, often in coordination with host reproduction. This highly adapted state tends to be genetically stable, sometimes generating almost clonal virus populations that retain genetic stability on an evolutionary time scale. In general, the state is highly tissue and species Future Virol. (2006) 1(5), 587–595

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specific, and will have numerous gene functions that are especially adapted for such specificity. I will further suggest that it is precisely the maladaption or simplification of these highly tuned systems into new hosts and tissues that underlie most acute viral disease. Therefore, this essay is mainly an exercise in shifting a long-held perspective. We will examine virology, not from the usual disease eyepiece, but from the larger lens of persistence and evolution. I will briefly consider the view of basic virology, medical science, epidemiology and evolutionary biology from this lens. Let us give much more respect to the phylogenetic congruence of virus and host (orders), which is common for persistence (including genomic persistence). In this light, I think we will see that persistence is not simply an accident, but a vital force that overlays clear and bright clades of virus that color the entire tree of life. General definitions & issues

The word ‘virus’ originates from Latin and designated a poisonous liquid or slime. Although modern definitions no longer include reference to either liquid or poison, the negative connotations of that original meaning have endured. ‘Virus’ remains a negative concept associated mainly with harm to the host. Thus, it is natural that evolutionary biologists have accepted this concept and consider viral agents simply as toxic or lethal agents that can be modeled with the same differential equations originally designed to understand predator/prey relationships. The successful application of such models to viral epidemic disease appears to validate such a widely held view. But wait. How does this perspective connect with a flurry of more recent proposals, which have argued that viruses appear to have been directly involved in the origin of numerous basic and highly complex functions of life? This includes the possible viral role in the origin of DNA-based genomes and DNA replication systems [7–10], eukaryotic nucleus [4,11–14], interference RNA innate and adaptive immune system [15,16], mammalian placenta and viviparous birth [17–22]. Such proposals imply that viruses are the busy handmaidens to the Mother of life! How can such creative roles fit with the inherently destructive life cycle of a virus? Is there some basic conceptual flaw in such new and seemingly radical proposals [23]? The flaw is that of perspective. The idea that viruses can provide a basic and creative role in the evolution of host is neither new nor radical, but is in fact old and mostly forgotten. In 1959, while contemplating the role 588

viruses might have in the evolution of host, S Luria wrote ‘…may we not feel that in the virus, in their merging with the cellular genome and re-emerging from them, we observe the units and process which, in the course of evolution, have created the successful genetic patterns that underlie all living cells?’ [24]. This concept, although mostly ignored, was originally put forward by one of the most accomplished and farsighted of all virologists. S Luria can also be credited with providing us with the first modern definition of a virus [25]. In modern terminology, a virus is a molecular genetic parasite that is dependent on its host for reproduction and/or maintenance. That is it: no slime, poison or disease. This definition does not specify life strategy (lytic vs persistence). Nor does it specify the extracellular role or composition of a virus. It is an encompassing definition that includes persisting genomic viruses (e.g., prophage, once a highly contentious issue). However, I would amend Luria’s definition to now include satellite viruses and defective viruses, including those that do not make extracellular forms (e.g., in fungi) or code for any viral genes in order to accommodate their role in persistence. All these viral elements are now well accepted and studied by virologists. Also, all these elements are often used as strategically important elements in the context of persistence (e.g., prophage, satellites and defectives). In fact, this looser definition enables us to better define persistence. Persistence is the stable capacity of such viruses to colonize an individual host and be maintained or re-emerge at some later time. However, this is not easy or trivial, it requires a molecular intimacy that avoids elimination by innate and adaptive host immune systems. This usually involves highly adapted viral genes that manipulate these exact immune systems, and must also compete with existing acute and persisting viral agents. In the era of genomics, we now have the evidence required to evaluate many such ideas, but we lack the perspective. Two prevailing and overpowering views account for this: • Viruses are simply lytic agents (run-away replicators); • The concept of selfish DNA that appears to account for viral-like sequences found in all genomes. Viral persistence provides an alternative view. How, then, might persisting viruses contribute to the tree of life? Consider the following scenario. Evolution of a new host lineage will often Future Virol. (2006) 1(5)

How viruses shape the tree of life – PERSPECTIVE

be associated with the acquisition of complex, multigene adaptations that are characteristics that are often limited to that specific lineage. In the context of bacteria, we can easily envision the need for the host to acquire a set of interacting proteins required for a new, more complex habitat. For example, multiple drug resistances or colonization of a new host are complex traits. Colonization and persistence by a new prophage can indeed provide exactly such a new and complex host phenotype. However, bacteria are not eukaryotes, so surely this scenario does not apply in eukaryote examples. Consider the recently characterized mimivirus of protozoa [26]. With 1000 genes, mostly of unknown function, it has a surprising scale of genomic complexity for a virus [27,28], especially one that now appears to be abundant in the oceans [29], thereby suggesting a vast genetic potential. Although we do not fully understand the protozoan life strategy of this virus, consider the evolutionary consequence that would result from the stable colonization of its host. All these 1000 mimiviral genes would become available to Darwinian selection to promote host survival and evolution. This potential promotion of host survival is not limited to novel genes that the virus might bring to the host. For example, filamentous fungi are essentially all colonized by doublestranded RNA viruses of various types, many of which often encode toxins that affect host survival by competing with other RNA viruses [30]. This suggests that persisting viruses can positively affect host survival as a consequence of the colonizing virus, precluding competition from other, usually similar acute viruses. African monkeys support replication with their own versions of foamy virus and simian immunodefiency virus. We do not currently understand why their immune systems respond differently than those of humans to these viruses (e.g., glycoprotein) and why they do not progress to AIDS-like disease, but there is reason to believe that their endogeneous retroviruses might be involved. Humans differ from their chimpanzee relatives by colonization patterns of various human endogenous retroviurs-k (HERV-K) viruses. What has been the effect to human survival and evolution as a consequence of this viral colonization? Currently, koala bears are undergoing colonization by exogenous retrovirus. How will this affect this species? Although we cannot answer these questions at present, they do suggest that persisting viruses are often associated with the evolution of their host. www.futuremedicine.com

In fact, I will offer the following challenge to my colleagues in virology and evolutionary biology. I assert that essentially all major transitions in the evolution of life are associated with specific and often peculiar patterns of colonization by persisting genomic and extragenomic parasites (viruses). The branches in the tree of life are all virus colored, but these are mainly persisting viruses that have been invisible to us. Viral footprints are everywhere if we simply adapt this perspective and look for them. Figure 1 represents how viruses shape and color the tree of life and notes some peculiar virus–host relationships. Blue represents high levels of levels of exogenous virus activity, whereas yellow represents genomic or persisting virus activity. Note that virus activity is high at the origin of domains of life. The Last Universal Common Ancestor is proposed to have had a viral character. Virology perspective

The fact that virologists can define and observe persistence should not lead anyone to think that this enables us to easily understand or even identify persistence. In fact, I would assert that we generally misunderstand and disrespect the impressive intricacy and evolutionary stability of persistence, mainly because we observe it strictly from a disease perspective. For example, most molecular biologists and virologists would think of the main regulatory protein (T-Ag) of small DNA tumor viruses (polyomavirus) from the context of cell cycle disregulation and tumor induction, and many text books introduce this subject from exactly this perspective. We estimate that as many as 4 billion people are likely to be persistently infected with either CJ or BK human polyomavirus. However, essentially no persistently infected kidneys (a major site for virus production) will develop tumors. As Keith Gottlieb and I have published, polyomavirus early genes are mainly evolved to enable a highly specific and temporal biological strategy, replication through the lungs which results in kidney persistence, not tumor production or cell cycle disregulation [31]. Large and middle T-Ags are really proteins designed for kidney persistence, not tumor generation [32]. However, the basic importance of persistence has failed to adequately penetrate our collective consciousness or move consensus. We are so focused on lytic replication and disease that we fail to see that on an evolutionary time scale, persistence is the much more successful strategy for almost all viral lineages, RNA and DNA. 589


Figure 1. Virus color of the tree of life. Crenarchaeota Euryarchaeota

Nonlytic dsDNA viruses

Archea protoLUCA/virus

Korarchaeota Nanoarchaeota

dinoflagellates

Mycobacterium spp.

green algae

Other bacteria

Green plants (viridophytae)

Eukarya

conifers

Monocots

Cyanobacteria

Chromalveolates Radiolaria, cercozoa foraminifera

Simpler plants

Angiosperms

Opisthokonta

Amitochondriate excavates Discricristales

Plantae

Higher plants +ssRNA viruses red algae Amoebozoa dsRNA viruses Fungi Choanazoa

Animalia Metazoa

dsDNA phage

Ecdysozoa Bilateria

Anabaena spp. Bacteria

Insects dsDNA viruses nematodes

Lophotrochozoa

Firmicutes

Bacillus subtilis

Enchinodermata, hemichordata Deuterostomia Vertebrata

sharks Bony fish -ssRNA rhabdoviruses Chordata Reptiles Birds monotremes marsupials eutherians

Proteobacteria Escherichia coli

dsDNA: Double-stranded DNA; ssRNA: Single-stranded RNA. Reproduced with permission from [4], ASM Press, Washington DC, USA.

Virologists are compelled by the consensus-based funding systems of disease research to become more and more focused on mechanisms of disease and pathology. They must now propose to understand the 3D protein structure of disease mechanisms if they are to maintain their research. Gone is any support for natural virus studies, such as Wally Rowe once performed, to understand the realistic avirulent and persistent biology of a polyoma virus, let alone study the molecular basis of this state [33,34]. Medical scientists, epidemiologists and evolutionary biologists are simply following this same path made by us. Thus, the oversimplified and incorrect views that viruses are only runaway replicators, composed of stolen genes (as pickpockets [35]), and the products of reductive evolution prevail. Although it is clear that viruses can lift genes from their host, genomic analysis (especially DNA viruses) clearly indicates that the large majority of viral genes are novel viral creations and not from the host. 590

Many of my colleagues may scoff at my suggestion to study persistence. After all, viruses clearly cause disease, so why should we study situations in which they do not? What would be learned? In answering this, I would point out that most model systems of viral disease ignore the study of persistent relationships (species and tissues) that provide the origin of the very genes they study. In following a primary disease focus, researchers are assured of not understanding the evolutionary forces that initially created these very genes causing pathology. Pathology mainly focuses on how the virus–host relationship goes wrong in new, nonpersisting hosts (species jumps). Let us consider two prominent examples of this assertion with RNA viruses that pose a serious disease threat to humans. Hantavirus pathology has received much attention since it was recognized as a human pathogen, and the molecular basis of this pathogenesis is intensely studied. However, we know that the virus persists in stable avirulent states in various Future Virol. (2006) 1(5)


species (but unknown tissue) of the three murid clades of rodents [36,37]. What do we know about the molecular biology of these same genes regarding natural persistence? Very little, although studies with one of the simplest RNA viruses (Borna) are starting to yield some information [38,39]. Another situation that has received worldwide attention and enormous press is pathogenic avian influenza. There is intense study of the avian influenza (H5N1), which appears to spontaneously emerge, adapt to humans and induce a lethal human disease (via a strong cytokine response that resembles severe acute respiratory syndrome [SARS] pathology). Avian influenza poses a serious pandemic threat. However, what do we know about how these viral genes persist or affect cytokines in their natural and avirulent host? Although H5N1 persists in, and can be isolated from, free-grazing ducks, which are considered (albeit with little evidence) to be the source of epidemic outbreaks [40,41], nothing is known regarding viral gene function in these avirulent states, let alone how they might interact at the 3D level (as grant reviewers are likely to ask). The high prevalence of influenza A in European ducks does support the idea of a persistent life strategy [42]. But even when we are sure of the persisting host and tissue (which is not often the case), we do not usually know anything regarding the molecular basis of persistence. Other emerging viral agents (Marburg virus, Ebola virus and Monkeypox) are also known to persist in specific host that can maintain a genetically stable (almost clonal) version of the virus, thereby implying strong but unknown selection on viral gene sequence and function. A quick search of PubMed® on any of these topics will confirm our general ignorance of the basis of persistence. Medical perspective

Medical science must focus on disease; however, this focus has sometimes led to strange and even distorted views concerning viruses and host evolutionary relationships. Concepts such as pathogenic fitness, or the belief that acute viral evolution will eventually result in stable persistence, have often been promoted. I have tired of correcting seminar speakers on this topic. However, long-established, human-specific viruses (e.g., measles and smallpox) never establish authentic persistence and thus can be eliminated by vaccination. Persistence would prevent such elimination. Virus evolution in medicine is almost exclusively considered from the perspective of acute disease. Hence, there is an endless www.futuremedicine.com

fascination with the genetic drift, instability and extinction of influenza hemaglutinin and neuroaminidase proteins while equal genetic stability in natural habitats of water-fowl sources is rarely mentioned. Regulatory genes of many persisting DNA and retroviruses are classified and considered only as oncogenes designed for runaway acute replicators. Cervical oncogenesis by human papillomavirus is one such major topic, but why cancer is an unusual biological outcome of these persistent infections, or why humans harbor 100 phylogenetically stable versions of human papillomavirus, is seldom considered. Retroviruses occupy much attention in medical education and research, but persistence is not a significant part of that attention. For example, it is not likely that most medical scientists will be very concerned with human endogenous retroviruses, unless it is to worry that these agents might induce some disease (such as autoimmune disease or transplanting pig tissues and porcine endogenous retroviruses). The phylogenetic congruence of these endogenous agents and their host, including primates, or their role in the evolution of vivipary, for example, will likely receive only a passing mention at best, and will not be used as an example of virus–host evolution that is highly intertwined or fundamental. Unless a virus causes a disease, it will not likely warrant much attention from the medical community. Epidemiology perspective

Epidemiology is also necessarily focused on disease transmission in human and animal populations. The basal models of transmission and disease focus only on acute transmission as measured by the net reproductive output or viable offspring per individual per lifetime (R0). The models have worked well in many epidemic situations, but the resulting faith in these mathematical models is sometimes curious to behold. For example, R0 approaches a mythical standard whose predictive value is often unquestioned. The real and sometimes chaotic nature of R0 in actual epidemics (such as the crucial initial role of super-spreaders for HIV and SARS [43]) does not appear to shake this arithmetic faith. As the R0 of a super-spreader is likely the result of other agents (such as HIV infection itself ) whose occurrence is not necessarily statistically predictable, R0 itself appears to be a variable. However, the models are more fundamentally problematic in that they do not really consider the origins of epidemics. For example, the recent outbreak of poliovirus in an American–Amish colony clearly appears to have been due to the 591


establishment of a persistent inapparent infection in an immunocompromised individual. This persistent situation resides outside of these mathematical premises since its establishment itself is not predictable. This identifies a general need to address the persistent source of most new epidemics. However, the occurrence of persistence, especially its temporal stability and biological conditionality, will violate the mathematical assumptions of all current epidemic models. Therefore, prediction of, for example, the probability that the Reston Ebola virus versus a Zaire/Sudan isolate (Ebola with similar genomes [44]), will develop into a human (not monkey) epidemic is not now possible. These Ebola isolates derive from different persistent sources, but we do not understand the relationship between these persisting reservoirs and human versus monkey disease. It is not even theoretically clear that this could be modeled given our current lack of knowledge regarding persistence. Another basic problem of epidemiological models also exists. Persistent states and their corresponding host species are treated simply as reservoirs whose biological and genetic parameters are considered to be equivalent to that of the acute replication in a new host. Given that persistence and acute viruses have vastly different genetic, population and reproduction parameters, the historic model is clearly oversimplified to the point of being misleading. Evolution perspective

Evolutionary biology has also considered viruses simply as agents of disease. The very same basic concepts used by epidemiology (predator/prey relationships, replicative fitness and no temporal component to relative fitness) have also limited the viral perspective in evolutionary biology. In addition, another concept, that of selfish DNA, has provided a seemingly satisfactory explanation for the widespread occurrence of parasitic genetic elements in the germlines of so many organisms. Persisting viruses, both genomic and epigenomic, are mostly ignored. However, defective versions of viruses are numerous in genomes. The selfish DNA concept has been used to account for these elements, but it fails to explain why all lineages of life have their own peculiar patterns of parasite acquisition, which is also associated with the origins of all lineages. The selfish DNA concept has accounted for many sequence data, but explains little of this biology. In this perspective, persistence has no role, viruses are simply trucks or thieves that horizontally transfer genetic material 592

from one cellular lineage to the other. Nevermind that viral lineages have clearly invented many exceedingly complex and virus-specific genes and gene sets (e.g., mimivirus or Simian virus 40 T-Ag). The vast viral genetic adaptability, diversity, creativity and ability to superimpose persisting viral identity onto the host have essentially been dismissed as a force in evolution. Viruses kill hosts, they do not colonize them. They are not symbiotic. Transposons (essentially persisting defective viruses and parasites of viruses) are considered to be somehow distinct from persisting viral genetic parasites. Persistence of genetic parasites is almost never mentioned as a significant issue that is relevant to evolutionary biology. However, all genomes can be considered as a complex mix of hyperparasites, including full viral elements, defectives and satellite-like elements. If we define these as inherently viral and persisting, we might be able to understand why a peculiar set of genetic parasites is acquired when species first diverge. From bacteria to human, this species-specific pattern of colonization remains. Similarly, all mammals have their own peculiar, but distinct, version of endogenous retroviruses. How then are we to understand the chromoviruses in lower eukaryotes, or Cer elements in Caenorhabditis elegans, or HERV-L in all placentals, or HERV-K in African primates? Are they simply examples of lineage-specific viral junk, elements that we can simply ignore as being of no consequence to evolution? Researchers who study long interspersed elements also think of them as being distinct from viruses. But I would argue that even they seem clearly viral derived (e.g., from chromoviruses and Cer elements) at their origins. We can continue to use the mantra that selfish DNA produces all the genomic junk; however, evolutionary biology should note that, of all the fields of biology, virology (the first field to introduce the study of genomic evolution) is really the most practical application of evolutionary principles because we can observe real-time evolution during the progression of an individual’s viral disease (i.e., HIV and hepatitis C). It is curious then, that the evolutionarily stable, nondisease, persisting virus–host relationships are mostly ignored by evolutionary biology. General implications

Obviously, we must continue to study and prevent viral disease. However, this should not preclude the study of persistence or result in its Future Virol. (2006) 1(5)


dismissal from consideration in host evolution. Persistence is a very difficult problem, worthy of study, funding and respect (although I doubt it will receive much more attention anytime soon). Persistence should merit more attention from the scientific community, and should not be relegated to the status of a less efficient acute viral infection that is currently the common viewpoint, especially among nonvirologists. However, the process of persistence is inherently inscrutable, tends to be silent and is normally under selection to maintain that silence until appropriate biological cues are encountered. Persistence has many features that are poorly understood. It tends to operate in highly specific situations that have precise biological controls and do not lend themselves to cell culture or biochemical studies, let alone structural analysis. Consider human herpes simplex virus (HSV), one of the most intensely studied models of viral persistence. HSV takes up life-long residence in a specific human site (trigeminal ganglion). Although much progress has been made in the last two decades, the exact mechanisms of persistence or reactivation are still unknown, such as the specific role latency-associated transcript in gene silencing and neuroprotection. HSV is only one of eight families of prevalent human-specific herpes virus, and all appear to have their own specific tissues and mechanism of persistence, despite the fact that they are all related to each other, genetically stable and mostly phylogenetically congruent with their host. When the tree of life is considered from the perspective of the viruses that persist on it, we see a very clear overlay of viruses and the tree. For example, humans and their close relatives, chimpanzees, like most mammals, differ in their corresponding herpes viruses, papillomaviruses and endogenous retroviruses. The perspective of persistence informs us about the demarcations in the tree and provides color to

all large and small clades of the tree of life. For example, collecting the CJ human polyoma virus excreted in the urine of persistently infected humans would be informative about the likely racial and geographical origin of the person. Persistent viruses present a fractal pattern in that no matter how close or far your gaze, genomic and epigenomic viruses will differentiate the host members. Viruses belong on and help shape the tree of life. They are clearly handmaidens to the Mother of life, and remain the most abundant life form on the planet. They are, in a very direct sense, our ancestors, and merit our respect. Conclusions

Viruses very much belong on the tree of life, but it is the persisting viruses that prevail on an evolutionary time scale and have had the biggest impact on the tree. Although acute disease has necessarily occupied the study of viruses, it is now time to understand viral persistence. Persisting viruses, including those found in genomes, are central agents that continue to determine the shape of the tree and diversity of all life. Future perspective

The era of genomics has established that viruses and other genetic parasites are the main biological entities on the planet. With the development of genomics of habitats (e.g., in oceans, in human blood or in various species), it is now possible to survey and identify nonapparent viral agents in most situations. We are starting to realize that our world is mainly viral, but that all domains of life have their own peculiar relationship with these agents. It is also time to understand the molecular basis of how these silent viruses work. Once the importance of persistence is accepted and better understood, evolutionary biology, medicine and virology will all be better able to understand emergence of both disease and new life.

Executive summary • Historically, viruses have not been considered to be members of the tree of life, primarily because they are considered to be agents of disease and destructive of life. • However, on an evolutionary time scale, persisting (usually asymptomatic) viruses are much more successful. • Persisting viruses have major effects on the tree of life. • In this article, viral persistence is defined and presented as the major perspective from which we understand virus and host evolution. • This perspective enables us to see the central and constructive role viruses have had on the tree of life.

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Affiliation • Luis P Villarreal, PhD University of California, Center for Virus Research, 3232 McGaugh Hall, Irvine, CA 92697, USA Tel.: +1 949 824 6074; Fax: +1 949 824 9437; [email protected]

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