Any living organism aims to increase its population and this also applies to viruses. After completing the life cycle in a host, the virus exits and infects the same or a different host to continue the life cycle. Generalist viruses have a higher probability of finding the correct host for infection since they infect more number of species than the specialist viruses [8Parrish CR, Holmes EC, Morens DM, et al. Cross-species virus transmission and the emergence of new epidemic diseases. Microbiol Mol Biol Rev 2008; 72(3): 457-70.
[http://dx.doi.org/10.1128/MMBR.00004-08] [PMID: 18772285] ]. In addition, if a virus has multiple hosts, one of the hosts can act as a reservoir where, in the absence of a preferred host, the virus stays in an alternate host until the preferred host becomes available. This increases the chances of successful propagation of a generalist virus. For example, Potato leafroll virus and Potato virus Y make use of a weed, hairy nightshade (Solanum sarrachoides), as a viral reservoir and this increases virus infection of potato plants [28Srinivasan R, Alvarez JM, Bosque-Pérez NA, Eigenbrode SD, Novy RG. Effect of an alternate weed host, hairy nightshade, Solanum sarrachoides, on the biology of the two most important potato leafroll virus (Luteoviridae: Polerovirus) vectors, Myzus persicae and Macrosiphum euphorbiae (Aphididae: Homoptera). Environ Entomol 2008; 37(2): 592-600.
[PMID: 18419933] , 29Cervantes FA, Alvarez JM. Within plant distribution of Potato Virus Y in hairy nightshade (Solanum sarrachoides): An inoculum source affecting PVY aphid transmission. Virus Res 2011; 159(2): 194-200.
[http://dx.doi.org/10.1016/j.virusres.2011.05.003] [PMID: 21601597] ]. Similarly, bats serve as a reservoir for several important human viruses like Ebola and Nipah viruses [30Calisher CH, Childs JE, Field HE, Holmes KV, Schountz T. Bats: Important reservoir hosts of emerging viruses. Clin Microbiol Rev 2006; 19(3): 531-45.
[http://dx.doi.org/10.1128/CMR.00017-06] [PMID: 16847084] ].

Viruses act as pathogens and hence, according to the Red Queen hypothesis, there is a race between a virus and its host, where on the one hand, the host aims to develop defense mechanisms that can either eliminate or render the virus harmless or less harmful [31Dawkins R, Krebs JR. Arms races between and within species. Proc R Soc Lond B Biol Sci 1979; 205(1161): 489-511.
[http://dx.doi.org/10.1098/rspb.1979.0081] [PMID: 42057] -34Rosenzweig ML, Brown JS, Vincent TL. Red Queens and ESS: The coevolution of evolutionary rates. Evol Ecol 1987; 1: 59-94.
[http://dx.doi.org/10.1007/BF02067269] ], but on the other hand, the virus aims to maximize its fitness in the host [35Anderson RM, May RM. Coevolution of hosts and parasites. Parasitology 1982; 85(Pt 2): 411-26.
[http://dx.doi.org/10.1017/S0031182000055360] [PMID: 6755367] ]. Fitness is a cumulative ability of the virus to utilize the host resources for its propagation, ability to counteract the host defense network by increasing its virulence and transmission potential. Hence, with time the host may evolve to become resistant to a virus. This has been observed in plants [32de Ronde D, Butterbach P, Kormelink R. Dominant resistance against plant viruses. Front Plant Sci 2014; 5: 307.
[http://dx.doi.org/10.3389/fpls.2014.00307] [PMID: 25018765] ]. For example, several plant species developed resistance to specific viruses through resistance genes that are either dominant or recessive in nature. Dominant resistance genes act by synthesising protein products that bind to the avirulence (Avr) proteins of the viruses, rendering the virus inactive. Recessive resistance genes code for the mutated forms of the host factors indispensable for viral propagation, as a result, the virus fails to utilise them. If both the copies of a recessive resistance gene are mutated, the virus fails to propagate in the host. Therefore, if a host develops resistance then it will pose a serious extinction threat to a specialist virus, whereas the generalist virus can complete its life cycle in its alternate host(s). In addition, if the population of one of the hosts dwindles or if the host gets extinct, a generalist virus can complete its life cycle in other hosts. However, a specialist virus may face an extinction risk with the extinction of its host. Thus, having more than one host may increase the chances of viral survival.

Generalist viruses propagate in more than one host. Different hosts pose varying selection pressure on the virus. This leads the virus to adapt differently in different hosts and thus, the selection of unique genotypes of the virus in each host. This can result in the evolution of a new species of the virus. The evolution aims to improve the fitness of the virus in the given host [36Froissart R, Roze D, Uzest M, Galibert L, Blanc S, Michalakis Y. Recombination every day: Abundant recombination in a virus during a single multi-cellular host infection. PLoS Biol 2005; 3(3)e89
[http://dx.doi.org/10.1371/journal.pbio.0030089] [PMID: 15737066] ]. Nonetheless, the evolved species of the virus may show fitness trade-offs in the original hosts [7Elena SF, Agudelo-Romero P, Lalić J. The evolution of viruses in multi-host fitness landscapes. Open Virol J 2009; 3: 1-6.
[http://dx.doi.org/10.2174/1874357900903010001] [PMID: 19572052] , 37Longdon B, Brockhurst MA, Russell CA, Welch JJ, Jiggins FM. The evolution and genetics of virus host shifts. PLoS Pathog 2014; 10(11)e1004395
[http://dx.doi.org/10.1371/journal.ppat.1004395] [PMID: 25375777] ].

The infection of a host with more than one virus has been observed [38Syverton JT, Berry GP. Multiple virus infection of single host cells. J Exp Med 1947; 86(2): 145-52.
[http://dx.doi.org/10.1084/jem.86.2.145] [PMID: 19871662] ]. Hence, a generalist virus may be exposed to different sets of genetic material in different hosts, given the host is infected with more than one type of virus at one time. However, a specialist virus will have limited exposure to foreign DNA. This provides the generalist virus higher ability to bring variations through recombination and reassortment and may lead to an evolution of a new strain/species of the virus. However, there is limited literature on this aspect of virus evolution. Reassortment was observed in the evolution of the Influenza virus since it has a segmented genome and hence viruses with different genotypes can exchange nucleic acid segments [39De Clercq E. Antiviral agents active against influenza a viruses. Nat Rev Drug Discov 2006; 5(12): 1015-25.
[http://dx.doi.org/10.1038/nrd2175] [PMID: 17139286] -41Reid AH, Taubenberger JK. The origin of the 1918 pandemic influenza virus: A continuing enigma. J Gen Virol 2003; 84(Pt 9): 2285-92.
[http://dx.doi.org/10.1099/vir.0.19302-0] [PMID: 12917448] ].

In a dynamic environment, where fluctuation in biotic and abiotic factors occurs, generalist viruses have higher chances of survival. This is because generalist viruses thrive on more than one host and different hosts pose varying selection pressure on the virus. This allows the virus to adapt differently in different hosts leading to higher standing variation at any point in time. This helps the generalist virus adapts faster in a dynamic environment [42Woolhouse ME, Taylor LH, Haydon DT. Population biology of multihost pathogens. Science 2001; 292(5519): 1109-12.
[http://dx.doi.org/10.1126/science.1059026] [PMID: 11352066] , 43Whitlock MC. The Red Queen Beats the Jack-Of-All-Trades: The Limitations on the Evolution of Phenotypic Plasticity and Niche Breadth. Am Nat 1996; 148: 565-77.
[http://dx.doi.org/10.1086/285902] ].

Co-evolution of the virus and its host results in the specialisation of the virus, which helps the virus to improve its fitness in the host. As a result, a specialist virus can evolve to achieve maximum fitness in its host [42Woolhouse ME, Taylor LH, Haydon DT. Population biology of multihost pathogens. Science 2001; 292(5519): 1109-12.
[http://dx.doi.org/10.1126/science.1059026] [PMID: 11352066] , 43Whitlock MC. The Red Queen Beats the Jack-Of-All-Trades: The Limitations on the Evolution of Phenotypic Plasticity and Niche Breadth. Am Nat 1996; 148: 565-77.
[http://dx.doi.org/10.1086/285902] ]. However, it will be a daunting task for a generalist virus to maximise its fitness in each of its hosts [44Bera S, Fraile A, García-Arenal F. Analysis of fitness trade-offs in the host range expansion of an rna virus, tobacco mild green mosaic virus. J Virol 2018; 92(24): 92.
[http://dx.doi.org/10.1128/JVI.01268-18] [PMID: 30257999] ] since higher fitness in a host may cause fitness trade-offs in other hosts and vice-versa [7Elena SF, Agudelo-Romero P, Lalić J. The evolution of viruses in multi-host fitness landscapes. Open Virol J 2009; 3: 1-6.
[http://dx.doi.org/10.2174/1874357900903010001] [PMID: 19572052] ]. Therefore, a generalist virus evolves to acquire fitness, which allows it to propagate in each of the hosts successfully, albeit with different fitness. The lower fitness of the generalist virus may be disadvantageous when it has to compete with another virus having higher fitness in a given host. The fitness cost of its adaptation in a new host could even lead to the loss of the original host(s) [7Elena SF, Agudelo-Romero P, Lalić J. The evolution of viruses in multi-host fitness landscapes. Open Virol J 2009; 3: 1-6.
[http://dx.doi.org/10.2174/1874357900903010001] [PMID: 19572052] , 45Sharp PM, Hahn BH. The evolution of HIV-1 and the origin of AIDS. Philos Trans R Soc Lond B Biol Sci 2010; 365(1552): 2487-94.
[http://dx.doi.org/10.1098/rstb.2010.0031] [PMID: 20643738] ].

Over time, evolution should help the virus increase its fitness in the host until it achieves an optimum possible fitness. Since the generalist virus propagates in more than one host, it has to face different selection pressures, thus may not be able to maximise its fitness, as explained earlier. On the other hand, the specialist virus will evolve to achieve maximum fitness in its host. Hence, a stable environment favours the evolution of specialist viruses [46Baronchelli A, Chater N, Christiansen MH, Pastor-Satorras R. Evolution in a changing environment. PLoS One 2013; 8(1)e52742
[http://dx.doi.org/10.1371/journal.pone.0052742] [PMID: 23326355] ].

The first step for a successful host shift by a virus is to land on a new host [8Parrish CR, Holmes EC, Morens DM, et al. Cross-species virus transmission and the emergence of new epidemic diseases. Microbiol Mol Biol Rev 2008; 72(3): 457-70.
[http://dx.doi.org/10.1128/MMBR.00004-08] [PMID: 18772285] ]. Viruses after completing the life cycle must exit the host and land on a new host to initiate a host shift event. Different viruses exploit different transmission agents like air, food, water, physical contacts between the hosts, vectors, etc. to enhance their spread [4Payne S. Virus Transmission and Epidemiology.Viruses: From Understanding to Investigation 2018; 53-60.-6Stevens WA. Transmission of Plant Viruses.Virology of Flowering Plants 1983; 41-68.
[http://dx.doi.org/10.1007/978-1-4757-1251-3_3] ].

Plant viruses are transmitted mostly through vectors, the majority of which are insects, which are host generalists and feed on a wide variety of plants [7Elena SF, Agudelo-Romero P, Lalić J. The evolution of viruses in multi-host fitness landscapes. Open Virol J 2009; 3: 1-6.
[http://dx.doi.org/10.2174/1874357900903010001] [PMID: 19572052] ]. Other modes of transmission include the use of contaminated tools, vegetative propagation of infected plant parts, infected seed, etc [12Hanssen IM, Lapidot M, Thomma BP. Emerging viral diseases of tomato crops. Mol Plant Microbe Interact 2010; 23(5): 539-48.
[http://dx.doi.org/10.1094/MPMI-23-5-0539] [PMID: 20367462] ]. These routes allow plant viruses to land on a wide variety of non-host plants (Fig. 2a). Similarly, animal viruses can also land on a wide variety of non-hosts as they are transmitted via micro-droplets through the air, contaminated food and water, direct physical contact and vectors [13Moriones E, Praveen S, Chakraborty S. Tomato leaf curl new delhi virus: An emerging virus complex threatening vegetable and fiber crops. Viruses 2017; 9(10)E264
[http://dx.doi.org/10.3390/v9100264] [PMID: 28934148] ].

Fig. (1) Life cycle of a plant virus and challenges to a successful host shift. Schematic representation of a plant virus life cycle. For a successful host shift, a virus has to overcome certain challenges. These challenges are indicated in black boxes (1 to 6) in the figure.

After landing on a new host, the virus or its nucleic acid must enter inside the cell for carrying out the life cycle and thus successfully achieves a host shift, and this step is one of the most challenging steps in the successful host shift event. Animal viruses enter the cell by endocytosis or membrane fusion [49Payne S. Virus Interactions With the Cell.From Understanding to Investigation 2018; 23-35.], which requires specific molecular interactions between the viral surface proteins and host cell surface receptors. However, this specificity is a limitation for the entry of the animal viruses to non-host cells [8Parrish CR, Holmes EC, Morens DM, et al. Cross-species virus transmission and the emergence of new epidemic diseases. Microbiol Mol Biol Rev 2008; 72(3): 457-70.
[http://dx.doi.org/10.1128/MMBR.00004-08] [PMID: 18772285] ]. An analysis of 64 human viruses showed that those with the widest host range used protein receptors whose sequences were more conserved [50Woolhouse M, Scott F, Hudson Z, Howey R, Chase-Topping M. Human viruses: Discovery and emergence. Philos Trans R Soc Lond B Biol Sci 2012; 367(1604): 2864-71.
[http://dx.doi.org/10.1098/rstb.2011.0354] [PMID: 22966141] ]. Mutation in the attachment protein of phi-6 phage allowed them to become generalists by allowing them to bind to the receptors of the non-host cells and enter the cell [51Duffy S, Turner PE, Burch CL. Pleiotropic costs of niche expansion in the RNA bacteriophage phi 6. Genetics 2006; 172(2): 751-7.
[http://dx.doi.org/10.1534/genetics.105.051136] [PMID: 16299384] ]. In the case of canine parvovirus (CPV), two mutations in the Feline panleukopenia virus surface protein allowed it to bind to canine transferrin receptor and thus expanded its host range [52Hueffer K, Govindasamy L, Agbandje-McKenna M, Parrish CR. Combinations of two capsid regions controlling canine host range determine canine transferrin receptor binding by canine and feline parvoviruses. J Virol 2003; 77(18): 10099-105.
[http://dx.doi.org/10.1128/JVI.77.18.10099-10105.2003] [PMID: 12941920] , 53Shimakage MI, Yutsudo M, Hakura A, Toyoshima K. Isolation and characterization of host range mutants of avian sarcoma virus. J Gen Virol 1983; 64(Pt 4): 921-6.
[http://dx.doi.org/10.1099/0022-1317-64-4-921] [PMID: 6300310] ].

However, in the case of plant viruses, the plant cell has a rigid cell wall, and therefore, such viruses can not enter the cell similar to animal viruses. Plant viruses can only enter the cell through the mechanical injuries inflicted by either the vectors feeding on the plants, which are majorly host generalist or agricultural practices which can cause such injuries [54Balique F, Lecoq H, Raoult D, Colson P. Can plant viruses cross the kingdom border and be pathogenic to humans? Viruses 2015; 7(4): 2074-98.
[http://dx.doi.org/10.3390/v7042074] [PMID: 25903834] ]. As a result, plant viruses can easily gain access to a wide variety of non-host plant species (Fig. 2b).

Host cells have developed defense mechanisms to eliminate the introduction of viruses [55Barber GN. Host defense, viruses and apoptosis. Cell Death Differ 2001; 8(2): 113-26.
[http://dx.doi.org/10.1038/sj.cdd.4400823] [PMID: 11313713] ]. There is a race between the virus and its host where the host aims to evolve defense mechanisms that can eliminate or render the virus harmless or less harmful. On the other hand, the virus aims to evolve to counteract the host defense mechanisms and optimise its virulence that can increase its fitness in the host [31Dawkins R, Krebs JR. Arms races between and within species. Proc R Soc Lond B Biol Sci 1979; 205(1161): 489-511.
[http://dx.doi.org/10.1098/rspb.1979.0081] [PMID: 42057] , 34Rosenzweig ML, Brown JS, Vincent TL. Red Queens and ESS: The coevolution of evolutionary rates. Evol Ecol 1987; 1: 59-94.
[http://dx.doi.org/10.1007/BF02067269] ].

Once inside the cell, the virus faces the host defense network. Higher animals, such as vertebrates, have a highly developed immune system. It consists of organs and cells dedicated to mediate the defense. The immune cells scan for incoming threats and can move from one part of the body to another through motility and circulatory system. The system contains both innate and adaptive immunity. Innate immunity is broadly non-specific in nature, whereas adaptive immunity is highly specific and generates memory, which reduces the response time on successive infection by the same pathogen [56Yatim KM, Lakkis FG. A brief journey through the immune system. Clin J Am Soc Nephrol 2015; 10(7): 1274-81.
[http://dx.doi.org/10.2215/CJN.10031014] [PMID: 25845377] , 57Iriti M, Faoro F. Review of innate and specific immunity in plants and animals. Mycopathologia 2007; 164(2): 57-64.
[http://dx.doi.org/10.1007/s11046-007-9026-7] [PMID: 17554637] ].

On the contrary, the plant immune system lacks dedicated immune cells and organs. Rather, their defense network is located in each cell of the plant. Also, plants lack adaptive immunity and they only contain innate immunity, which is mainly provided by pattern recognition receptor (PRR), R-genes, RNA interference and Jasmonic acid signalling pathway [57Iriti M, Faoro F. Review of innate and specific immunity in plants and animals. Mycopathologia 2007; 164(2): 57-64.
[http://dx.doi.org/10.1007/s11046-007-9026-7] [PMID: 17554637] -59Jones JD, Dangl JL. The plant immune system. Nature 2006; 444(7117): 323-9.
[http://dx.doi.org/10.1038/nature05286] [PMID: 17108957] ]. RNA interference in plants is highly efficient in combating viral infections [60Rosa C, Kuo YW, Wuriyanghan H, Falk BW. RNA interference mechanisms and applications in plant pathology. Annu Rev Phytopathol 2018; 56: 581-610.
[http://dx.doi.org/10.1146/annurev-phyto-080417-050044] [PMID: 29979927] ]. But, it employs a conserved pathway and viruses can develop resistance against the conserved proteins of the RNAi in plants [61Voinnet O. Induction and suppression of RNA silencing: Insights from viral infections. Nat Rev Genet 2005; 6(3): 206-20.
[http://dx.doi.org/10.1038/nrg1555] [PMID: 15703763] ]. Resistance in one species may be able to provide resistance in related species because of the involvement of conserved proteins.

Since plants lack adaptive immunity and dedicated immune cells and organs in vertebrates, they may not be as efficient as vertebrates in eliminating viruses during a host shift event. Thus, plants may provide a more conducive environment for a successful host shift event.

Fig. (2) Entry and spread of plant virusesa. Insect vectors are generalist in nature and feed on different plants. b. Viruses are then released through the stylet of the insect into mesophyll cells primarily. c. Viruses then spread to neighbouring cells and enter a sieve tube to infect distant cells via plasmodesmata. Viruses may experience varying fitness in different cells of the plant. For example, in the given figure, the virus experiences high fitness in bundle sheath cell and cell ‘X’ as indicated by the replicative potential of the virus. ‘X and Y’ could be any other living cells of the plant.

Inside a non-host cell, the virus may experience lower fitness resulting in an unsuccessful host shift event. For a successful host shift event, the virus should improve its fitness in the new host. Fitness is a cumulative ability of the virus to utilize the host resources for its (i) multiplication, (ii) ability to counteract the host defense network and (iii) virulence and transmission potential. The majority of plant viruses are RNA viruses [62Joshi S, Haenni LA. Review: Plant RNA viruses: Strategies of expression and regulation of Viral Genes. FEBS Lett 1984; 177.], and these viruses have the highest mutation rates [63Duffy S, Shackelton LA, Holmes EC. Rates of evolutionary change in viruses: Patterns and determinants. Nat Rev Genet 2008; 9(4): 267-76.
[http://dx.doi.org/10.1038/nrg2323] [PMID: 18319742] ]. Mutations can result in variations on which natural selection could act to improve the fitness of the virus [64Zhao L, Duffy S. Gauging genetic diversity of generalists: A test of genetic and ecological generalism with RNA virus experimental evolution. Virus Evol 2019; 5(1)vez019
[http://dx.doi.org/10.1093/ve/vez019] [PMID: 31275611] ]. Therefore, plant viruses can adapt faster during a host shift event. This could also explain the generalist nature of RNA viruses [37Longdon B, Brockhurst MA, Russell CA, Welch JJ, Jiggins FM. The evolution and genetics of virus host shifts. PLoS Pathog 2014; 10(11)e1004395
[http://dx.doi.org/10.1371/journal.ppat.1004395] [PMID: 25375777] ].

After replicating inside a cell, the virus must infect neighbouring (short distance travel) and distantly located (long distance travel) cells in a multicellular organism. However, the virus faces the cell membrane and/or cell wall as barriers while exiting the infected cell and entering a new cell. Transmission of viruses inside an organism can occur either by cell-free mode or by cell-cell connections. In cell-free mode, viruses exit the cell by exocytosis or cell lysis and diffuse to infect the neighbouring or the distantly located cells [65Mothes W, Sherer NM, Jin J, Zhong P. Virus cell-to-cell transmission. J Virol 2010; 84(17): 8360-8.
[http://dx.doi.org/10.1128/JVI.00443-10] [PMID: 20375157] , 66Zhong P, Agosto LM, Munro JB, Mothes W. Cell-to-cell transmission of viruses. Curr Opin Virol 2013; 3(1): 44-50.
[http://dx.doi.org/10.1016/j.coviro.2012.11.004] [PMID: 23219376] ]. In the cell-cell mode of transmission, viruses use cell-to-cell connections like a tight junction, gap junction, cytonemes, plasmodesmata, etc. for their spread. Cell-to-cell transmission is advantageous for the virus since it is faster, protects the virus from the immunological mediators like antibodies and anti-viral factors present in the extracellular space, evades the need for exocytosis or cell lysis and protects the virus from the extracellular environment, which may destabilise viruses [65Mothes W, Sherer NM, Jin J, Zhong P. Virus cell-to-cell transmission. J Virol 2010; 84(17): 8360-8.
[http://dx.doi.org/10.1128/JVI.00443-10] [PMID: 20375157] -67Sherer NM, Mothes W. Cytonemes and tunneling nanotubules in cell-cell communication and viral pathogenesis. Trends Cell Biol 2008; 18(9): 414-20.
[http://dx.doi.org/10.1016/j.tcb.2008.07.003] [PMID: 18703335] ].

The majority of the animal viruses use the cell-free transmission method [49Payne S. Virus Interactions With the Cell.From Understanding to Investigation 2018; 23-35., 68Bird SW, Kirkegaard K. Escape of non-enveloped virus from intact cells. Virology 2015; 479-480: 444-9.
[http://dx.doi.org/10.1016/j.virol.2015.03.044] [PMID: 25890822] ], whereas plant viruses exclusively use a cell-to-cell mode of transmission through plasmodesmata, which are fine cytoplasmic channels running between two plant cells [69Benitez-Alfonso Y, Faulkner C, Ritzenthaler C, Maule AJ. Plasmodesmata: Gateways to local and systemic virus infection. Mol Plant Microbe Interact 2010; 23(11): 1403-12.
[http://dx.doi.org/10.1094/MPMI-05-10-0116] [PMID: 20687788] ]. This is because plant cells have a rigid cell wall and hence viruses cannot carry out a cell-free mode of transmission. Movement through plasmodesmata is assisted by movement proteins, some of which have been found to be conserved across species (Unpublished data). Therefore, plant viruses exploit plasmodesmata to infect neighbouring cells and also enter phloem sieve elements for long distance travel to infect distantly located cells [69Benitez-Alfonso Y, Faulkner C, Ritzenthaler C, Maule AJ. Plasmodesmata: Gateways to local and systemic virus infection. Mol Plant Microbe Interact 2010; 23(11): 1403-12.
[http://dx.doi.org/10.1094/MPMI-05-10-0116] [PMID: 20687788] -71Elisabeth Waigmann SU, Trutnyeva K, Citovsky V. The Ins and Outs of Nondestructive Cell-to-Cell and Systemic Movement of Plant Viruses. Crit Rev Plant Sci 2010; 23: 195-250.
[http://dx.doi.org/10.1080/07352680490452807] ] (Fig. 2c). Thus, it may be easier for a plant virus to adapt to spread inside the plant during a host shift event than animal viruses.

The entry of the animal viruses inside the cell is mediated via a specific receptor present on the host cell surface, as explained earlier [51Duffy S, Turner PE, Burch CL. Pleiotropic costs of niche expansion in the RNA bacteriophage phi 6. Genetics 2006; 172(2): 751-7.
[http://dx.doi.org/10.1534/genetics.105.051136] [PMID: 16299384] -53Shimakage MI, Yutsudo M, Hakura A, Toyoshima K. Isolation and characterization of host range mutants of avian sarcoma virus. J Gen Virol 1983; 64(Pt 4): 921-6.
[http://dx.doi.org/10.1099/0022-1317-64-4-921] [PMID: 6300310] ]. Therefore, animal viruses, after entering the organism, find the target tissue(s) and infect specific cell(s) of the tissue(s). Hence, an animal virus can only infect one or a few cell types of the organism [72Samuel Baron MF, Albrecht T. Viral Pathogenesis.Medical Microbiology 1996.]. On the contrary, plant viruses use plasmodesmata for short distance travel to infect neighbouring cells and phloem sieve elements for long distance travel to infect distantly located cells [70Hipper C, Brault V, Ziegler-Graff V, Revers F. Viral and cellular factors involved in Phloem transport of plant viruses. Front Plant Sci 2013; 4: 154.
[http://dx.doi.org/10.3389/fpls.2013.00154] [PMID: 23745125] , 71Elisabeth Waigmann SU, Trutnyeva K, Citovsky V. The Ins and Outs of Nondestructive Cell-to-Cell and Systemic Movement of Plant Viruses. Crit Rev Plant Sci 2010; 23: 195-250.
[http://dx.doi.org/10.1080/07352680490452807] ]. Therefore, plant viruses gain access to different cell types of the plant and often lead to systemic infection [71Elisabeth Waigmann SU, Trutnyeva K, Citovsky V. The Ins and Outs of Nondestructive Cell-to-Cell and Systemic Movement of Plant Viruses. Crit Rev Plant Sci 2010; 23: 195-250.
[http://dx.doi.org/10.1080/07352680490452807] ]. Different cell types of the plant provide different cellular environments to the virus. Thus, plant viruses may experience different fitness in different cell types. This improves the chances of a virus to find the right cell type where the fitness is high and it can multiply and increase the chances of a successful host shift (Fig. 2c).