viruses, characteristics, and transmission.pptx

This presentation is aimed to provide core concepts about viruses, their characteristics, and how they transmit inside plants

1. Bacteriology & Virology The Science of Microbes

2. I n t r oducti o n Viruses are all around us, comprising an enormous proportion of our environment, in both number and total mass All living things encounter billions of virus particles every day. For example, they enter our lungs in the 6 liters of air each of us inhales every minute; They enter our digestive systems with the food we eat; And they are transferred to our eyes, mouths, and other points of entry from the surfaces we touch and the people with whom we interact. Our bodies are reservoirs for viruses that reside in our respiratory, gastrointestinal, and urogenital tracts.

3. I n t r oducti o n Compared with eukaryotic and even prokaryotic cells, most Viruses are much smaller and simpler in structure. Lacking the Structures and metabolic machinery found in a cell, a virus Is an infectious particle consisting of little more than genes Packaged in a protein coat .

4. Viruses: Defination: An infective agent that typically consists of a nucleic acid molecule in a protein coat, is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host.

5. Introduction to viruses Viruses do not have cells that divide; new viruses are assembled in the infected host cell But unlike still simpler infectious agents, viruses contain genes, which gives them the ability to mutate and evolve. Evolved from plasmids : pieces of DNA that can move between cells while others may have evolved from bacteria. Over 5,000 species of viruses have been discovered.

6. Introduction to viruses A virus consists of two or three parts: ge n e s , m ade f rom e i ther DNA o r RNA , long molecules that carry genetic information protein coat that protects the genes; and in some viruses, an envelope of fat Viruses vary in shape from the simple helical and icosahedral to more comple x structures. Viruses range in size from 20 to 300 nanometres;

7. Properties of virsuses Viruses have a nucleic acid genome of either DNA or RNA. Compared with a cell genome, viral genomes are small, but genomes of different viruses range in size by over 100-fold ( c . 3000 nt to 1,200,000 bp) Small genomes make small particles – again with a 100-fold size range. Viral genomes are associated with protein that at its simplest forms the virus particle, but In some viruses this nucleoprotein is surrounded by further protein or a lipid bilayer. Viruses can only reproduce in living cells. The outermost proteins of the virus particle allow the virus to recognize the correct host cell and gain entry into its cytoplasm

8. Introduction Are viruses living or nonliving? Early on, they were considered Biological chemicals; the latin root for virus means “poison.” Viruses can cause a wide variety of diseases, so researchers In the late 1800s saw a parallel with bacteria and proposed that Viruses were the simplest of living forms. However, viruses cannot Reproduce or carry out metabolic activities outside of a host Cell. Most biologists would probably agree that viruses are not Alive, but instead exist in a shady area between life-forms and Chemicals. The simple phrase used by two researchers describes them aptly: viruses lead “a kind of borrowed life.”

9. DISCOVERY OF VIRUSES Although much is known about viruses it is instructive and Interesting to consider how this knowledge came about. It was only just Over 100 years ago at the end of the nineteenth century that the germ Theory of disease was formulated, And pathologists were then confident that a causative microorganism would be found for each infectious disease

10. DISCOVERY OF VIRUSES Further they believed that these agents of disease could be seen with the aid of a microscope, could be cultivated on a nutrient medium, and could be retained by filters. There were, admittedly, a few organisms which were so fastidious that they could not be cultivated in vitro (literally, in glass, meaning in the test tube), but the other two criteria were satisfied However, a few years later, in 1892, Dmitri iwanowski was able to show that The causal agent of a mosaic disease of tobacco plants, manifesting As a discoloration of the leaf, passed through a bacteria-proof filter, and could not be seen or cultivated. Iwanowski was unimpressed by his discovery, but beijerinck repeated the experiments in 1898, and became convinced this

11. Discovery In 1884 the French microbiologist Charles Chamberland invented a filter, known today as the Chamberland filter or Chamberland–Pasteur filter, that has pores smaller than bacteria. Thus he could pass a solution containing bacteria through the filter and completely remove them from the solution. In the early 1890s the Russian biologist Dmitri Ivanovsky used this filter to study what became known as the tobacco mosaic virus. His experiments showed that extracts from the crushed leaves of infected tobacco-plants remain infectious after filtration.

12. DISCOVERY OF VIRUSES In the same year Loeffler and frosch came to the same conclusion regarding the cause of Foot-and-mouth disease. Furthermore, because foot-and-mouth disease Could be passed from animal to animal, with great dilution at each passage, The causative agent had to be reproducing and thus could not be a Bacterial toxin. Viruses of other animals were soon discovered. Ellerman And bang reported the cell-free transmission of chicken leukemia in 1908, And in 1911 rous discovered that solid tumors of chickens could be transmitted By cell-free filtrates. These were the first indications that some viruses can cause cancer.

13. Discovery: In 1899 the Dutch microbiologist Martinus Beijerinck observed that the agent multiplied only in dividing cells. Having failed to demonstrate its particulate nature he called it a " contagium vivum fluidum ", a "soluble living germ". In the early 20th century the English bacteriologist Frederick Twort discovered viruses that infect bacteria With the invention of the electron microscope in 1931 by the German engineers Ernst Ruska and Max Knoll came the first images of viruses.

14. DISCOVERY OF VIRUSES Finally bacterial viruses were discovered. In 1915, published an Account of a glassy transformation of micrococci. He had been trying to Culture the smallpox agent on agar plates but the only growth obtained was that of some contaminating micrococci. Upon prolonged incubation, Some of the colonies took on a glassy appearance and, once this Occurred, no bacteria could be subcultured from the affected colonies

15. DISCOVERY OF VIRUSES If Some of the glassy material was added to normal colonies, they too took On a similar appearance, even if the glassy material was first passed through Very fine filters. Among the suggestions that Twort put forward to explain the phenomenon was the existence of a bacterial virus or the secretion By the bacteria of an enzyme which could lyse the producing cells.

16. DISCOVERY OF VIRUSES This idea of self-destruction by secreted enzymes was to prove a controversial Topic over the next decade. In 1917 d’Hérelle observed a similar Phenomenon in dysentery bacilli. He observed clear spots on lawns of Such cells, and resolved to find an explanation for them. Upon noting the lysis of broth cultures of pure dysentery bacilli by filtered emulsions Of feces, he immediately realized he was dealing with a bacterial virus.

17. DISCOVERY OF VIRUSES Since this virus was incapable of multiplying except at the expense of living bacteria, he called his virus a bacteriophage (literally a bacterium eater) or phage for short. Thus the first definition of these new agents, the viruses, was presented entirely in negative terms: They could not be seen, could not be cultivated in the absence of cells and, most important of all, were not retained by bacteria-proof filters.

18. DISCOVERY OF VIRUSES Scientists detected viruses indirectly long before they were able to see them. The story of how viruses were discovered begins In 1883. A german scientist named Adolf mayer was studying Tobacco mosaic disease, which stunts the growth of tobacco plants and gives their leaves a mottled, or mosaic, coloration. Mayer discovered that he could transmit the disease from plant to plant by rubbing sap extracted from diseased leaves onto healthy plants.

19. DISCOVERY OF VIRUSES After an unsuccessful search for an infectious Microorganism in the sap, he suggested that the disease was caused by unusually small bacteria that were invisible under a microscope. This hypothesis was tested a decade later by Dmitri Ivanowsky , a russian biologist Who passed sap from Infected tobacco leaves through a filter designed to remove Bacteria. After filtration, the sap still produced mosaic disease.

20. DISCOVERY OF VIRUSES But Ivanowsky reasoned that perhaps the bacteria were small enough to pass through the filter or made a toxin that could do so. The second possibility was ruled out when the Dutch botanist martinus beijerinck carried out a classic series of experiments that showed that the infectious agent in the filtered sap could replicate

21. ORIGIN OF VIRUSES The question of the origin of viruses is a fascinating topic but as so often happens when hard evidence is scarce, discussion can generate more heat than light. There are two popular theories: viruses are either degenerate cells or vagrant genes. Just as fleas are descended from flies by loss of wings, viruses may be derived from pro- or eukaryotic cells that have dispensed with many of their cellular functions ( degeneracy ).

22. The Progressive Hypothesis According to this hypothesis, viruses originated through a progressive process. Mobile genetic elements, pieces of genetic material capable of moving within a genome, gained the ability to exit one cell and enter another.

23. The Regressive Hypothesis In contrast to the progressive process just described, viruses may have originated via a regressive, or reductive, process. Microbiologists generally agree that certain bacteria that are obligate intracellular parasites, like  Chlamydia  and  Rickettsia  species, evolved from free-living ancestors. Indeed, genomic studies indicate that the mitochondria of eukaryotic cells and  Rickettsia prowazekii  may share a common, free-living ancestor. It follows, then, that existing viruses may have evolved from more complex, possibly free-living organisms that lost genetic information over time, as they adopted a parasitic approach to replication

24. ORIGIN OF VIRUSES Alternatively, some nucleic acid might have been transferred accidentally into a cell of a different species (e.g. through a wound or by sexual contact) and, Instead of being degraded, as would normally be the case, might have survived and replicated ( escape ). Although half a century has elapsed since these two theories were first proposed, we still do not have any firm indications if either, or both, are correct

25. ORIGIN OF VIRUSES Two processes that contribute significantly to virus evolution are recombination and mutation. Recombination takes place infrequently between the single molecule genomes of two related DNA or RNA viruses that are present in the same cell and generates a novel combination of genes. Of far greater significance is the potential for genetic exchange between related viruses with segmented genomes. Here, whole functional genes are exchanged, and this type of recombination is called reassortment .

26. ORIGIN OF VIRUSES The only restriction is the compatibility between the various individual segments making up the functional genome. Fortunately, this seems to be a real barrier to the unlimited creation of new viruses, Although it is not invincible, since pandemic influenza A viruses can be created in this way Mutation is of particular significance to the evolution of RNA genomes as, in contrast to DNA synthesis, There is no molecular proof-reading mechanism during RNA synthesis. Mutations accumulated at a rate of approximately 3 × 10 4 per nucleotide per cycle of replication, whereas with DNA this figure is 10− 9 to 10− 10 per nucleotide per cycle.

27. ORIGIN OF VIRUSES In other words, an RNA virus can achieve in one generation the degree of genetic variation Which would take an equivalent DNA genome between 300,000 and 3000,000 generations to achieve. Once formed by reassortment, an influenza A virus evolves so rapidly that it takes only 4 years on average to mutate sufficiently to escape recognition by host defenses and to re-infect that same individual.

28. Introduction to virus structure

29. Introduction to virus structure Outside their host cells, viruses survive as virus particles, also known as virions. The virion is a gene delivery system; it contains the virus genome, and its functions are to protect the genome and to aid its entry into a host cell, Where it can be replicated and packaged into new virions. The genome is packaged in a protein structure known as a capsid.

30. Introduction to virus structure Many viruses also have a lipid component, generally present at the surface of the virion forming an envelope, which also contains proteins with roles in aiding entry into host cells. A few viruses form protective protein occlusion bodies around their virions. Before looking at these virus structures we shall consider characteristics of the nucleic acid and protein molecules that are the main components of virions.

31. Virus genomes A virion contains the genome of a virus in the form of one or more molecules of nucleic acid. For any one virus the genome is composed of either RNA or DNA. If a new virus is isolated, one way to determine whether it is an RNA virus or a DNA virus is to test its susceptibility to a ribonuclease and a deoxyribonuclease. The virus nucleic acid will be susceptible to degradation by only one of these enzymes.

32. Virus genomes Each nucleic acid molecule is either single-stranded (ss) or double-stranded (ds), giving four categories of virus genome: dsDNA, ssDNA, dsRNA and ssRNA The dsDNA viruses encode their genes in the same kind of molecule as animals, plants, bacteria and other cellular organisms, while the other three types of genome are unique to viruses. It interesting to note that most fungal viruses have dsRNA genomes, most plant viruses have ssRNA genomes and most prokaryotic viruses have dsDNA genomes. The reasons for these distributions presumably concern diverse origins of the viruses in these very different host types.

33. Virus genomes A further categorization of a virus nucleic acid can be made on the basis of whether the molecule is linear, with free 5 and 3 ends, or circular, as a result of the strand(s) being covalently closed. Examples of each category are given in Figure 3.1. In this figure, and indeed throughout the book, molecules of DNA and RNA are colour coded. Dark blue and light blue depict (+) RNA and (−) RNA respectively;

34. Virus genomes It should be noted that some linear molecules may be in a circular conformation as a result of base pairing between complementary sequences at their ends This applies, for example, to the DNA in heap dna virus virions and to the RNA in influenza virions .

35. Viral capsids The capsid is a complex structure made up of many identical subunits of viral protein – often termed a capsomer . The capsid functions to provide a protein shell in which the chemically labile viral genome can be maintained in a stable environment. The association of capsids with genomes is a complex process, but it must result in an energetically stable structure. a very large number assume one of two regular shapes. The first is the helix , in which the capsomers associate with helical nucleic acid as a nucleoprotein – these can either be stiff or flexible depending upon the properties of the capsid’s proteins themselves.

36. The other highly regular shape is the icosahedron , in which the capsomers form a regular solid structure enfolding the viral genome. Despite the frequency of such regular shapes, many viruses have more complex and/or less regular appearances, these include spindle, kidney, lemon, and lozenge shapes. Further, some viruses can assume different shapes depending upon the nature of the cells in which they mature, And some groups of viruses – notably the pox viruses – are distinguished by having a number of different shapes characterizing specifi c members of the group Viral capsids

37. Viral Envelops A naked capsid defines the outer extent of bacterial, plant, and many animal viruses, But other types of viruses have a more complex structure in which the capsid is surrounded by a lipid envelope . This envelope is made up of a lipid bilayer that is derived from the cell in which the virus replicates and from virus-encoded membrane- associated proteins. The presence or absence of a lipid envelope (described as enveloped or naked, respectively) is another important defining property of different groups of animal viruses.

38. Viral Envelops The shape of a given type of virus is determined by the shape of the virus capsid and really does not depend on whether or not the virus is enveloped. This is because for most viruses, the lipid envelope is amorphous and deforms readily upon preparation for visualization using the electron microscope.

39. CLASSIFICATION SCHEMES

40. CLASSIFICATION SCHEMES As we have noted above, since it is not clear that all viruses have a common origin, a true Linnaean classification is not possible, But a logical classification is invaluable for understanding the detailed properties of individual viruses and how to generalize them. Schemes dependent on basic properties of the virus, as well as specific features of their replication cycle, Afford a useful set of parameters for keeping track of the many different types of viruses. A good strategy for remembering the basics of virus classification is to keep track of the following:

41. CLASSIFICATION SCHEMES 1 What kind of genome is in the capsid: is it DNA or RNA? Is it single stranded or double stranded? Is the genome circular or linear, composed of a single piece or segmented? 2 How is the protein arranged around the nucleic acid; that is, what are the symmetry and dimensions of the viral capsid? 3 Are there other components of the virion? (a) Is there an envelope? (b) Are there enzymes in the virion required for initiation of infection or maturation of the virion?

42. The Baltimore scheme of virus classification Knowledge of the particulars of a virus’s structure and the basic features of its replication can be used in a number of ways to build a general classification of viruses. In 1971, David Baltimore suggested a scheme for virus classification based on the way in which a virus produces messenger RNA (mRNA) during infection. The logic of this consideration is that in order to replicate, all viruses must express mRNA for translation into protein, but how they do this is determined by the type of genome utilized by the virus.

43. The Baltimore scheme of virus classification In this system, viruses with RNA genomes whose genome is the same sense as mRNA are called positive ( + )-sense RNA viruses , while viruses whose genome is the opposite ( complementary ) sense of mRNA are called negative ( - )-sense RNA viruses . Viruses with double-stranded genomes obviously have both senses of the nucleic acid.

44. The Baltimore scheme of virus classification The Baltimore Classification System initially included six classes of viruses. However, a seventh class was added to accommodate the gapped DNA genome of Hepadnaviridae (hepatitis B virus). The seven classes of viruses in the Baltimore Classification System are as follows:

45. Class I: Double stranded DNA (dsDNA) viruses A double stranded DNA virus enters the host nucleus before it begins to replicate. It makes use of the host polymerases to replicate its genome, and is therefore highly dependent on the host cell cycle. The cell must therefore be in replication for the virus to replicate. Examples of Class I viruses include Herpesviridae , Adenoviridae , and Papoviridae .

46. Class II: Single stranded DNA (ssDNA) viruses Most ssDNA viruses have circular genomes and replicate mostly within the nucleus by a rolling circle mechanism. Some examples of Class II viruses are Anelloviridae , Circoviridae , and Parvoviridae .

47. Class III: Double stranded RNA (dsRNA) viruses Double stranded RNA viruses replicate in the core capsid in the host cell cytoplasm and do depend as heavily on host polymerases as DNA viruses. The genomes of Class III viruses may be segmented, and unlike viruses with more complex translation, each gene codes for only one protein.

48. Class IV: Single stranded RNA (ssRNA) viruses Class IV ssRNA viruses have positive-sense RNA genomes, meaning they can be directly read by ribosomes to translate into proteins. They are further divided into viruses with polycistronic mRNA and those with complex transcription. Polycistronic mRNA is translated into a polyprotein that is subsequently cleaved to form separate proteins. Viruses with complex transcription use ribosomal frameshifting and proteolytic processing to produce multiple proteins from the same gene sequences.

49. Class V: Single stranded RNA (ssRNA) viruses Class V viruses have a negative-sense RNA genome, meaning they must be transcribed by a viral polymerase to produce a readable strand of mRNA. The genomes of Class V viruses may be segmented or non- segmented.

50. Class VI: Positive-sense ssRNA reverse transcriptase viruses Group VI viruses have a positive sense, single-stranded RNA genome, but replicate through a DNA intermediate. The RNA is converted to DNA by reverse transcriptase and then the DNA is spliced into the host genome for subsequent transcription and translation using the enzyme integrase.

51. Class VII: Double stranded DNA (dsDNA) reverse transcriptase viruses Class VII viruses have a double-stranded DNA genome, but unlike Class I viruses, they replicate via a ssRNA intermediate. The dsDNA genome is gapped, and subsequently filled in to form a closed circle serving as a template for production of viral mRNA. To reproduce the genome, RNA is reverse transcribed back to DNA. Hepatitis B virus is a Class VII virus.

52. CLASSIFICATION ON THE BASIS OF DISEASE The first, and most common, experience of viruses is as agents of disease and it is possible to group viruses according to the nature of the disease with which they are associated. can discuss hepatitis viruses or viruses causing the common cold. However, this method of grouping viruses, though reflecting an important characteristic, suffers from serious deficiencies. First, this approach is very anthropomorphic, focusing as it does on diseases that we recognize because they affect humans or our domestic livestock. This ignores the fact that most viruses either do not cause disease or cause a disease that we do not recognize because of a lack of understanding of the host; for example we understand little of the diseases caused by viruses of fish or amphibians.

53. CLASSIFICATION ON THE BASIS OF DISEASE Similarly, it is possible for a single virus to cause more than one type of disease; a good example of this is varicella zoster virus which causes chickenpox in a first infection but when reactivated later in life causes shingles. A classification based on disease, while it may be helpful in some settings, also fails in the important feature of being able to use the groupings to predict common fundamental features of the viruses in question.

54. CLASSIFICATION ON THE BASIS OF HOST ORGANISM An alternative approach has been to group viruses according to the host that they infect. This has the attraction that it emphasizes the parasitic nature of the virus–host interaction. However, there are several difficulties with this approach. This form of classification implies a fixed, unchanging, link between the virus and host in question. Some viruses are very restricted in their host range, infecting only one species, such as hepatitis B virus infecting humans, and so a designation based on the host is appropriate.

55. CLASSIFICATION ON THE BASIS OF HOST ORGANISM However, others may infect a small range of hosts, such as poliovirus which can infect various primates, and the designation here must reflect this rather than name a single species. The most serious difficulty arises with viruses which infect and replicate within very different species. This can be seen with certain viruses which can infect and replicate within both plants and insects.

56. CLASSIFICATION ON THE BASIS OF HOST ORGANISM Designation of a virus by the host it infects is therefore not always straightforward. Overriding all of these difficulties is the problem that even if a number of viruses infect a single species, This characteristic does not imply any other similarities in terms of disease or genetic makeup of the various viruses

57. Classification on viral structure When viruses were first visualized in the electron microscope, defining classification groups on the basis of the observed particle shape or morphology was relatively simple. A key structural feature is whether or not the virus particle has a lipid envelope and this alone can be used as a designated feature, giving enveloped and nonenveloped viruses. If the virion is nonenveloped three morphological categories are defined, isometric, filamentous, and complex. Isometric viruses appear approximately spherical but are actually icosahedrons or icosadeltahedrons.

58. Classification on viral structure While a classification scheme based on morphology is simple and describes an unchanging feature of the virus, it suffers from several drawbacks. Primary amongst these is that knowing the shape of a virus particle does not allow us to predict anything about the biology, pathology, or molecular biology of similarly shaped viruses. Thus, two viruses with very similar morphologies may differ in all of their other fundamental Characteristics For example, the polyomaviruses and the papillomaviruses

59. THE VIROSPHERE The International Committee on Taxonomy of Viruses (ICTV) published their eighth report in 2005. More than 5450 viruses arranged in greater than 2000 species, 287 genera, 73 families, and three orders are described. While this is a notable achievement, it is not a complete one – the pace of discovery of new viruses and characterization of the genes they encode ensures that the number will change. Further, it is increasingly evident that the very nature of virus replication and association with their hosts leads to complications not found in classification schemes for cell-based life.

60. THE VIROSPHERE The best generalization that can be made concerning virus classification is that It depends on analysis of a number of features, and the importance of such features may vary depending upon the use being made of the classification. A classification scheme that combines the Baltimore basis along with the nature of the host and detailed genetic characterization of critical viral proteins can be combined to generate a global view of viruses as a virosphere

61. The virosphere. Classifi cation of a major portion of the currently known genera of viruses (– viridae ) using criteria defi ned by the International Committee on the Taxonomy of Viruses. Major groupings are based on the nature of the viral genome and the nature of the host.

62. Virus Transmission Spread of virus

63. Virus Transmission A minimum proportion of the virions produced in infected hosts must be transmitted to new hosts in which more virions can be manufactured. If this does not happen the virus will die out. The only other possibility for the survival of virus genes is for them to be maintained in cells as nucleic acids, which are replicated and passed on to daughter cells when the cells divide.

64. Virus Transmission Viruses of bacteria and other microbial hosts are released from infected cells into the environment of the host, where further susceptible cells are likely to be present. These viruses are dependent upon chance encounters with susceptible cells, To which they may bind if receptors on the surface of those cells come into contact with virus attachment sites.

65. Virus Transmission Viruses of multicellular animals and plants must also find new cells to infect. An infection may spread to adjacent cells, or to cells in a distant part of the host after transport in the blood of an animal or in the phloem of a plant, But ultimately a virus must find new hosts to infect if it is to survive.

66. Virus Transmission On their journeys between hosts viruses may have to survive adverse conditions in an environment such as air, water or soil; There are some viruses, however, that can be transmitted to new hosts without ‘seeing the light of day’, in other words without exposure to the outside environment. These are viruses that can be transmitted directly from host to host, Also included in this , transmitted directly from a parent to members of the next generation. Transmission in these cases is said to be vertical; otherwise it is described as horizontal

67. Virus Transmission Viruses may be moved over long distances in a variety of ways. Rivers and winds can move viruses to new areas. The foot and mouth disease outbreak on the Isle of Wight, UK, in 1981 was initiated by virus that had spread via the air from Brittany, more than 250 km away. Viruses of birds, fishes, humans and other hosts are transported within their hosts to other parts of the planet as a result of migration, travel and animal export, for example Bird migration (avian influenza viruses) Human travel (SARS virus) Animal export (monkeypox virus).

68. Virus Transmission In theory, a single virion can initiate an infection, but in practice it is often found that a host must be inoculated with a minimum number of virions in order for that host to become infected. The reasons for this are probably many and varied, and may include some virions being defective and some being inactivated by the host’s immune systems. This minimum amount of virus required for infection of a host is known as the minimum infective dose.

69. Transmission via vectors: General principles Many viruses of plants and animals are transmitted between hosts by organisms that feed on them; these organisms act as vectors. The principle of vector transmission is that the vector acquires a virus when it feeds on an infected host and subsequently transmits the virus to one or more new hosts. Some viruses are transmitted after virions have become attached to the mouthparts of their vectors during feeding. Transmission in this way may occur within seconds or minutes of the vector acquiring virus.

70. Transmission via vectors: General principles Many vector-transmitted viruses, however, cross the gut wall of the vector and enter its circulatory system. The virus ultimately reaches the salivary glands and is secreted into the saliva, which may transport virus into new hosts when the vector feeds. This mode of transmission is said to be circulative, and transmission does not occur until hours or days after the vector has acquired the virus.

71. Transmission of plant viruses Plant cells are surrounded by thick cell walls that present significant barriers to virus entry; Most plant viruses are carried across these barriers by vectors. A wide variety of organisms use plants as sources of nutrition and some of these organisms, especially invertebrates, act as virus vectors Many of the vectors (e.g. aphids, nematodes) feed by piercing cell walls and ingesting the contents, while beetles feed by biting.

72. Transmission of plant viruses The most common vectors of plant viruses are aphids, which, as we have already pointed out, feed by ingesting the contents of cells. The reader may question how an invertebrate that feeds by removing the contents of plant cells can introduce virus into cells that subsequently support replication of the virus. The answer appears to be that these vectors probe a number of cells before selecting one on which to feed, So virus may be transmitted into cells that are probed, but not significantly damaged by the vector.

73. Transmission of plant viruses The nematodes that transmit viruses are soil dwelling animals that pierce root cells and then ingest their contents. Virus transmission ceases after a nematode moults, indicating that virus does not move from its gut into its body. An interesting feature of virus vector specificity concerns transmission of viruses with different shapes by different types of nematode. Tobra viruses have rod-shaped virions and are transmitted by nematodes in the family Trichodoridae , While nepoviruses have isometric virions and are transmitted by nematodes in the family Longidoridae

74. Transmission of plant viruses The basis of some cases of plant virus-vector specificity lies in specific amino acid sequences in capsid proteins. In other cases important roles are played by virus-coded non- structural proteins (helper factors) that are synthesized in the infected plant cell. Virions may bind specifically to structures in the mouthparts of their vectors via specific sequences on the surfaces of capsids and/or helper factors.

75. Transmission of plant viruses Some plant-parasitic fungi can also act as virus vectors, for example Spongospora subterranea , which infects potato causing powdery scab disease, is a vector of potato mop-top virus. If a plant is infected with both a fungus and a virus, then virions may be taken into developing fungal spores. The virus may survive in a spore for months or years until it germinates on a new host, which then becomes infected, not only with the fungus but also with the virus. Some fungus-transmitted plant viruses have been classified in a genus, the name of which reflects their mode of transmission and the virion shape: the genus Furovirus ( fu ngus-transmitted ro d-shaped).

76. Transmission of plant viruses About 20 per cent of plant viruses can be transmitted vertically; in other words, seed can be infected, leading to infection of the next generation. Most seed-transmitted viruses are carried in the embryo, which may have acquired its infection from either an infected ovule or an infected pollen grain. Examples of viruses that can be transmitted via seed include the nepo viruses and the tobra viruses, two groups of nematode-transmitted viruses mentioned above. Many plant viruses can also be transmitted by artificial means; for example, grafting material from a virus-infected plant can introduce virus into a new host.

77. The process of infection Life history of viruses in Plants

78. The process of infection The process of infection begins with the coming together of a virus particle with its target cell, but this union occurs by different means with each of bacteriophages, plant viruses, and animal viruses. The initial interaction of animal viruses with animal cells occurs by simple diffusion, since particles the size of a virus are in constant Brownian motion when suspended in liquid. Diffusion of bacteriophage is probably also the force influencing their union with bacterial cells.

79. The process of infection By contrast, plant viruses are, in most cases, injected directly into the cell cytoplasm by the activities of virus-carrying pathogens, or else plants become infected following mechanical damage, very often as a result of wind action. Consequently, the way in which the union of virus and cell occurs is not so important in plant systems. However, viruses can also be transmitted from infected tissue to a non- infected plant from grafting, and diffusion of virus through the vascular system is most likely responsible for infection in this situation. Plants are a special case as all cells directly communicate with their neighbors, and functionally a plant behaves as a single cell.

80. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL Viruses attach to animal cells via receptor molecules found on the cell surface. These are usually proteins, but carbohydrates and, very occasionally, lipids are also used (Table 5.1). The virus–receptor interaction is highly specific, but a family of viruses may use the same receptor. One notable exception is the sugar, N -acetylneuraminic acid, which often forms the terminal moiety of a carbohydrate group of a glycoprotein or glycolipid, and is used as a receptor by members of several different families of viruses

81. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL Some viruses can use more than one type of molecule as primary receptor (e.g. reoviruses bind to the β-adrenergic receptor or N - acetylneuraminic acid). The unequivocal demonstration that a molecule serves as a receptor for virus infection requires some stringent tests

82. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL Viruses bind up to three different types of receptor molecule on the cell surface in succession. These are low affinity receptors, primary receptors and co- or secondary receptors. In principle, receptors serve to overcome any repulsive forces that may exist between the virus and the cell, To allow the virus particle to have intimate contact with the lipid bilayer of the cell membrane, and to trigger the release of the viral genome into the cell.

83. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL The first type of receptor is a high abundance molecule that has a low specificity, low affinity interaction with the virus. This serves to get the virus out of the fluid bathing the cell and in direct contact with molecules on the cell surface. Several viruses, including HIV-1, use heparans while others use the sugar, N -acetyl neuraminic acid (NANA), as their first receptor

84. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL This binding is usually followed by interactions with further cell- surface molecules that lead to infection. The binding of HIV-1 to its target cell, for example, is complex and it uses three cell receptors and three virus attachment sites. However, NANA is the sole receptor for the influenza viruses.

85. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL Some viruses can actually use non-neutralizing, virus-specific antibody as an additional receptor. The antibody binds via its constant regions to Fc receptors that certain cells have in their plasma membranes and this leads to infection. Such cells do not carry a regular virus receptor, and would not normally be infected

86. INFECTION OF ANIMAL CELLS – ATTACHMENT TO THE CELL This process is known as antibody-dependent enhancement (ADE) of infectivity. While ADE can be readily demonstrated in cells in culture, it is rare in vivo . The classic example occurs with dengue fever virus (a flavivirus). This virus normally causes a mild subclinical or febrile illness in humans but in the presence of antibody is able to infect macrophages and to cause life-threatening infections (dengue hemorrhagic fever and dengue shock syndrome).

87. INFECTION OF PLANTS The cell wall that surrounds the plasma membrane of all plant cells prevents viruses from attaching and entering them in the ways described for animal cells. Viruses can only reach the cytoplasm of plant cells when the tissue is damaged. Thus plants are infected either with the help of vectors , namely animals that feed on plants, or invading fungi, Or by mechanical damage caused by the wind or passing animals, all of which allow viruses to enter directly into cells.

88. INFECTION OF PLANTS In the laboratory, this is mimicked by the gentle application of abrasive carborundum to leaves during local lesion assays of virus- containing material Many plants that become infected naturally do so because virus- carrying animals feed upon them. However, this transmission is not a casual process which occurs whenever any animal chances to feed on an uninfected host plant after feeding on an infected one. Rather, the transmission of most plant viruses is a highly specific process, requiring the participation of particular animals as vectors.

89. INFECTION OF PLANTS Although some viruses, such as tobacco mosaic virus (TMV), require no vector and can be transmitted mechanically in a nonspecific manner, Most have a specific association with their animal vectors that feed by piercing plant tissues with their mouthparts (leafhoppers, aphids, thrips, whiteflies, mealy bugs, mites, or nematodes