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Virus.pptx
- 1. Virus Ranjeet Kumar Taram SoSin Life Science Pt. Ravishankar Shukla university Raipur
- 2. • Virus • Virusis defined as a nucleoprotein complex a small infectious agent which infect cell and uses their metabolic machinery to replicate. It is simple acellular entities. • Characteristics :- • Obligate intracellular parasites of bacteria, protozoa, algae, fungi, plants and animals. • Ultramicroscopic size ranging from 20 nm to 400 nm diameter. • All viruses have a nucleocapsid composed of a nucleic acid genome surrounded by a protein capsid. Some viruses have a membranous envelope that lies outside the nucleocapsid. • The nucleic acid of the virus can be RNA or DNA, single-stranded or double stranded, linear or circular. • Capsids may have helical, icosahedral, or complex symmetry. They are constructed of protomers that self-assemble through noncovalent bonds. • The typical virus life cycle consists of five steps: attachment to the host cell, entry into the host cell, synthesis of viral nucleic acid and proteins within the host cell, self-assembly of virions within the host cell, and release of virions from the host cell • Viruses are not affected by antibiotics ,affected only by antiviral drugs and interferons.
- 3. Historical account • TheRussian botanist Ivanovski (1892) was the first to give clear cut evidence of a virus • M.Beijerinck (1897)was first to coined the term virus. • Bacteriophages were discovered by Twort and D. Herelle(1917). • Schelsinger (1933)was the first to determine the composition of a virus. He showed that a bacteriophage consists of only protein and DNA. • In 1935, Stanley crystallized the virus causing tobacco mosaic disease and demonstrated that crystals retained their infectivity when inoculated into healthy plants. • In 1952, Hershey and Chase studied the T2 bacteriophage and demonstrated that the genetic information is carried in the phage DNA and that infection is the result of penetration of viral DNA into cells.
- 4. Classification • Virus classificationis the process of naming viruses and placing them into taxonomic system. • Before discovery:- i. Dermotrophic – infect skin cells. ii. Neurotrophic - infect nerve cells. iii. Viscerotrophic - infect digestive tract. iv. Pneumotrophic - infect respiratory system. After discovery viruses are classified on the basis of – Types and structure of their nucleic acid. Method of replication. Host range. Chemical and physical characteristics.
- 5. • ICTV(International committeeon Taxonomy of viruses) is responsible for the classification of the viruses. • Suffixes used for classification – • Taxa Suffix For ex. –Rhabdovirus Realm Viria Riboviria Kingdom Virae Orthonavirae Phylum Viricota Negarnaviricota Class Viricetes Monjiviricetes Order Virales Mononegavirales Family Viridae Rhabdoviridae Genus Virus Rhabdovirus
- 6. • On thebasis of morphology virus capsids are classify as – 1. Icosahedral capsid – in this type of capsid 20 triangular faces and 12 corner or vertices are present with regularly arranged unit called capsomers and nucleic acid is densely coiled. a) Naked capsid – Adeno virus, Polio virus. b) Enveloped capsid - Herpes Simplex virus. 2. Helical capsid – in this type of capsid shaped like hollow tube with protein walls. Protomers are arranged helical or spirals and produce long rigid tube like structure and capsid enclosed nuclear material. a) Naked capsid – TMV, bacteriophage tail. b) Enveloped capsid – Influenza virus. 3. Complex capsid – most viruses have either icosahedral or helical symmetry but some viruses are not classified as above they placed in the complex capsid category. Ex.- Bacteriophage, Vaccinia virus, Pox virus etc.
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- 8. Baltimore classification • DavidBaltimore and Howard Temin gave the Baltimore classification system. • This classification is based on genome type and mode of replication and transcription. Class Description of genome and replication strategy Example I Double stranded DNA (ds DNA) Herpes virus, Pox virus II Single stranded DNA (ss DNA) Pervovirus III Double stranded RNA (ds RNA) Reovirus IV Single stranded RNA with positively sensed (+ss RNA) Picornavirus, Flavivirus V Single stranded RNA with negatively sensed (-ss RNA) Influenza virus, Rhabdovirus VI Single stranded RNA genome that replicated with DNA intermediate (ss RNA- RT) Retrovirus VII Double stranded DNA genome that replicates with RNA intermediate (ds DNA) Hepadnavirus, Hepatitis B virus
- 9. Tobacco Mosaic virus(TMV) • Introduction • TMV is the most serious plant pathogen causing mosaic on tobacco plant. • It is a plant virus that have positive single stranded RNA that infects a wide range of plant especially tobacco and Solanaceae family. • TMV is the most resistant virus known so far of which the thermal death point is 90˚C for 10 min. • This is the first virus that was crystallized in 1935 by W. M. Stanley. Kingdom Orthonavirae Phylum Kitrinoviricota Class Alsuviricetes Order Martellivirales Family Virgaviridae Genus Tobamovirus Species Tobacco mosaic virus Classification
- 10. • Structure :- •It is a rod shaped helical virus about 300 nm long and 15-18 nm in diameter. • It consist of capsid made from 2130 capsomeres arranged in a hollow right handed helix. • It contains a single stranded RNA of 6400 nucleotide. • Each protein subunit is made up of a single polypeptide chain consisting of 158 amino acid residue whose sequence has been established. • This protein self assemble to form a hairpin loop structure. • The molecular weight of TMV is 2.06x106 Dalton.
- 11. • Mode ofinfection:- • TMV enters plants through wounds, Damage to the plant cell membrane and permit entry of infectious particle into cytoplasm. • The virus spreads from an initial infection site to all parts of the plant via the phloem, the plants nutrient transport network. • It is also transported by mechanical means in the field by wind or water. Fig.- Pathogenicity of TMV
- 12. • Symptoms • Symptomsinclude mosaic pattern on leaves, mottling, necrosis and leaf curling. • The lighting of leaf color among the veins in early stage. • In later stage, it turn into light and dark green mosaic symptoms. • Yellow streaking of leaves.(especially monocots) • Yellow spotting on leaves.
- 13. • Control • TMVoccurs in tobacco growing areas so it is controlled by crop rotation. • Crop rotation should also be employed to avoid infected soil/ seed beds for at least two years. • One of the common control methods for TMV is sanitation, which includes removing infected plants and washing hands in between each planting. • As for any plant disease, looking for resistant strains against TMV may also be advised. • The proliferation of aphids will aid in the spread of foliar diseases, and killing them can effectively reduce the rate of foliar disease infection. Aphid control can be carried out with the choice of oxaliplatin, vanillin, imidacloprid, etc. • Spraying with disinfectant can be used for prevention during agricultural processes such as leaf-cutting, seed removal, and topping, and can last for two weeks at a time.
- 14. Cucumber Mosaic Virus(CMV) • Introduction Cucumber mosaic virus (CMV) is one of the most widespread and troublesome viruses infecting cultivated plants worldwide. The virus is made up of many and varied strains that differ in a number of aspects including host range, symptoms, and means of transmission. The strains of CMV are differentiated on the basis of symptoms on indicator host plants. Classification Realm Riboviria Kingdom Orthornavirae Phylum Kitrinoviricota Class Alsuviricetes Order Martellivirales Family Bromoviridae Genus Cucumovirus
- 15. • Structure • Virion-non-enveloped, spherical virion about 29 nm in diameter with T=3 icosahedral symmetry, composed of 180 coat proteins, 12pentamers and 20 hexamers. • The capsid is composed of 60 asymmetric units made of 3 protein (T=3) ,for a total 180 capsid proteins.
- 16. • Genome- segmented,tripartite linear positively sensed ss RNA(+). • Its genome size is 8.623 kb and it is divided among RNA1(3357bp), RNA2(3050 bp) and RNA3(2216 bp), all of which has a tRNA-like structure and 5’ cap. • These three RNAs encode five proteins, proteins 1a, 2a, 2b, movement protein (MP) and coat protein (CP). • proteins 1a and 2a are responsible for the replication of the virus, protein 2b is the host- silencing suppressor(viral suppressor of RNA silencing VSR).
- 17. Mode of infection •Virus transmission- • Arthropods: - CMV is vectored and transmitted by cucumber beetles and more than 60 species of aphids. • Mechanically: - CMV is readily transmitted between plants via plant sap and by mechanical inoculation via pruning tools. • Seeds: - Transmission to new plants through seeds occurs to varying degrees for 19 host species, including some important weeds. • Parasitic seed plants:- This virus can also be transmitted between plants by parasitic seed plants such as dodder (Cuscuta spp.), whose vine-like stems bridge the hosts aerially or at the ground surface.
- 18. Life cycle ofvirus in host plant. 1.Virus penetrates into the host cell. 2.Uncoating, and release of the viral genomic RNA into the cytoplasm. 3.Expression of protein 1a and 2a to produce replication proteins. 4.Replication occurs in viral factories made of membrane vesicles derived from the ER (spherules). A dsRNA genome is synthesized from the genomic ss RNA(+). 5.The dsRNA genome is transcribed/replicated thereby providing viral mRNA/new ssRNA(+) genomes. 6.Subgenomic RNA4 is translated producing capsid proteins. 7.Assembly of new virus particles. 8.Viral movement protein triggers the formation of tubular structures that mediate virion cell-to-cell transfer via a tubule-guided mechanism.
- 19. • Symptoms Cucurbit plantsmay become infected at stage of growth, from emergence of the seedling to near maturity. CMV symptoms in cucumber are more severe on plants exposed to short days or reduced light than on plants exposed to long days and bright light. Cucurbit plants rarely become infected in the seedling stage. When this happens, the cotyledons may turn yellow and wilt. New leaves are slightly mottled a yellowish green, remain small, wrinkled, and distorted. Plants infected in the seedling stage remain dwarfed or may die. Leaves are often stunted, distorted, crinkled, and curled downward. Vines are sometimes dwarfed and may be yellowish near the center of the hill and "bunchy" because of shortening of the stem between
- 21. • Disease management •Manage infected weeds and alternate hosts for CMV and vectors before planting. • Exclude CMV from production houses. Exclusion in a production house means physically preventing CMV from infecting susceptible hosts. • Manage aphids and CMV in production houses before out planting. Establish host-free zones around production houses by using cement, mulch, rocks, or herbicides to reduce nearby vector and virus populations. Apply insecticides within production houses to minimize vector numbers. • Plant CMV-resistant host varieties. Resistant plants are the best management practice, because they require fewer inputs, are easy to use, and don’t have adverse effects on the environment. • Fumigate greenhouses regularly to control aphids and other insects. • Apply insecticides regularly in and around the greenhouse, garden, or field to eliminate aphids, cucumber beetles, and other insects. It is important to kill insects before they have an opportunity to infect vine crops and move from plant to plant in a cucurbit planting.
- 22. Human Immunodeficiency Virus(HIV) • The human immunodeficiency virus is a lentivirus that causes the acquired immunodeficiency syndrome (AIDS), a condition in humans in which progressive failure of the immune system allows opportunistic infections and cancers to prosper. • Unlike some other viruses, the human body cannot get rid of HIV. That means that once you have HIV, you have it for life. • Scientists identified a type of chimpanzee in West Africa as the source of HIV infection in humans. They believe that the chimpanzee version of the immunodeficiency virus (called simian immunodeficiency virus, or SIV) most likely was transmitted to humans and mutated into HIV when humans hunted these chimpanzees for meat and came into contact with their infected blood. HIV was first described in USA in 1981 amongst homosexuals, Haitians and heroine addicts. Realm Ribovira Kingdom Pararnavirae Phylum Artverviricota Class Revtraviricetes Order Orthovirales Family Retroviridae Subfamily Orthoretrovirinae Genus Lentivirus Species HIV1 /HIV2
- 23. Morphology • It isroughly spherical - diameter of about 120 nm. • Composed of two copies of positive single stranded RNA (Held together by protein P7) enclosed by a conical capsid composed of viral protein P24 • Very high genetic variability. • The RNA genome consists of 9 genes - Three of these genes: gag, pol, and env, contain information needed to make the structural proteins for new virus particles. • Inside of capsid are three enzymes required for HIV replication: reverse transcriptase, integrase and protease. • A matrix composed of the viral protein P17 surrounds the capsid ensuring the integrity of the virion particle. • The matrix is surrounded by phospholipids – 2 layers – Embedded by 70 copies of a complex HIV protein (glycoprotein) – Spikes: 2 units – Gp41 and Gp120.
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- 27. • Attachment-Attachment ofvirus into the host cell by Specific binding of the virus to the CD4 receptors is by the envelope glycoprotein gp120. • Cell to cell fusion – For infection to take place the cell fusion is essential. • This is brought about by the transmembrane glycoprotein gp 41. HIV-1 utilizes two major co- receptors along with CD4 to bind to, fuse with, and enter target cells; these co-receptors are CCR5 and CXCR4, which are also receptors for certain endogenous chemokines. • Strains of HIV that utilize CCR5 as a co-receptor are referred to as macrophage tropic viruses (M –tropic viruses) • Strains of HIV that utilize CXCR4 are referred to as T - tropic viruses. • Many virus strains are dual tropic in that they utilize both CCR5 and CXCR4. • Uncoating of the viral envelope and entry of nuclear capsid core into the cell , After fusion of virus with the host cell membrane, HIV genome is uncoated and internalized in to cell. Viral RNA is released into the core cytoplasm Life cycle of HIV
- 28. • Viral transcription •Viral reverse transcriptase mediates transcription of its RNA. • RNA-DNA hybrid is formed . • Original RNA strand is degraded by ribonuclease H, followed by. • Synthesis of second strand of DNA to yield double strand HIV DNA. • Integration into the host DNA • The double stranded DNA bis integrated in to the genome of the infected host cell through the action of the viral integrase enzyme , causing a latent infection. • Fate of provirus • From time to time, lytic infection is initiated releasing progeny virions, which infect other cells. • The long and variable incubation period of HIV is because of the latency. • In an infected individual the virus can be isolated from the blood , lymphocytes, cell free plasma, semen , cervical secretion, saliva, urine and breast milk.
- 29. • Transcription backinto RNA • The viral DNA is transcribed into RNA and multiple copies of viral RNA are produced. • There are only nine gene in HIV RNA, and these code for the production of structural proteins, accessory proteins and enzymes that essential for the virus's replicative cycle. • Virion assembly- With the help of viral protease the new virion are assembled into the polypeptide sequences needed for HIV virion formation and infectivity. • Cell lysis- the infected cell is made to burst open, presumably by the action of cellular proteins.
- 31. Treatment • There aretwo principal approaches to treatment :- immunotherapy and anti-HIV drug treatments. • A. Immunotherapy:- Immunotherapy is transfusion based treatment designed to replace lost immunoglobulins needed to fi ght HIV infection (passive immunotherapy), to provide cellular factors such as interleukins (IL2) or to introduce selected or altered immune cells to attack cells harboring the virus (adoptive im munotherapy). • B. Anti-HIV drug treatment:- • Treatment with anti-HIV drugs attempts to reduce viral load by blocking new infection in the host cell. • The drugs target two major enzymes of HIV which are needed for the infection cycle: Reverse transcriptase and Proteases. • Ex.- Nucleoside Reverse transcriptase inhibitor- zydovudine, stavudine. • Non-nucleoside Reverse Transcriptase inhibitor – Efavirenz, Nevirapine. • Protease inhibitor – Atazanavir, Darunavir.
- 32. Treatment C. Combination Treatment:- Since reverse transcriptase inhibitors and protease inhibitor address different stage of viral replication, using both families of drugs in combination has been shown to be more effective than monotherapy in impending the spread of HIV in the body and reducing viral loads. This communication of two reverse transcriptase inhibitor, one of which is a thymidine analogue, and a protease inhibitor, block infection both before and after integration and in both activated and resting T cells. This combinational therapy is termed as highly active anti-retroviral therapy. D. In future :- In addition to the positive results shown by combination therapy trials, a number of development may hold promise for the near future. These include genetically engineered killer T cells which attack HIV before it reproduces, and research into genetically deactivating the CXCR4 and CCR5 T cell co-receptors, which are a path for HIV entry into cells.
- 33. Prevention • There isno vaccine to prevent HIV infection and no cure for AIDS. But it is possible to protect ourself and other from infection. • It means educating everyone about HIV and avoid any behavior that allows HIV infected fluids into our body.
- 34. Herpes virus • Herpesis the name of a group of viruses that causes painful blister and sore. • These viruses are enveloped and show host specificity. • They are double stranded DNA viruses with relatively large complex genomes and replicate in the nucleus of a wide range of vertebrate hosts. • Herpes simplex is a viral infection that typically affects the mouth, genital or anal area . • It is contagious and can cause outbreak of sores and other symptoms. • These are blister that develop on the surface of the skin and may be itchy or uncomfortable. • Herpes virus have ability to persist indefinitely in their host by establishing latent infection that may lead to recurrent symptoms. Classification Realm Duplodnaviria Kingdom Heunggongviriae Phylum Peploviricota Class Hervivicetes Order Herpesvirales Family Herpesviridae Genus Simplex virus
- 36. Morphology • All herpesvirusvirions have four structural elements:- • Core. The core consists of a single linear molecule of dsDNA in the form of a torus. • Capsid. Surrounding the core is an icosahedral capsid with a 100 nm diameter constructed of 162 capsomeres. • Tegument. Between the capsid and envelope is an amorphous, sometimes asymmetrical, feature named the tegument. It consists of viral enzymes, some of which are needed to take control of the cell's chemical processes and subvert them to virion production, some of which defend against the host cell's immediate responses, and others for which the function is not yet understood. • Envelope. The envelope is the outer layer of the virion and is composed of altered host membrane and a dozen unique viral glycoproteins. They appear in electron micrographs as short spikes embedded in the envelope.
- 37. Morphology Genome structure The herpesvirus genome contain a non- segmented, linear , ds- DNA molecule. Genome length range approximately 120 to 250 kbp and encode for 60-120 genes. HSV-1 and HSV-2 each contain at least 74 genes within their genome. These genes encode a variety of proteins involved in forming the capsid, tegument and envelope of the virus, as well as controlling the replication and infectivity of the virus.
- 38. Life cycle ofHerpes virus
- 39. Pathogenicity Stages Of Infections:-their are different stages of infection:- (i) Primary Stage :- This stage starts 2 to 8 days after infection. The area under the blister will be red and painful, the fluid in the blister may be cloudy. The blister break and become open sores. (ii) Latent Stage:- during this stage, there are no blister, sores or other symptoms. The virus is travelling from skin into the nerves . (iii) Shedding Stage:- in the shedding stage, the virus starts multiplying in the nerve ending. If these nerve ending areas of the body that are in contact with body fluids, include- saliva, semen or vaginal fluid , this means that herpes is very contagious during this stage.
- 40. • Treatment • Infectionswith herpes simplex virus 1 and 2 and varicella-zoster virus are currently the most amenable to therapy; acyclovir, valaciclovir and famciclovir are all licensed therapeutics. • Alternatively, zinc containing cream or slightly anesthetic cream can be applied. • Prevention • People with active symptoms of oral herpes should avoid oral contact with other. • A vaccine to prevent varicella-zoster virus infections was recently licensed in the United States. Vaccines against herpes simplex virus 2, and cytomegalovirus are undergoing extensive evaluations in field trials. • Passive immunization with immunoglobulin or hyperimmune globulin is used either to prevent infection or as an adjunct to antiviral therapy.
- 41. Pox virus • Introduction •Term “pox” derives from English pocks, blister like skin lesions. • Pox virus infection typically result in the formation of lesions, skin nodules or disseminated rashes. • Family pox virideae causes various disease, small pox is one of them. • Small pox is an infectious, contagious and some times fatal disease unique only in human. • It is caused by either of two Variola virus:- • 1.Variola major • 2. Variola minor. Classification Realm Varidnaviria Kingdom Bamfordvirae Phylum Nucleocytoviricota Class Pokkesviricetes Order Chitovirales Family Poxviridae Genus Orthopoxvirus Species Variola virus
- 42. Morphology • Pox virusare largest virus, size 300x200x100 nm with a single linear double stranded DNA genome 186 kbp in size and containing a hairpin loop at each end. • It consist of central biconcave DNA core. • Brick or oval shape.
- 43. Life cycle ofPox virus Abbreviation:- EEV- External Enveloped Virion IEV- Intracellular Enveloped Virion IMV- Intracellular Mature Virion CEV- Cell-associated Enveloped Virion
- 44. Even though theyare DNA viruses, poxviruses replicate in the cytoplasm. Accordingly, they are only minimally dependent on the host cell for DNA and RNA replication, and they encode their own proteins for these processes. • Step 1- attachment and entry of EEV- The mechanisms by which either the IMV or the EEV infectious forms of vaccinia virus attach to and enter susceptible host cells are not well understood and will be constrained by the number of membranes enveloping the virus. After fusion of the viral and cellular membranes, primary uncoating takes place, and the viral core is released into the cytoplasm. • Step 2- All later steps in the infectious cycle take place in this cellular compartment. The core contains, in addition to the viral genome, the viral DNA-dependent RNA polymerase, the ‘‘initiation’’ proteins necessary for specific recognition of the promoters of viral early genes, and several RNA processing enzymes that modify viral transcripts. Life cycle of Pox virus
- 45. • Step 3-On release into the host-cell cytoplasm, the core synthesizes viral early mRNAs, which exhibit the features typical of cellular mRNAs and are translated by the cellular protein- synthesizing machinery. Approximately half of the viral genes are expressed during this early phase of infection. • Step 4- Some early proteins are secreted from the cell and have sequence similarity to cellular growth factors, which can induce proliferation of neighboring host cells, or are proteins that counteract host immune defense mechanisms. • Step 5 - The synthesis of early proteins also induces a second uncoating reaction in which the core wall opens and a nucleoprotein complex containing the genome is released from the core. • Step 6- This core disassembly leads to cessation of viral early gene expression. Other early proteins catalyze the replication of the viral DNA genome.
- 47. • Step 7and8 - Newly synthesized viral DNA molecules can serve as templates for additional cycles of genome replication , and they are the templates for transcription of viral intermediate- phase genes. • Step 9 -The activation of transcription of intermediate genes also requires specific viral proteins (the products of early genes) that confer specificity for intermediate promoters on the viral RNA polymerase, as well as a host-cell protein (Vitf2) that relocates from the infected cell nucleus to the cytoplasm. • Step 10- The proteins encoded by intermediate mRNAs include those necessary for transcription of late-phase genes. The latter genes encode the proteins from which virions are built as well as the virion enzymes and other essential proteins, such as the early initiation proteins, that must be incorporated into virus particles during assembly.
- 48. • Step 11– once these protein are synthesized by the cellular translation machinery the assembly of progeny virus particles begins. • Step 12- The viral membrane proteins are un- glycosylated, and the role of cellular membranes in early stages of assembly is controversial. • Step 13- The initial assembly reactions result in formation of the immature virion , which is a spherical particle delimited by a membrane that may be acquired from an early compartment of the cellular secretory pathway. • Step 14&15- This virus particle matures into the brick shaped IMV, which is released only on cell lysis.
- 49. • Step 16-However, the particle can acquire a second, double membrane from a trans Golgi or early endosomal compartment to form the intracellular enveloped virion (IEV) . • Step 17- The IEVs move to the cell surface on microtubules where fusion with the plasma membrane forms cell-associated virions (CEV). • Step 18- These CEV induce an actin polymerization that promotes a direct transfer to surrounding cells; they can also dissociate from the membrane as EEV.
- 51. Pathogenicity:- This is airbornedisease therefore it spread readily. Incubation period 7-17 days. Initial symptoms (Prodrome) duration – 2 to 4 days which is sometimes contagious Early rash – (duration: about 4 days) most contagious Rash distribution Pustular rash – (duration: about 5 days) –contagious pustules and scabs –(duration: about 5 days)- contagious resolving scabs – (duration : about 6 days)- contagious Scabs resolved – not contagious smallpox may be most contagious during prodrome phase. Most infectious during the first 7 to 10 days following rash onset .
- 52. Mode of infection:- Prolongedface-to-face contact with someone who has smallpox . Direct contact with infected bodily fluids or an object such as bedding or clothing that has the virus on it. Exposure to an aerosol release of smallpox (the virus is put in the air ). Treatment There is no proven treatment for small pox. Prevention • The smallpox vaccine is made from a virus called vaccinia which is a pox type virus related to smallpox . • The smallpox vaccine contain “live” vaccinia virus – not dead virus like many other vaccines. • Edward Jenner (1796)- first successful vaccine to be developed against smallpox using cowpox virus(variolation) . • The only smallpox vaccine currently licensed by the food and drug administration is Dryvax .
- 53. • One ofthe most serious bioterrorist threats. • It is used as a biological weapon during the French and the Indian wars(1774 to1776)when British soldiers distributed smallpox infected blankets to American Indians . • several factors contribute to the concern about the use of smallpox as a biological weapon 1) Variola can spread easily from person to person. 2) There is no widely available or licensed treatment for the disease . 3) High fatality rate. 4) Variola is relatively stable as an aerosol. 5) Infectious dose is small. Small pox as biological weapon
Editor's Notes
- #17 Genomic RNA serves as messenger RNAs. RNA1 and RNA2 encode respectively proteins 1a and 2a, both involved in genome replication and internal transcription of sgRNA4 from the minus-strand copy of RNA3. RNA3 and sgRNA4 are translated respectively into movement and capsid proteins. ORF2b encodes a viral suppressor of RNA silencing (VSR) and is expressed probably as a subgenomic RNA (sgRNA4A).
- #37 The enveloped virion measures about 200 nm and the naked virion about 100 nm.