Viral molecular genetics
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The document discusses the different types of nucleic acids that viruses can use to store their genetic information, including double-stranded DNA, single-stranded DNA, double-stranded RNA, negative-sense RNA, positive-sense RNA, and positive-sense RNA retroviruses. It provides details on how each type replicates and produces viral mRNA.
Viral molecular genetics
- 1. Viral Genetics Viruses can store their genetic information in six different types of nucleic acid which are named based on how that nucleic acid eventually becomes transcribed to the viral mRNA Only a (+) viral mRNA strand can be translated into viral protein
- 2. Viral Genetics (+/-) double-stranded DNA DNA-dependent DNA polymerase enzymes copy both the (+) and (-) DNA strands DNA-dependent RNA polymerase enzymes copy the (-) DNA strand into (+) viral mRNA Examples include most bacteriophages, Papovaviruses, Adenoviruses, and Herpesviruses
- 3. Replication of a Double-Stranded DNA Viral Genome and production of Viral mRNA
- 4. Viral Genetics (+) single-stranded DNA DNA-dependent DNA polymerase enzymes copy the (+) DNA strand of the genome producing a dsDNA intermediate DNA-dependent RNA polymerase enzymes copy the (-) DNA strand into (+) viral mRNA Phage M13 and Parvoviruses
- 5. Replication of a Single-Stranded DNA Viral Genome and Production of Viral mRNA
- 6. Viral Genetics (+/-) double-stranded RNA RNA-dependent RNA polymerase enzymes copy both the (+) RNA and (-) RNA strands of the genome producing a dsRNA genomes RNA-dependent RNA polymerase enzymes copy the (-) RNA strand into (+) viral mRNA Reoviruses
- 7. Replication of a Double-Stranded RNA Viral Genome and Production of Viral mRNA
- 8. Viral Genetics (-) RNA RNA-dependent RNA polymerase enzymes then copy the (+) RNA strands producing ss (-) RNA viral genome RNA-dependent RNA polymerase enzymes then copy the (+) RNA strands producing ss (-) RNA viral genome Orthomyxoviruses, Paramyxoviruses, Rhabdoviruses
- 9. Replication of a Single-Stranded Minus RNA Viral Genome and Production of Viral mRNA
- 10. Viral Genetics (+) RNA RNA-dependent RNA polymerase enzymes copy the (+) RNA genome producing ss (-) RNA RNA-dependent RNA polymerase enzymes then copy the (-) RNA strands producing ss (+) RNA viral genome Picornaviruses, Togaviruses, and Coronaviruses
- 11. Replication of a Single-Stranded Plus RNA Viral Genome and Production of Viral mRNA
- 12. Viral Genetics (+) RNA Retroviruses reverse transcriptase enzymes (RNA-dependent DNA polymerases) copy the (+) RNA genome producing ss (-) DNA strands DNA-dependent DNA polymerase enzymes then copy the (-) DNA strands to produce a dsDNA intermediate DNA-dependent RNA polymerase enzymes then copy the (-) DNA strands to produce ss (+) RNA genomes DNA-dependent RNA polymerase enzymes copy the (-) DNA strand into (+) viral mRNA HIV-1, HIV-2, and HTLV-1
- 13. Replication of a Single-Stranded Plus RNA Viral Genome and Production of Viral mRNA by way of Reverse Transcriptase
- 14. Viral Genetics Viruses grow rapidly, there are usually a large number of progeny virions per cell. There is, therefore, more chance of mutations occurring over a short time period Viruses undergo genetic change by several mechanisms Genetic drift: where individual bases in the DNA or RNA mutate to other bases Antigenic shift: where there is a major change in the genome of the virus. This occurs as a result of recombination
- 15. Mutants Spontaneous mutations These arise naturally during viral replication (Replication, Tautomeric base pairing) DNA viruses tend to more genetically stable than RNA viruses (DNA repair) Induced mutation by physical (UV light or X-rays) or chemical means (nitrous acid)
- 16. Mutants Types of mutation point mutants insertion/deletion mutants
- 17. Phenotypic changes seen in virus mutants Conditional lethal mutants:These mutants multiply under some conditions but not others A.temperature sensitive B.host range
- 18. Phenotypic changes seen in virus mutants Plaque size :may be larger or smaller than in the wild type virus Drug resistance: The possibility of drug resistant mutants arising must always be considered Enzyme-deficient mutants: Some viral enzymes are not always essential and so we can isolate viable enzyme-deficient mutants
- 19. Phenotypic changes seen in virus mutants "Hot" mutants These grow better at elevated temperatures than the wild type virus. They may be more virulent since host fever may have little effect on the mutants but may slow down the replication of wild type virions
- 20. Phenotypic changes seen in virus mutants Attenuated mutants Many viral mutants cause much milder symptoms (or no symptoms) compared to the parental virus - these are said to be attenuated vaccine development
- 21. Recombination Exchange of genetic information between two genomes "Classic" recombination :This involves breaking of covalent bonds within the nucleic acid, exchange of genetic information, and reforming of covalent bonds This kind of break/join recombination is common in DNA viruses or those RNA viruses which have a DNA phase (retroviruses). The host cell has recombination systems for DNA
- 22. Recombination Recombination of this type is very rare in RNA viruses (No host enzymes) "copy choice" kind of mechanism in which the polymerase switches templates while copying the RNA So far, there is no evidence for recombination in the negative stranded RNA viruses giving rise to viable viruses
- 23. Recombination
- 24. Reassortment Reassortment is a non-classical kind of recombination If a virus has a segmented genome and if two variants of that virus infect a single cell, progeny virions can result with some segments from one parent, some from the other This is an efficient process - but is limited to viruses with segmented genomes orthomyxoviruses, reoviruses, arenaviruses, bunya viruses
- 25. Reassortment
- 26. Applied genetics vaccine called Flumist for influenza virus The vaccine is trivalent – it contains 3 strains of influenza virus cold adapted strains: grow well at 25 degrees C ,grow in the upper respiratory tract temperature-sensitive and grow poorly in the warmer lower respiratory tract viruses are attenuated strains and much less pathogenic than wild-type virus
- 27. Applied genetics The vaccine technology uses reassortment to generate reassortant viruses which have six gene segments from the attenuated, cold-adapted virus and the HA and NA coding segments from the virus which is likely to be a problem in the up-coming influenza season
- 28. Applied genetics
- 29. Complementation Interaction at a functional level NOT at the nucleic acid level two mutants with a ts (temperature-sensitive) lesion in different genes neither can grow at a high temperature infect the same cell with both mutants, each mutant can provide the missing function of the other and therefore they can replicate
- 30. Multiplicity reactivation If double stranded DNA viruses are inactivated using ultraviolet irradiation, we often see reactivation if we infect cells with the inactivated virus at a very high multiplicity of infection?
- 31. Defective viruses Defective viruses lack the full complement of genes necessary for a complete infectious cycle (many are deletion mutants) they need another virus to provide the missing functions - this second virus is called a helper virus
- 32. Defective interfering particles The replication of the helper virus may be less effective than if the defective virus (particle) was not there This is because the defective particle is competing with the helper for the functions that the helper provides This phenomenon is known as interference, and defective particles which cause this phenomenon are known as "defective interfering" (DI) particles Not all defective viruses interfere, but many do
- 33. Phenotypic mixing If two different viruses infect a cell, progeny viruses may contain coat components derived from both parents and so they will have coat properties of both parents IT INVOLVES NO ALTERATION IN GENETIC MATERIAL We can also get the situation where a coat is entirely that of another virus