topic 16 Flashcards
contrast bacterial growth with viral growth? What are the different periods of viral growth?
Cells reproduce by fission of a parental cell–>fast steady growth
• Viruses reproduce by de novo assembly of newly synthesized components
eclipse period-Virus infects cell so you can see some viruses,virus disassembles and thus while its making its machinery you don’t see any viruses
exponential growth period (viruses are being assembled
What are 4 viral replication patterns?
- Lytic infection: Accumulation of viruses in the cell followed by rupture of the cell (lysis) to release progeny viruses (e.g., Adenovirus). Also called an acute infection-it eventually ends.
- Persistent infection: An infection that lasts indefinitely.
- Chronic infection: A persistent infection in which viral replication is continuous (e.g., Hepatitis C virus, Hepatitis B virus).
- Latent infection: A persistent infection in which viral production is not continually present (e.g. Herpesvirus). Viral gene expression is shut off and the virus “hides” in the cell. Viral replication can reactivate and start lytic replication. The cell types supporting latent and lytic phases of a viral infection are not necessarily the same.
What are 2 types of viral genetic change with two examples of each?
• Two types of genetic change:
–Mutations
- Nucleotide substitution
- Insertion or deletion
–Recombination (between 2 similar viruses in the same cell)
- Molecular recombination (crossing over)
- Reassortment (exchanging segments)
What are the results of viral genetic changes?
• Results of genetic changes:
–Silent mutations
–Lethal mutations
–Adaptive mutations
–Immune escape
–Drug resistance
–Tropism changes (which species it infects)What are viral mutation rates?
• Viral mutation rates vary greatly
–Most DNA viruses mutate at ~1x10-8 to 1x10-9 mutations per base pair per replication cycle
–RNA viruses mutate at ~1x10-3 to 1x10-4
–Cellular DNA mutates at ~1x10-10
• High error rate (generation size, generation time) results in very rapid evolution
What determines the accumulation of mutations in a viral population?
• Accumulation of mutations in a viral population depends on:
–Mutation rate
–Viral replication rate
–Selective pressure on the virus
- Rapidly replicating viruses evolve more rapidly
- Viruses with high mutation rates evolve more rapidly
What determines the final product of viral mutations?
• A virus will evolve to a “most fit” genotype in a
host
• A virus population will evolve to a “most fit”
genotype for the host population
What are quasispecies?
Many viral mutation rates are greater than 1 mutation per genome per replication cycle.
These high mutation rates and selective pressures create quasispecies (basically, even within a species, the individual viruses are quite different, hence quasispecies instead of species)
This often leads to effecient immune evasion and rapid development of drug resistance (because even before the immune response starts or a drug is given, there is probably already a resistant virus due to the great amount of variability that already exists)
What are defective viruses?
• Most viral particles produced during an
infection are not infectious –100’s of defective particles per functional particle is common
• Complementation can permit defective genomes
to persist in the viral population
What are 5 host factors governing viral spread and some subfactors of each?
- Population density –Higher density increases transmission rate
- Social factors –Housing arrangements –Dietary habits, overall nutrition –Cyclical mobility –Social attitudes
- Herd immunity –Proportion of the population that is resistant to a pathogen –High herd immunity greatly impedes viral spread –High herd immunity is the major goal of mass vaccinations
- Public health –Surveillance –Sanitation –Education –Prophylactic vaccination
- Medical care –Vaccination –Antiviral therapy –Quarantine –Mistakes can increase spread (HCV in Egypt)`
What are 6 viral factors governing viral spread and subfactors of each?
• Viral stability and delivery route –Stable viruses can persist in the environment and spread indirectly –Transmission by aerosols, urine, feces etc. is more
efficient than transmission by blood, semen, etc.
• Degree and duration of infectivity: –Higher production of viruses increases transmission –Persistent infections lengthen the period over which
transmission to a new host can occur
• Disease: –Onset of transmissibility prior to symptoms increases chance of spread beyond immediate contacts
- onset of transmissibility after symptoms reduces chance of spread to general public and increases chance of spread to immediate contacts
- rapid lethality reduces spread
• Antigenic variation (a.k.a. immune escape) –Highly variable immunodominant epitopes permit virus to
avoid removal by antigen-specific immune responses –Variation is tolerated by virus because variable sequences are non-essential –Acts through both B- and T-cell epitopes
- Immune evasion –Active subversion of immune system by virus –Very common; almost universal among persistent viruses
- Animal reservoirs –Animals can be alternate hosts for some viruses (e.g., Influenza Virus, Yellow Fever Virus, Hantavirus….) –Infection of animal reservoirs increases persistence of virus in the host populations
What are some characteristics of arthropod borne viruses (arboviruses)?
• Grouping is based on viral mode of
transmission –Transmission between mammalian or avian hosts requries an intermediate infection of an insect or arachnid (vector ) –Arboviral infections are therefore zoononotic
• Arboviruses cause a wide variety of
diseases –Examples: yellow fever, many hemorrhagic fevers…
- Replication cycle: –Arthropod vector is infected when it takes a blood meal from an infected host –The virus replicates to high titers in the vector –The vector infects another host when it takes another blood meal
- Humans are not natural hosts for most arboviruses
–Viruses are usually maintained in wild or domestic animals (enzootic and rural epizootic cycles)
–Infection of natural hosts rarely causes disease
–A few arboviruses can establish self-sustaining infections of humans without infection of another mammalian/avian maintenance host (urban epidemic cycle)
What are some effects of the multiple host replication cycle of arboviruses?
• Greater viral persistence in a geographic area –2 types of animal hosts provide a larger reservoir for
viral replication
- Harder to eradicate if virus has an animal maintenance host –Vector-borne transmission permits viral control by vector control
- Yellow fever, mosquitoes, and the Panama Canal
- Viral genetics –Virus must replicate in vastly different host species and tissues –Tends to reduces viral genetic diversity
- Less genetic drift
- Tighter quasispecies clouds
How do viruses enter the body? What are some barriers?
• Entry sites –Viruses can enter the body at any site where cells could be exposed to the environment –Common routes include through the respiratory, GI tracts, or urogenital tracts, the eyes, or skin punctures
• Barriers to entry
–Physical barriers such as the dead cells on the surface of skin
–Dynamic barriers such as flow of mucous out of the respiratory tract
–Physiological barriers such as the low pH in the stomach
–Viruses have adapted to overcome the primary
barriers they typically face –Example: viruses that infect the GI tract are resistant to low pH
How do viruses disseminate throughout the body? How does this effect pathology?
• Viral replication can spread beyond the entry site
–Viruses usually start replicating in cells near the entry site
–Progeny virus can either remain localized (e.g., dermal papillomavirus infection), or can spread to other tissues (e.g., pox viruses)
–Virus is released into the blood, lymph or gastric fluids, or transported within lymphocytes or through nerves
• Pathology is dependent on viral dissemination patterns
–Replication at the entry site usually causes unapparent or limited disease (papillomaviruses
and skin warts), but disease can occasionally be severe (influenza virus infection of the respiratory tract)
–The more serious viral diseases are usually associated with replication at secondary sites
(disease type depends on tissue infected)
