Chapter 13 revamp

Characteristics of Viruses

-Minuscle, acellular, infectious agents having DNA or RNA

-cause infections of humans, animals, plants, and bacteria.

-Cannot carry out any metabolic pathway.

-Neither grow nor respond to the environment.

-Cannot reproduce independently.

-Recruit the cell’s metabolic pathway to increase their number.

-No cytoplasmic membrane, cytosol, or organelles.

-Have an extracellular and intracellular state.

Extracellular state

-Called Viviron

-Protein coat caspid sorrunding the nucleic acid.

-Nucleic acid and caspid are called Nucleocaspid.

-some have a phosophlipid envelope.

-Outermost layer provides protection and recongition sites for host cells.

Intracellular State

-Caspid removed

-Virus exists as Nucleic Acid

Genetic Material of Viruses

-Show more variety in the nature of their genome than they do in cells.

-May be DNA or RNA but never both.

-May be linear, segmented, single, or circular.

-Much smaller than the genome of cells.

Caspids

-Provides protection for viral nucleic acid.

-Means of attachment to host cells.

-Composed of proteinaceous subunits called capsomeres.

-Capsomeres made be made of singular or multiple types of proteins.

Helical

tube structure capsid forms a spiral shape around the genome.

Polyhederal

3D structure that has a bunch of different sides and repeated sub units.

Complex

doesn’t fit into any category can be any shape.

Viral envelope

-Aquired from the host cell from viral replication or release.

-Envelope is the portion of the membrane system of the host.

-Composed of Phospholipid Bilayer and Proteins

(some are encoded as glycoproteins)

-Viral envelope proteins and glycoproteins allow the virus to recongize and attatch to specific receptors on the host cell.

-Envelope can provide some protection from recognition by immune system.

-Envelope is more fragile than naked viruses.

Lytic Replication

Viral replication that usually results in death or lysis of the host cell.

Five stages of lytic replication cycle

-Attatchment

-Entry

-Synthesis

-Assembly

-Release

Lytic cycle in bacteria phages

Attatchment: Tail fibers bind to receptor proteins on the host surface.

Entry: Release enzyme lyszome that weakens the cell wall.

Synthesis: Bacterium stops synthesizing it’s own molecules begins to only synthesize viral parts.

Assembly: Capsomeres and Caspid heads assemble

Release: New Vivrons are released and lyzsomes breaks down the cell wall causing the cell to burst.

Burst time

The amount of time to complete the lytic cycle

Burst Size

How many vivrons are released after burst

Lysogenic Replication of Bacteriophages

-Modified replication cycle.

-Infected host cells grow and reproduce normally for generations before lyse.

-Temperate phages:

-Prophage:Viral DNA integrated in a viral choromsome (inactive phage)

-Not permanent can transition into lytic replication cycle.

-Lysogenic conversion:

Results when phages carry genes that alter the phenotype of bacteria.

Prophage

Viral DNA integrated into the viral chromosome an inactive phage.

Lysogenic conversion

Results when phages carry genes that alter the phenotype of the bacterium.

Lysogenic steps

1. Phage attatches to the cell with it’s tail and inserts viral DNA into the cell.

2. Viral DNA integrates into chromosome becoming a prophage.

3. Everytime the cell replicates an infected chromosome the prohage is replicated.

4. All the daughter cells of the lysogenic cell are infected with the inactive virus.

2. Prohage is excised by induction and rejoins the lytic cycle.

Replication of animal viruses

Chemical attraction between viral proteins and cell receptor.

Animals proteins do not have tails or tail fibers.

-have glycoproteins spikes or attatchment molecules that mediate attatchment.

Entry and Uncoating of Animal Viruses.

Enter the host cell by at least three different mechanisms:

Direct Pentration

Membrane Fusion

Endocytosis

Differences in Replication of Animal Viruses

-Same basic replication pathway as bacteriophages.

Differences result from:
-Presence of envelope around some viruses.

-Eukaryotic nature of animal cells.

-Lack of cell walls in animal cells.

Direct Pentration

-Naked Viruses Use it.

-Nakes Vivirons attatches to the receptor squirts Nucleic Acid into the Animal Cell’s Host.

Membrane Fusion

Viral glycoproteins on the viral envelope merge with cell membranes which allow it uncoat viral caspid exposing nucleicacid.

Endocytosis

Naked Viruses after attatchment phase they use endocytosis and engulf the virus which eventually uncoats releasing nucleic acid.

DsDNA

similar replication of cellular DNA

viral genome is replicated in the nucleus

viral proteins made in the cytoplasm.

Some Expectations:

Heptasis B replicate DNA from RNA intermediary.

SSDNA viruses

-Cells do not use ssDNA

-Paraviruses have ssDNA Genomes

-DNA strands fold back to form dsDNA which replicated by cellular DNA polymerase.

-Newly replicated strand is release as ssDNA

Positive Sense RNA

Viral RNA can act as mRNA.

Negative Sense RNA

Viral RNA cannot be directly translated.

Synthesis of proteins and genomes (+SSRNA)

-ssRNA complementary to the genome is synethsized by viral RNA polymerase in the cytoplasm to act as template.

Synthesis of proteins and genome(-ssRNA)

transcription forms +ssRNA to serves both as mRNA and template for -ssRNA genome.

Synthesis of proteins and genome (DsDNA)

genome unwinds so that positive sense strand serves as mRNA each strand acts like a template for it’s complement.

Four types of RNA viruses

+ssRNA

-ssRNA

dsDNA

retrovirus

Retro Virus

Does not use genomes as mRNA

-Use DNA intermerdiary transcribed by viral reverse transcriptase to produce viral genomes

Assembly and Release of Animal Viruses

-Most DNA viruses assemble in the nucleus.

-Most RNA viruses assemble in cytoplasm.

-Enveloped viruses are released in a process called budding.

-Enveloped viruses can cause persistent infections.

-Naked viruses are released by excoytosis or lysis.

Proviruses or Latent Viruses

-when animal viruses remain dormant in their host cells.

-may prolonged for years for no viral activity.

-Incorporation of pro virus into it’s host cell is permeant.

Cell division is under genetic control

-Genes ditate when cells can no longer divide at all.

-Cells that divide are prevented from unlimited division.

-Genes for cell division turns off or genes inhibiting division turns on.

Neoplasia

-Uncontrolled cell division in a multicellular animal

-Mass of neoplastic cell is called a tumor.

Benign Tumor

tumors that remain in one place they’re not harmful

Malignant tumors

Tumors that invade neighboring tissues they’re also called cancer.

Metasis

occurs when a tumor spreads.

Protocongenes

promotes cell growth and division

Uncontrolled activation of onocongenes

Can lead to cancer

Environmental factors to contribute to acitvation of oncogenes

-Ultraviolet light

-Radiation

-Carcinogenes

-Viruses

Some viruses can cause human cancers

-Burkitt’s lymphoma

-Hodgkin Disease

-Kaposis Sacroma

-Cervical Cancer

Vivirods

-exetremely small circular pieces of ssRNA that infectious and pathogenic in plants.

-Similar RNA viruses lacks caspids.

-Vivirods RNA does not code for proteins

-Viviroid RNA adheres complementary plant RNA.:

-Plants enzymes degrade dsRNA

results in disease state

Characteristics of prions

-Proteinaceous infenctious agents

Cellular Prp:

-Made by all mammals.

-Normal functional structure that has a helices.

Prion Prp:

-Disease Causing forms b pleated sheets.

Prion Prp causes Cellular to refold into Prion Prp

Prion diseases

-Spongiform encephalopthies

-BSE, Scrapie, Kuru, CWD, and VCJD

-transmitted through ingestion, transplation, and contact with mucous membrane with infected tissue.

-No treatment for prion disease.

Destroying Prions

-Normal sterilization does deactiviate prions.

-Prions are destroyed by in incernation or autoclaving in concentrated sodium hydroxide.