Chapter 13 - Viruses, Viroids, and Prions Flashcards
Obligatory Intracellular Parasites
-require living host cells to multiply
Viruses
-contain a single type of nuclei acid, DNA, or RNA
-contain a protein coat
-multiply inside living cells by using synthesizing machinery of the cell
-synthesize special structures that transfer viral nucleic acid to other cells
Viruses Have no Enzymes
-no enzymes for their own metabolism, protein synthesis, ATP generation
-take over metabolic machinery of host cell
Host Range
-spectrum of host cells the virus can infect
Virion
-a complete, fully developed, infectious viral particle
-composed of nucleic acid and surrounded by a protein coat outside a host cell
Virus DNA
-have DNA or RNA but never both
Capsid
-protects the nucleic acid of a virus
-a protein coat
-allows lab ID
-allows transmission between hosts
-used for attachment
Capsomeres
-composition of capsid (subunit)
-protein subunits
-arrangement is particular to the virus
Envelope
-covers some capsids in a virus
-combination of lipids, proteins, carbohydrates
-a phospholipid bilayer
-extra layer of protection
-aids in ID
Spikes
-may cover envelopes
-carbohydrate-protein complexes
-how some viruses attach to host cells
-can be used as a means of ID (vaccine target)
Hemagglutination Spike
-resulting clumping of red blood cells by spikes
-viruses bind to RBCs and form bridges between them
-sharp
Neuraminidase Spike
-separation from host cell after infection
-rounded bulb shape
Non-enveloped Viruses
-viruses whose capsids aren’t covered by an envelope
-capsid protects nucleic acid from enzymes
-capsid promotes virus attachment to host
Complex Viruses
-bacterial viruses that have complicated structures
How are viruses grouped?
-according to how their mRNA is produced
Viral Species
-a group of viruses sharing the same genetic information and ecological niche
Parasite
-a virus
-usually asymptomatic
-use host as mixing vessel (bird, bats) to transfer genes to humans
Influenza
-can transmit from different species to others (humans)
H1N1
-influenza strain
-mutates, protein spikes change
-annual flu
Cell Cultures
-preferred type of growth medium for many viruses
-cells grown in culture media in the lab
Cytopathic Effect (CPE)
-viruses infecting a monolayer of normal cells that cause the monolayer to deteriorate as they multiply
One-Step Growth Curve
-demonstrates the multiplication of viruses
-data obtained by infecting every cell in a culture then testing for virions and viral proteins
Lytic Cycle
-mechanism of multiplication
-ends with lysis and death of the host cell
Lysogenic Cycle
-mechanism of multiplication
-host cell remains alive
Retroviruses
-goes against the central dogma of geneties
-Reverse Transcriptase uses the viral RNA as a template to produce double stranded DNA
Reverse Transcriptase Enzyme
-enzyme used in Retrovirus
-also degrades original viral RNA
-makes ss DNA from ss RNA
-the part that makes HIV dangerous
Provirus
-integrated viral DNA in the host cell chromosome
-never leaves the chromosome
-protects HIV from the host’s immune system and antiviral drugs
Human Immunodeficiency Virus (HIV)
-attacks T-cells
-virion has RNA genome (2 identical ss RNA)
-a backup strand
-has capsid, envelope, and spikes
Retrovirus Multiplication and Inheritance
- virus enters via fusion between spikes and host receptors (has 2 identical ss RNA)
- uncoating releases two viral RNA strandsand viral enzymes reverse transcriptase
- reverse transcriptase copies viral RNA to prouduce ds DNA
- new viral DNA transported to host cell nucleus, integrated into chromosome as a provirus (viral integrase) and may be replicated
- transcription of provirus may occur, producing RNA for new retrovirus
- viral proteins processed (viral protease), some viral proteins moved to host plasma memb.
- mature retrovirus leaves host cell and acquires envelope and attachment spikes as it buds out
Receptor Mediated Endocytosis
-how HIV gets into host cell
-HIV attaches to CD4 receptors found on host cell and releases its genome into the cell
Provirus Stage
-makes new baby virions to keep the infection cycle going
-may become latent and emerge later
-can convert infected cell into a cancer cell (end stage of HIV - Kaposi’s Sarcoma)
HIV Progression
-usually ~10 YEARS
-3 stages
Syndrome
-a collection of symptoms
HIV Stage A
-1/3 of TH cells diminished
-about 500/µm or mm³
Lymphadenopathy
-viral load determines the speed of the pathogen
Normal TH Cell COunt
-1500-3000
HIV Transmission
-blood: 1000-10 000 infectous particles/µL
-semen: 10-1000 IP/mL
-saliva: 1 IP/mL
HIV Treatment
-highly active retroviral therapy (HART)
-a cocktail of several antiviral drugs used to reduce viral replication (Zidovudine and Lamivudine)
Why no HIV mRNA vaccine?
-small mutations within the person make the vaccine not possible
Lytic Infection
-cells don’t make themselves permanent residents
-kill host cell
-ie. cold, influenza
Persistent Infection
-don’t kill host cell
-ie. measles (SSPE/brain degeneration and death?)
Latent Infection
-hide and become latent in cells
-emerge and produce new virions
-ie. Herpes (cole sores, genital warts, shingles)
Cancer
-turns normal host cells into cancer cells
-ie. EB virus (herpes 4), Burkitt’s lymphoma, nasopharyngeal cancer
