Microbiology Final Flashcards
Can viruses be linked to cancer progression?
Yes: Viruses like HPV can lead to certain cancers.
Capsid
-the protein shell that surrounds the genome of a virus (found in both enveloped and naked viruses)
-Capsomere proteins form the protein coat (capsid)
-usually only made up of one protein due to limited genome space
-self-assembly of capsomeres
Naked Virus
-Have no other layers
-Nucleic acid genome
-Capsid
-Most bacterial
Enveloped Virus
-Most animal viruses
-Mostly infect animal cells because the envelope is unable to get through a cell wall
-have an outer layer consisting of a phospholipid bilayer (from the host cell membrane)
-Viral proteins
-Envelope, Glycoprotein, nucleic acid genome, and capsid
Nucleocapsid
nucleic acid and protein in enveloped viruses
Why are virion surface proteins important?
-They are important for host cell attachment and may include enzymes involved in infection and/or replication
-Need a viral protein- glycoprotein or spike protein
General Characteristics of Viruses
-Obligatory intracellular parasites (require a host cell to multiply)
-Contain DNA or RNA
-No ribosomes
-No ATP-generating mechanisms
Do most viruses effect many cells?
No: most viruses infect only specific types of cells in one host.
-Once a virus is inside a cell, however, all cells can be infected
-Ex.) COVID: Would not infect skin cells but would infect respiratory cells
Bacteriophage
viruses that infect bacteria
Virus Classification
-Based on Host range (determined by specific receptors)
-Based on genome structure (DNA or RNA) (can be other versions like HIV that changes between RNA and DNA)
Does the genome of a virus determine the shape of it?
No
DNA Viruses
-Class I: Classical Semiconservative
-Class II: Classical Semiconservative, discard (-) strand
-Class VII: Transcription followed by reverse transcription
RNA Viruses
-Class III: make ssRNA (+) and transcribe from this to give ssRNA (-) complementary strand
-Class IV: make ssRNA (-) and transcribe from this to give ssRNA (+) genome
Class V: make ssRNA (+) and transcribe from this to give ssRNA (-) genome
Class VI: make ssRNA (+) genome by transcription of (-) strand of dsDNA
Virion
-Complete, fully developed viral particle
-Spikes: projections from the outer surface
-Important for attachment and release
-HIV: some are immune (HIV cannot bind to CD4 cells without CCR5)
Virus Infection: Transformation
-Transforms the cells
-Cause of cancer formation (Like HPV)
Virus Infection: Lysis
-Causes direct cell death
-One of two main kinds of infection
Virus Infection: Persistent Infection
-Virus buds out of cell without death
-One of two main kinds of infection
Virus Infection: Latent Infection
-Virus is present but not replicating
-Ex: HIV, herpes
Steps in a Replication Cycle
-One-step growth curve: Virion numbers increase when cells burst
-Eclipse Phase: genome replicated and proteins translated
-Maturation: packaging of nucleic acids in capsids
-Latent period: eclipse and maturation
-Release: cell lysis, budding, or excretion
-Burst Size: number of virions released
Replication Cycle of a Lytic Bacterial Virus
1.) Attachment (absorption of phage virion)
2.) Penetration of viral nucleic acid
3.) Synthesis of a viral nucleic acid and protein
4.) Assembly and packaging of a new virus
5.) Cell lysis and release of new virions
Lytic Pathway
-lytic events are initiated
-phage components are synthesized and virions are assembled
-lysis of the host cell and release of new phage virions
Lysogenic Pathway
-viral DNA is integrated into host DNA
-Viral DNA is replicated with host DNA at cell division
Induction
When the cycle changes from lysogenic to lytic
What are the advantages of lytic viral replication?
The virus has the ability to make and spread many copies, and spread between the host and other cells
What are the advantages of lysogenic replication?
Lysogenic viruses replicate quietly in host DNA, we cannot detect it
Why would a temperate virus switch from lysogenic to lytic replication (or vice versa)?
When the environment is very favorable or very unfavorable
How would someone intervene at each step of the replication cycle?
By stopping attachment
Cro and CII proteins and lysogeny
-High nutrients (more host cells)- CII cleaved, so Cro induces
-Multiple phages infect single host cell- increase in CII, leads to lysogeny
-Once in prophage form, few proteins are expressed (one is CI) which prevents other phages from infecting host cell (prevents other viruses from infecting)
Latency replication switch
When CII > Cro = (Lysogenic) Integration and become a prophage (most viruses cannot do this)
-When Cro > CII =(Lytic)
Viral Genome integration selection
-HIV and other lentiviruses
-stretch of DNA transcribed more often than other DNA
-Could use host to transcribe viral DNA
Ebola
-Caused by a Filovirus
-Negative stranded RNA virus
-Transmitted through direct bodily fluid contact
-Spread stopped through proper PPE usage
-Flu-like symptoms at first then severe symptoms like unexplained hemorrhaging, and hiccups
Ebola Replication Cycle
-Viral protein that inhibits intracellular immune pathways then hijacks the track (Anti-viral RNA sensor)
-Attaches in endothelial cells
Ebola Pathophysiology
-Excess cytokines (allows for increased permeability)
-Destroys cellular immune response
Virion
-Complete, fully developed viral particle
Envelope
-Lipid, protein, and carbohydrate coating on some viruses
-Phospholipid bilayer is a product of the host
Envelope acquisition
-Viral capsid moves to the plasma membrane (docking site for capsid)
-Begins to bud using host to create a membrane (Need to bud!)
Enveloped Viruses
-Easier to get rid of in the environment
-Sensitive to drying, heat, detergents, acids
-Consequences of enveloped viruses is that they have an advantage when spreading (respiratory illnesses, STIs)
Naked Viruses
-Stable in most environments and not sensitive to drying, heat, detergents, acid
-can be identified more easily by host cells (food borne illnesses)
DdDP
-DNA dependent DNA Polymerase
-DNA is the template, and makes DNA
- (HOST)
DdRP
-DNA dependent RNA Polymerase
-DNA is template, RNA is made
- (HOST)
What does mRNA =?
+ssRNA (our RNA)
-our ribosomes can only recognize +
( + to - to postitive)
RdRP
-RNA dependent RNA Polymerase
- RNA template forms RNA
-Viral (not in humans)
-Does not happen in human biology
RdDP
-RNA dependent DNA Polymerase
-RNA template makes DNA
-Reverse transcriptase (What HIV does)
RNA dependent polymerases
-ssRNA uses RdRP to create +ssRNA to host ribosomes
+ssRNA uses RdRP to make -ssRNA
Human Herpes Virus 3
-Varicella Zoster (Chickenpox)
-Lysogeny (causes latent virus (Shingles))
-Never truly integrates into the genome (not a true prophage)
-Latent form (immediate early (expressed immediately)) (late (wont express unless making active viral proteins))
-T Cell Tropism (chickenpox is airborne!)
ssRNA viral replication
- T sense viruses don’t need to bring RdRP (they can make it)
-Cannot do anything in our cells without RdRP, which they carry in the capsid
Poliovirus- A model for polyprotein synthesis
-Replicates in neuron
- (+ssRNA)(Immediately goes through replication)
-Makes one ling polypeptide chain which is then cleaved into smaller more usable proteins
-Important organization (genome organization is important for translation)
-Looks like human RNA
Coronaviruses- A model for multistep synthesis/replication
- +ssRNA
-Being translated
-Replicase makes a lot of -ssRNA
-Synthesis of monocistronic mRNAs–> Each code for 1 protein
-Synthesis of genome copies–> difference in how much has been copied
Rabies- The need for viral proteins
- (-ssRNA)
-not a perfect process - Negative parental RNA strand uses RdRP (and RNA replicase in capsid) to make mRNAs (+ sense)
- +strand RNA is the template for genome replication
dsRNA and Retroviruses
-dsRNA is the best of both worlds
-Retroviruses- version of ssRNA but requires dsRNA intermediate
Reoviruses- dsRNA leads to unique process
-dsRNA is easier to find in cytoplasm and is highly immunogenic and has to be very unique
-Reoviruses hide their genome
-RNA replication in capsid
-Protein translation in cytoplasm
-Staying in capsid it cannot be detected by the immune system
-In cytoplasm when single stranded
-In capsid when double stranded
Reverse Transcriptase
-3 enzymatic activities
1.) Reverse transcription: Synthesize DNA from RNA
2.) Ribonuclease activity degrades RNA strand of RNA: DNA hybrid
3.) DNA polymerase to make dsDNA from ssDNA
-Viral tRNA serves as primer
-dsDNA with long terminal repeats forms; repeats assist in integration into genome by integrase
Measles
-Caused by a paramyxovirus
- (-ssRNA)
-Airborne virus
-Affects susceptible children and is highly infectious
Measles Pathology
-MeV (measles virus) replication stage affects multiple cell types
-Prodromal phase (before symptoms appear) can still be infectious
-Long-term consequences to measles (leaves immune system weak and therefore susceptible)
Mumps
-Caused by a paramyxovirus
-highly infectious with some outbreaks
-Less infectious than measles
-Characterized by inflammation of salivary glands
Rubella (German Measles)
-Similar process to covid
-Makes virus in the golgi apparatus
-Severe consequences for pregnant women
Virus impact on cancer development
Some viruses have ties to cancer development like HPV and cervical cancer, and HIV/AIDS and Kaposi’s Sarcoma
Viroids
-Naked RNA; no protein capsid (infect plants)
-ssRNA forms hairpin-shaped ds molecules
-enters plant through wound
-completely dependent on plant RNA polymerases for replication
Prions
-Self-replicating
-Infectious proteins whose extracellular form contains only proteins
-known to cause disease in animals (Chronic wasting disease, Mad cow disease, Kuru, etc)
Prions Proteins and Prion Infection Cycle
-Host cell contains gene (Prnp) that encodes native form of prion proteins (Prp) that is found in neurons/brain of healthy animals
-Mammalian prion proteins are similar in amino acid sequence
-Destroys brain and other nervous tissue
