Prokaryotic Viruses

true or false: animal viruses come in with proteins while bacteriophage do not

true

what is the central dogma and list the necessary enzymes

dsDNA→ssRNA→protein

transcription: RNA polymerase (DNA dependent)

translation: ribosomes

DNA replication: DNA polymerase

how are viruses able to deviate from the central dogma

if they deviate, they come in with their own enzymes (or at least the genetic instructions to do so)

what direction does replication go to?

3’ to 5’

how are RNA viruses able to replicate their RNA?

because RNA is single stranded, there is no enzyme that can literally copy a strand. we have to have a complementary strand made first, and then, that strand will be used as the template strand to make more of the original. the end result will be dsRNA

what enzyme is replicate RNA?

RNA polymerase that is RNA dependent

when an RNA is positive sense, what does this mean? what about negative sense?

positive: it can directly translated with host cell ribosomes

negative: it can NOT be directly translated with host cell ribosomes

if a negative sense RNA is used as a template, what will be the complimentary strand

positive sense (aka can be directly translated)

which is more stable: DNA or RNA

DNA (foreign RNA is more likely to be successfully challenged than foreign DNA)

what are some benefits to viruses having dsDNA as their nucleic acid? consequences?

(+) they can use host cell machinery (more likely to be following the central dogma) and it is more stable

(-) it will take longer to replicate (more steps), will have to travel, and it takes more time for the respective proteins to be made

what are some benefits to viruses having RNA as their nucleic acid? consequences?

(+)if it is positive sense, it can be directly translated and can adapt rapidly (because it lacks the necessary mechanisms for proofreading)

(-) if it is negative sense, it cannot be directly translated (longer to make the necessary components. also, it is less stable and with lack of proofreading mechanisms can result it in mistakes in making the necessary material for assembly. it would not be able to remain dormant for a long period of time because RNA degrades quickly

while viruses can bring in the necessary instructions for making respective enzymes, what do they have to use from the host in order to make proteins?

ribosomes (they lack them and ribosomes are absolutely needed in order to make proteins)

what organisms do bacteriophage infect?

bacteria

what does tropisin mean?

host “preference”

for bacteriophage, it can look like preferring gram positive vs gram negative

for human viruses, there can be preference for certain tissues or cell types

how would you describe the shape of a bacteriophage?

its head is icosahedral and its tail is helical

to entire part is considered COMPLEX

can TRUE icosahedral viruses have helical components? what about if TRUE helical viruses have icosahedral components?

true icosahedral viruses cannot have helical components and VICE VERSA (if it did it would be complex)

what is the standard behavior of virsues?

1. attach

2. enter

if they are dormant then latency (animal) or lysogeny (bacteria)

3. replicate

4. assemble

5. exit

how do bacteriophage attach? aka what facilitates attachment?

contact and attachment are mediated via cell-surface receptors

what are cell surface receptors? do bacteria make this just to help viruses?

they are proteins that are specific to host species, and they normally produced because they are necessary for host cell function (ex: LPS or flagellar motor).

bacteria do make this specifically for viruses

what makes a bacteria more susceptible to infection?

if it has ore cell-surface receptors that the viruses are attracted to

lytic vs lysogenic cycle

lytic: when bacteriophage quickly replicate and kill the host cell

lysogenic: bacteriophage are dormant and usually integrate into cell chromosome=prophage. it can reactivate to become lytic

why do viruses try to replicate quickly

they are try to get all the necessary materials made before the host cell potentially lyses(could lyse early)

if it lyses early, then the phage will not be assembled and cannot infect other hosts (hindering its purpose)

what is a prophage

host cell with viral DNA

what are the two points where we see full phage in the lytic cycle?

at attachment and assembly

if the bacteriophage is lysogenic, what is its standard behavior

1. host cell recognition and attachment

2. genome entry

3. integration into host chromosome (dormant)→prophage (it can stay here for prolonged periods of time)

4. reactivation and replication of genome/synthesis of proteins

5. assembly

6. exit and transmission

if the host is already stressed, is it likely for the bacteriopage to be dormant?

if it is stressed, the bacteriophage are not likely to integrate their DNA into the chromosome and be dormant

it is more likely that the bacteriophage will not even attach because it the host cell is stressed, it can lack the necessary machinery for the virus to replicate (since the host will not be actively replicating) and the host is more likely to lyse (hindering the virus from replicating)

what is the most common trigger from lysogenic to lytic

stress

how is it advantegeous for bacteriophage to be lysogenic

integrates into chromosome→daughter cells all have viral DNA→more viruses/higher potential for more virus formation

what are the three types of infection

productive, persistent, and dormant

what is productive infection? how long does it last in animal viruses

active virus replicaiton (steps 1-5)

in animal viruses, it can last 2-3 weeks

what is persistent infection? how long does it last in animal viruses

active virus replication but occurs slowly (NOT DORMANT). in animal viruses, it occurs over months to years

what is dormant infection

virus is not actively replicating, assembling, or exiting

does productive infection always result in lysis? what about persistent?

productive usually does but persistent does not always result in infection

is it common to see bacteriophage be persistent?

no because they already have a shorter life expectancy (the bacteria) so they do not have the time availability to be persistent or replicating slowly

why is animal virus tropism more complicated

because it involve the animal, then the tissue, and then the cell

what is host tropism? tissue tropism? and cellular tropism?

host: looking at the host a virus wants to infect (ex: some strains of influenze prefer human and have a human host tropism)

tissue/organ/area: for animals, it is the part of the body it infects (ex: influenza has respiratory tissue tropism)

cell: the cell type it infects (ex: influenza has a epithelial cell tropism)

what are the two ways animal viruses can enter?

endocytosis or membrane fusion

endocytosis vs membrane fusione

endocytosis: after the virus binds with the surface receptors host membrane literally engulfs the who virus and results in a intracellular vesicle that transports the virus into the cell

membrane fusion: the viral envelop attaches and fuses with the membrane to allow for the entry of the virus (aka everything that was surrounded by the envelope so everything within the capsid)

what are the three ways animal viruses are released?

lysis of cell, exocytosis, and budding

which method of animal virus release results in cell death

lysis and sometimes exocytosis (budding does not result in IMMEDIATE death)

lysis vs exocytosis vs budding

lysis: burst the cell membrane and results in immediate cell death

exocytosis: a vesicle transports the virus out without destroying the membrane

budding: the viruses passes through the membrane but leaves enveloped because it takes host membrane cell lipids to surround its capsid

is budding the only way for the virus to get host cell lipids

no, exocytosis involves some viruses taking lipids from the host membrane or even other places but budding is EXCLUSIVE for enveloped viruses that use lipids from the membrane

which method for release always results in an enveloped virus

budding (and has host cell lipids)

do viruses that have RNA have to have DNA?

no but they should if they want to remain around longer

what is the shape of the herpesvirus

icosahedral

is a herpesvirus enveloped or unenveloped

enveloped

what are the three distniguishable aspects of the herpesvirus?

nucleocapsid, tegument, and envelope

for herpesvirus, what is the tegument layer? what is it used for?

layers of proteins, and it is used for infectivity

describe the nucleic acid for herpesvirus

it is dsDNA (and this can change shape—linear or circular)

what kind of enzyme does it use to replicate? what about translation?

it does not use human polymerase; it has its own DNA polymerase. it still uses host cell ribosomes

viruses have to rely on when host cells are replicating in other to replicate themselves, but does this apply to herpesvirus

it can replicate independent of when our cells replicate (probably because it has its own enzymes and necessary material when actively dividing)

true or false: herpesvirus is only transmittable if there is an active sore

true

what are the three ways herpesvirus can be transmitted

• direct contact with saliva or spores (or skin to skin)

• oral (epithelial)-genital contact

• close personal contact/surface contact

how long is the herpesvirus “viable” for

minutes to hours on surfaces

what are the four ways to prevent herpesvirus

• avoid direct contact during outbreaks

• use barriers for protection

• practice skin hygiene

• educate partners

what is the cellular tropism for herpes simplex type 1 (cold sores) for productive infection? what about latent infection?

productive: epithelial cells of mucosal tissue

latent: sensory neurons in ganglia (potentially problematic if you have a history of herpesvirus and it remains dormant)

what are the two treatments(not cures) of herpes simplex type 1 and how do they work

1. acyclovir: it is antiviral and acts as nucleotides incorporated into viral DNA. it stops polymerization (monomer→polymer)

2. docosanol: a fatty acid that coats the host cell membrane which prevents viral entry (especially for new epithelial cells)