Introduction to Virology Flashcards
1
Q
Description of viruses? (4)
A
- small
- filterable- small enough to pass through filter that bacteria cannot
- not visible by light microscopy - obligate intracellular pathogens
- replicate only in living cells
- cannot be cultured like bacteria
- no sub cellular organelles - progeny visions are assembled, the virus does not divide
2
Q
How do viruses infect cells?
A
- attachment
- can’t infect if it can’t bind cell - entry/coating
- genome needs to be released into host cell - macromolecular synthesis
- genome gets copies
- viral protein gets transcribed/translated - assembly and release
- new viral particles self assemble
- released from host cell and spread to infect new cells
3
Q
What are viruses composed of? (7)
A
- nucleic acid- genome
- DNA or RNA, but not both
- genome and associated enzymes make up viral core - protein shell called capsid
- helical or icosahedral (crystal-20 sided)
- protects genome
- core + capsid = nucleocapsid - envelope
- capsid surrounded by lipid bilayer
4
Q
Viral envelope?
A
- host derived lipid membrane
- viral encoded proteins
- matrix proteins (assembly, acts as bridge)
- surface glycoproteins (viral attachment-VAPs, viral cell fusion-fusion between envelope and lipid membrane of cell, allows capsid to get released )
5
Q
How to classify viruses?
A
- Type of genome
- DNA or RNA - presence or absence of a viral envelope
- naked or envelope - type of capsid
- helical or icosahedral
6
Q
DNA vs RNA virus?
A
- DNA:
- genome can persist over time, not readily degraded
- genome resides in nucleus, may integrate
- can use host polymerase, some encode their own (DNA dependent DNA pol made by host)
- interacts with host transcription factors - RNA
- genome is labile, degraded sooner
- genome remains in cytoplasm
- has to encode their own polymerase (RNA dependent RNA pol)
- more prone to mutations
7
Q
Clinical consequences of type of genome?
A
- DNA and retroviruses
- transformation- trigger cancer
- latent infections- remains dormant - RNA viruses
- variability- quasi species (variance of initial infection strain), can escape immune response, antigenic variation
- more labile
8
Q
Shapes of capsid?
A
- helical
- icosahedron
- icosadeltahedron- herpes
9
Q
Functions of viral capsids?
A
- protects genome
- involved in attachment- naked viruses
- viral attachment protein (VAP) - involved in entry/uncoating
- involved in assembly
- packaged viral enzymes if necessary
10
Q
Properties of naked icosahedral viruses?
A
- can dry out and retain infectivity
- can survive acidic conditions of GI tract
- resistant to temp extremes, detergents, poor sewage treatment
- released by cell lysis- allows it to spread
11
Q
Clinical properties of naked icosahedral viruses?
A
- survive in the GI tract enables transmission via fecal oral route
- shed in stool
- present in sewage contaminated water - survival in environment enables transmission by fomites (infecting object then someone touches object)
- responsible for most cases of viral gastroenteritis
12
Q
Properties of enveloped viruses?
A
- must stay wet to retain infectivity
- cannot survive in GI tract (acid labile)
- infectivity is destroyed by organic solvents
- need not kill infected cell to spread- can bud out
- some induce cell to cell fusion
13
Q
Clinical properties of enveloped viruses?
A
- transmitted through droplets/secretions
- respiratory route, blood, organ transplants - cannot survive in GI tract
- need not kill infected cells to spread
- virus can be shed over time
14
Q
Attachment of virus to cell? (19)
A
- mediated by surface glycoproteins of enveloped viruses
- mediated by capsid proteins of naked viruses
- important determinant viral tropism- ability of virus to infect a certain type of cell
15
Q
Viral receptors?
A
- proteins or carbohydrates on glycoproteins or glycolipids
- physiological role in host cell, some other role, virus takes advantage of pre existing cell receptors
- types of receptors:
- molecules involved in cell to cell interactions
- hormone, cytokine, complement receptors
- enzymes
16
Q
Examples of viral receptors? (22)
A
see table
-cell receptor determines what cells can be infected
17
Q
Entry of virus to cell? (19)
A
- through plasma membrane
- viral cell fusion (enveloped viruses)
- hydrophobic interactions create a channel through the membrane (naked virus) - receptor mediated endocytosis
- most common route of entry
- used by both enveloped and naked viruses
18
Q
Viral cell fusion at plasma membrane? (24)
A
- viral attachment protein binds to host cell receptor
- lipid bilayers mix, makes pore
- capsid gets released into cytoplasm
19
Q
Receptor mediated endocytosis? pH dependent entry? pH independent?
A
- viral attachment protein binds to host cell receptor
- pH dependent entry:
- virus is internalized into endosome
- endosome becomes acidic and fuses with lysosome, dumps its enzymes in to activate fusion proteins
- acidic environment activates fusion activity of viral fusion protein
- fusion occurs between viral envelope and endosomal membrane
- more common
- pH independent:
- virus in internalized into vesicle that does not fuse with lysosomes and there is no acidification of vesicle
- the viral fusion protein is active at a neutral pH and can mediate fusion without exposure to an acidic environment
20
Q
Entry of naked icosahedral viruses?
A
- plasma membrane or receptor mediated endocytosis
- virus forms a pore through the membrane
- virus lyses the membrane (endosome)
- conformational change in capsid proteins:
- expose hydrophobic region (make a pore)
- dissociate to release genome (uncoating)
21
Q
What is uncoating? (27)
A
- release of genome into cell
- objectives:
- get rid of capsid
- get RNA into cytoplasm- uncoating coincides with entry, happen at same time
- get DNA into nucleus (two separate events, entry then uncoating at nucleus)
- triggers for uncoating include:
- binding to receptor
- change in pH
- proteolytic degradation
22
Q
Taking over the host cell?
A
- transcription of viral mRNA (viruses doesn’t have ribosomes)
- replicate genome
- controls protein synthesis:
- make viral proteins
- shut down synthesis of host proteins
23
Q
Transcription of viruses general properties?
A
- early transcripts
- encode regulatory enzymes and proteins:
- control transcription of viral mRNA
- initiate replication of viral genome
- shut down host protein synthesis - late transcripts
- encode viral structural proteins
24
Q
DNA viruses?
A
- transcription and replication occurs in nucleus (exception= pox viruses)
- genome = template for viral mRNA
- genome is infectious
- virus uses host cell DNA dependent RNA polymerase- more complex DNA viruses will encode their own polymerase
25
Q
replication of DNA viruses? (31)
A
see pic
26
Q
+ strand RNA virus? (32)
A
+ strand has same sequence as mRNA
- genome can function as mRNA
- translated as polyprotein, then cleaved into viral proteins - virus encodes an RNA dependent RNA polymerase
- transcription produces (-) strand RNA
- template for mRNA
- template for genomic RNA - genome is infectious
27
Q
(-) strand RNA virus? (33)
A
- virus encodes an RNA dependent RNA polymerase
- core protein - genome is template for mRNA
- strand copy of genome is template for genomic RNA
28
Q
Retroviruses? (35)
A
+ strand RNA is transcribed into DNA
- reverse transcriptase (RNA dependent DNA polymerase) is core enzyme- makes DNA from RNA
- DNA travels to nucleus where it integrates into host chromosome
- transcription of DNA produces mRNA and genomic RNA
29
Q
Assembly and release? (37)
A
- capsids self assemble
- package genome and core enzymes - naked virions are released upon cell lysis
- DNA virus pass through nuclear pore and is released upon cell lysis - enveloped viruses bud
- matrix proteins determine site of budding
- plasma membrane, ER, Golgi, nuclear membranes, released via exocytosis
- act as a bridge between nucleocapsid and surface glycoproteins
30
Q
Types of viral infections at cell level?
A
- productive infection
- progeny virus is produced
- infected cells are permissive for that virus - non productive infection
- no progeny are produced
- cells are non permissive
31
Q
Types of productive infection?
A
- lytic infection
- destruction or lysis of host cell
- naked virus produces lytic infections - persistent (chronic) infection
- continual shedding of virus
- no destruction of host cell (budding)
- envelope virus
32
Q
Types of nonproductive infection?
A
- abortive
- host cell cannot support viral replication
- viral genome is lost - latent infection
- virus is dormant in host cell
- viral genome is maintained
- viral transcripts may be detected, few or no viral proteins are expressed
- occurs in DNA or retroviruses
- reactivation of a lytic infection is possible - immortalizing and transforming infections
- one or few viral genes are expressed
- immortalized cells continually go through cell cycle- may or may not be transformed
- transformed cells are phenotypically altered
- cells are considered semi permissive for virus
33
Q
Viruses that can cause latent infections? (41)
A
see chart
34
Q
Possible consequences of transformation?
A
- uncontrolled cell growth
- alteration of morphology and metabolism
- decreased requirement for serum growth factors
- alterations in cell surface components
- increased metabolic rate - loss of contact inhibition of growth
35
Q
Examples of transforming viruses? (44)
A
see chart
36
Q
Summary of viral infections at cell level? (45)
A
see chart
-latent is a way to escape host immune response
37
Q
Consequences of viral replication? (46)
A
see chart
