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BOD > Virology > Flashcards

Virology Flashcards

1
Q

Virus

A

Obligate intracelluar parastie

Need host cell machinery to express proteins

Very small 20nm
can be just capsid and nucleic acid

capsid helical or icosahedral
lipid membrane

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2
Q

Viral genome

A

ssRNA
+ if mRNA so can be used in translation
- if complementary to mRNA

dsRNA
ssDNA
dsDNA

small RNA genomes due to error prone RNA pol, 20kb
mutate rapidly

DNA genomes much bigger
1500kb
more stable, less mutation
genes for everything instead

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3
Q

Studying virus

A

Electron microscope
Polymerase chain reaction (PCR)
Haemagglutination
Plaque assay

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4
Q

Virus life cycle

A

Binding and penetration

eclipse phase-No viral proteins present, genome fused and being replicated

assembly and burst

yiels is mean burst size
depends on virus and cell metabolic activity

Virus bind to different proteins
HIV binds CD4 so cause immune problems
influenza binds sialic acid on most things

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5
Q

virus membrane fusion

A

In HIV Binding to CD4 proteins can cause conformational change allwoing viral envelop to fuse

In influenza haemagglutinin, binds sialic acid allowing endocytosis

Acidification of vesicle to cause fusion then release

For non enveloped virus, they bind to receptor, conformational change to allow transfer of genome or capsid into cell

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6
Q

viral genome

A

ssRNA-ve
needs own RNA pol to make mRNA as host won’t have it

dsRNA- also needs own RNA pol

ssRNA+- can be replicated immediately

Some ssRNA+ uses revertranscriptase to form DNA then mRNA using host RNA pol

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7
Q

Negative strand ssRNA viruses (measles virus, rabies virus, Ebola virus and influenza
virus)
dsRNA viruses (rotavirus)

A

Pre packaged virus-encoded
RNA-dependent RNA
polymerase needed to make mRNA

REplicate in cytoplasm except influenza which is in the nucleus

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8
Q

Positive strand ssRNA viruses (poliovirus, foot and mouth disease virus, hepatitis A
virus, rubella virus, yellow fever virus, chikungunya virus).

A

As already mRNA translation starts

MAkes a RNA-dependent RNA polymerase to replicate the initial viral RNA into -ssRNA which is then used to make more viral RNA

Purified viral RNA is infectious

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9
Q

Retroviruses

A

+ve ssRNA viruses, has reverse transcriptase prepacked
Reverse transcriptase makes dsDNA which is integrated into host genome by integrin
Provirus

Uses host DNA-dependent RNA polymerase II to make viral proteins
May need to be slpiced

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10
Q

dsDNA viruses (adenoviruses, herpesviruses, papillomaviruses).

A

Replicate in nucleus and use host cell machinery and host DNA dependent RNA polymerase II.

Some viral proteins and capsid brought back into to nucleus where viral DNA replicated and packaged

viral DNA alone is infectious.

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11
Q

Poxviruses

A

have dsDNA genomes but replicate in the cytoplasm
Have (DNA-dependent RNA polymerase, and capping and
polyadenylating enzymes) packaged
Needs RNA pol so viral dna not infectious

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12
Q

Virus gene expression

A

Temporal control
herpesviruses and poxviruses have genes regulated in a cascade where expression of the next class of gene being dependent on proteins of the
previous class

Quantative
Early proteins are enzymes needed in small amount
LAter proteins are the new virus particles so lots

Polyprotein processing
As eukaryotes only translate 1 peptide, viral RNA is translated as 1 giant polypeptide and post transcriptionally cleaved

Retroviruses use RNA splicing to form multiple proteins

Ribosomal frameshifting.
Ribosomes, pause, slip into another reading frame and restart. Used by other viruses too e.g. SARS-CoV-2.

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13
Q

Assembly and release

A

“self-assembly” can occur, i.e. no catalytic process is involved.

Protein added around genome

Virus express their proteins on cell surface and when they bud out they take some of the host plasm membrane with their proteins

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14
Q

Latent infection

A

Some viruses can remain quiescent within the infected cell
Contains viral genome but no replication

In retroviruses Once provirus made if not transcribed latent, cant be cleared by immune system HIV

Herpesviruses:
viral DNA enters the nucleus but doesnt integrate
and is an extrachromosomal circular molecule called an episome.

Can be reactivated later if changes in transcription factors allow recognition of viral promoter
herpes simplex virus-repeated cold sores

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15
Q

shut-off of host protein synthesis

A

only virus proteins are made

Ribosomes recognise host
mRNAs by binding to
methylated 5’-cap. Poliovirus
encodes a protease that cleaves cap binding complex so capped mRNA not translated

Polio RNA has internal ribosome entry
site (IRES) so ribosome recognises even without cap so only polio proteins made

DEstroy host DNA or mRNA

poxviruses have decapping enzymes, virus mRNA more abundant so likely to be translated

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16
Q

Cell stimulation
by causing division

A

DNA viruses require high levels of deoxyribonucleotides (dNTPs)

herpesviruses synthesise cyclin D1 that cause the cell cycle in order to make dNTPs

vaccinia virus expresses an epidermal growth factor to cause nearby cells to divide

Cells not in the cell cycle have dNTPases to decrease dNTP available for viruses

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17
Q

Changes in nucleotide metabolism

A

poxviruses and herpesviruses encode enzymes like , thymidine kinase to make dNTP

Withoit these enzymes grow poorly in resting cells

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18
Q

Membrane modification

A

Virus insert their proteins into plasma membrane to enable budding

Measles virus induces the infected cell to fuse with surrounding uninfected cells so spreading virus
without exposure to antibody outside the cell
cell-associated viruses, virus doesnt have to leave cell

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19
Q

Cytopathic effect

A

different morphology to uninfected cells
alterations to the cytoskeleton
(actin and tubulin containing filaments), which are exploited by the virus to facilitate intracellular
movement of virus particles.

Rabies virus: Negri bodies in Purkinje cells in cerebellum

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20
Q

lytic and non lytic infection

A

The productive cycle of DNA viruses is lytic.
Non-enveloped RNA viruses are lytic.
Viruses that cause host shut-off are lytic

enveloped RNA viruses, including retroviruses, can multiply in cells without killing them and
so release virus particles over a long period of time.

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21
Q

Cell Transformation
and cancer

A

Some DNA viruses stimulate cell metabolism to create a suitable environment for virus replication

Virus replication fails but stimulation continues creating cacner
human papilloma viruses (HPVs)- cervical cancer, attacks p53

Retrovirus integration into DNA
Can activate oncogenes of inserted above or disrupt tumour supressor, Needs to affect both copies, rare
When replicated may aquire host oncogene,

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22
Q

Rous sarcoma virus.

A

Picked up src gene
tyrosine kinase,
host oncogene, causes expression in large amounts

Can lose envelope so needs second infecting virus with an envelope to bud off.

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23
Q

Detecting virus

A

viral DNA and RNA are PAMPs
Activate nuclear factor kappa B (NF-κB) or the interferon
response factors (IRFs)

Make interferons and TNF-alpha

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24
Q

Interferons

A

secreted glycoproteins that bind to specific receptors on cells to induce
activation of an anti-viral state
IFNα and IFNβ-upregulate MHC I
IFNγ-inflammation and tH1 response
IFNλs

Interferons important as without greater susceptibility
Viruses all have ways to interfere

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25
Q

IFNα and IFNβ

A

Virus detected by TLR
nuclear factor kappa B (NF-κB), activated and cause transcription of IFN-a/b

Secrted and bind to IFN receptor

Causes JAK STAT pathway, to activate
interferon stimulated gene factor 3 (ISGF-3)
Binds to interferon
stimulated response element (ISRE) and make antiviral proteins like

protein kinase R (PKR)
Mx
Can stop protein synthesis

26
Q

Interfering with interferon

A

stopping activation of the PRR-induced signalling cascades
soluble proteins to bind IFNs and stop them from binding to receptor,
Vaccina makes B18 protein to bind IFN
inhibiting the JAK-STAT signalling
targetting the ISG proteins directly

27
Q

Apoptosis
virus

A

PAMP detection can cause death

by blocking the action of caspases or targeting Bcl-2 family pro-apoptotic proteins at the mitochondria

28
Q

Chemokines

A

chemo-attractant cytokines that recruit leukocytes
produce more IFNs or cytokines to activate T cells and macrophages to
fight the infection.

29
Q

Cytokines

A

Promote inflammatory response,with IL-1, IL-12, IL-18
IFN-γ activates cytotxic T cell

herpesviruses and poxviruses secret proteins to block them

Epstein-Barr virus expresses a viral cytokine (vIL-10) to cause TH2 response instead of TH1
Wekaer cytotoxic response, instead mor B cells which EB replicates in

30
Q

Natural killer cells

A

If viral infected cell expresses antigen on MHC NK cell can kill
If MHC removed by virus, missing self response so can kill, antigen independent

31
Q

Adaptive immunity

A

bind to and neutralise virus particles
diminish spread by free virions
Mucosal IgA is important in preventing infection by viruses that enter by the respiratory system.

Cytotoxic T lymphocytes
DEstroy virus infected cells

Herpes evasion
Block generation of peptides by the proteasome
Block transport of peptides into endoplasmic reticulum-HSV
Destroy class I MHC molecules-HCMV
Retain class I MHC molecules intracellularly-vzv

32
Q

other ways to escape from adaptive immunity

A

Latency. Hide from the immune system

Express Fc receptors on cells and virions. The Fc region of antibodies are bound to viral Fc receptor so not available to bind host Fc receptors.

Antigenic variation: influenza, HIV and hepatitis C virus

33
Q

Factors affecting the outcome of infection.

A

Virus dose
High doses may overwhelm the local innate response and cause disease.

Route of entry
variola virus (smallpox) dangerous if enters by respiratory tract but less by dermal

Age and sex
Varicella-zoster virus (VZV) , mild as child, dangerous as adult

Hepatitis B virus (HBV) has a high chance of chronic infection(cancerous) early in life, acute later on
Worse for males, higher chance of chronic infection

Physiological state
Stress and immunological deficiency

34
Q

Local versus systemic infections.

A

Superficial infections:
Virus replication occurs in the epithelium at the initial infection site, no spread
acute infections with a short incubation period and of short duration.
influenza

Systemic infections-
spreads by various routes (lymphatics, bloodstream,
nerves)
More severe
measles

35
Q

Factors affecting spread

A

Temperature-
Rhinoviruses (common cold) grow well at 32 ºC but not at
37 ºC and so replicate well only in upper respiratory tract epithelium

Budding site
apical or basal
Influenza apical so into airways
If basal may be systemic

36
Q

Acute, persistent or latent infections

A

Acute infections:
The virus is cleared after an acute infection.
Variola, influenza

Persistent (chronic) infections
virus is detectable in the host for years, or even lifelong.
HIV and hepatitis C virus almost always establish persistence.
Hepatitis B virus 90% acute 10% chronic
,90% of infected male neonates become infected chronically.

Latent (persistent) infection
primary infection but reappears (reactivates), years later, to cause
a recurrence of disease. All herpesviruses establish latency and are not cleared.

37
Q

Herpesviruses latency

A

Varicella zoster virus
acute disease is chickenpox
varicella

virus genome resides in neurones of sensory ganglia and may cause shingles (zoster).

some cells are permissive for productive infection,
while others are non-permissive
A stimulus may cause a non permissive cell to allow replication

eg The differentiation
of a latently-infected monocyte to a macrophage results in production of HCMV, acute in macrophage

Varicella and HSV-acute in mucosla epithelium, latent in sensory neuron

Epstein-Barr virus- acute in B cell, latent in memory B cell

38
Q

Factors affecting transmission
Stability

A

Virion stability
Enveloped viruses are less stable
The lipid envelope
is fragile and can be disrupted easily
Since the envelope contains the virus attachment protein(s),
loss of the envelope results in loss of infectivity
Spread by clos contact

small non-enveloped viruses are very stable outside the host and can be transmitted over long distances

39
Q

Duration of shedding
and conc

A

Acute infection short so high quantities of virus made, shed in high conc
persistent virus make less virus but shed repeatedly over a long period, lower conc

40
Q

Availability of susceptible hosts

A

population size
Measles virus is physically unstable and survives for only a short time outside host, after intial infection long immunity, no non human hosts so disapperas so no one to infect

Yellow fever virus and rabies virus infect multiple hosts
zoonotic infections are very hard to eliminate due to animal reservoir

41
Q

The reproduction number: R value

A

The average number of infections produced by each infected host
R > 1 = the epidemic is expanding,
R < 1 = the epidemic is declining

42
Q

Vertical transmission

A

Congenital infection (transplacental infections)
rubella, HIV, human cytomegalovirus

Perinatal: infection during birth or from breast milk
HSV,Human cytomegalovirus
Hepatitis B virus

Germ line transmission
Retrovirus as provirus can be inherited as endogenous retroviruses.
Can reactivate

43
Q

Virus-induced disease

A

MOst virus cause little disease as have co evolved with host, harmful if in abnormal host

Foot and mouth disease virus
Cost 8 billiion as killed many sheep and cow

Myxoma
harmless poxvirus to South America rabbits, fatal to European rabbits

Yellow fever
flavivirus, female mosquito Aedes aegypti.
Infects humans and primates

44
Q

Influenzas
structure and entry

A

-ve ssRNA, helical capsid
lipid membrane
haemaglutinin HA (agglutinates RBC)
neuraminidase NA
M2 ion channel
RNA-dependent RNA
polymerase pre packaged
replicates in nucleus

4 types, A,B,C,D, A causes most disease
natural Reservoir in birds
Many HA and NA variants, diverse

transmitted via aerosol and inhaled virions, infects respiratory epithelial cells

HA trimer, HA1 binds sialic acid. Endocytosis,
HA2 has a hydrophobic fusion peptide so in acidic conditions fuses viral membrane and endosome membrane
At low pH M2 ion intakes H+ intp core, promotes uncoating
amantadine and rimantidine inhibit M2

45
Q

Influenza replication

A

After entry the nucleocapsid is transported into the nucleus
viral RdRp transcribes -ssRNA into mRNA

Viral mRNA obtains 5’ cap by cap snatching host mRNA so still needs host RNA pol II

More +ssRNA made and used to make -ssRNA for new virions by viral RdRp

New nucleocaspid leaves by budding
Needs neuraminidase to cleave sialic acid or viral HA would bind to same cell or agglutinate together

Tamiflu-siacilic acid analogue, inhibits NA, virus agglutinates and sticks to cell

Antigenic drift
HA protein changes over time as mutations due to error prone RNA pol change amino acids, slow, gradual

Antigenic shift
If a cell is infected with 2 viruses, human and avian, during reassembly virus can pick up RNA from both parents
If human virus picks up avian HA, dangerous as can replicate in humans and escape immunity, pandemic

46
Q

Avian influenza in humans

A

Sialic acid galactose with 2-3 and 2-6 linkage
human virus prefers 2-6, avian 2-3

The PB2 subunit of RNA pol influences replication
E627 to K627 causes better replication in humans for avian flu

non-structural protein 1 (NS1) confers resistance to interferons, avian NS1 not great in humans so needs to adapt

Antigenic shift mostly occurs in pigs, swine flu

47
Q

Hepatitis A

A

picornavirus
+ve ssRNA
icosahedron capsid
Transmits by fecal matter
infects epithelial cells of the oropharynx or intestine
Can spread via blood to liver, virions in bile into faeces

Acute, causes jaundice
asymptomatic in children, adults develop acute hepatitis, fever, jaundice,diar

Vaccine
Live attenuated vaccine
Inactivated virus

Like polio
expresses protein by cleaving polyprotein

48
Q

Hepatitis B

A

hepadnavirus
DNA virus, reverse transcription
Acute and chronic hepatitic and liver cancer
icosahedral capsid
lipid envelope
Australia antigen surface protein (HBsAg)

small DNA genome, uses 4 overlapping reading frames
HBsAg binds hepatocytes, target for anitbody and used in vaccine

Reversivirus
Uses reverse transcriptase to makes it genome
but does not integrate its DNA into host genome, No latency, packages DNA not RNA
Hard to grow in culture

Transmission
Infected mother to child
infected blood product
Needles

Acute infection with jaundice
Chronic- virus not cleared, high HBsAg, liver disease and leads to hepatocellular carcinoma

Males and young children mor likely to develop chronic

Prevention
Scrren blood products
Vaccination
uses yeast to make HBsAg and purify

49
Q

Hepatitis C

A

flavivirus
icosahedral capsid
lipid envelope
E1, E2 glycoprotein
+ve ssRNA
Huge diversity, hard to make vaccine

Acute and chronic infection, 70% chronic
liver cirrhosis then cancer

Screen blood products

Treatment
Interferons
Drugs to target proteases and RNA pol
Effective drugs availabe but expensive

HCV RNA virus, hard to make vaccine so drugs used, HBV DNA virus, vaccine used

50
Q

Prions

A

infectious proteins
transmissible spongiform encephalopathies (TSEs) chronic, progressive neurodegenerative diseases

Scrapie in sheep.

Kuru in the Fore tribes in Papua New Guinea, transmitted by cannibalism.

Creutzfeldt-Jakob disease (CJD) and variant CJD (vCJD) in humans.

Bovine spongiform encephalopathy (BSE) in cattle (also called mad cow disease)

Found by infecting primate with kuru, no bacteria or virus, irradtion destroying nucleic acid had no effect, was a protein

51
Q

Prion protein

A

PrP
alpha helical, GPI-anchored, cell surface glycoprotein
Highly conserved
Found in CNS

PrP can form PrPSc(scrapie) a beta sheet, stable and hard to digest
Catalyses normal protein to misfold
Can spontaneously form

52
Q

Bovine spongiform encephalopathy (BSE)

A

feeding cattle with meat and bone meal ) infected with prions, from scrapie-infected sheep

53
Q

Creutzfeldt-Jakob disease (CJD) and variant CJD (vCJD)

A

like BSE in that:
* the disease had florid plaques in the cerebellum, like BSE prions in primates
* the PrP glycoform typing showed the same pattern as BSE

Transmitted by eating infected BSE meat

54
Q

Detetction of prions

A

No adaptive immune response
Monoclonal antibodies can distinguish
bio assay, infect mice

55
Q

Sars Cov 2
COVID 19

A

Prominant surface spike like corona
nucleocapsid
lipid envelope
+ve ssRNA
30kb genome, big for RNA

RNA pol has proof reading
nsp14 exonuclease
Still more mutation than DNA viruses
If 2 Cov infect same cell can recombination

Spike protein trimer, binds cells via angiotensin converting enzyme II (ACE-2) and causes fusion

From horseshoe bats
related to pangolins

asymptomatic, or cause severe acute respiratory syndrome (SARS)
0.3% fatality rate, higher when older,obese,lung conditions

Social distancing
person protective eq
hygiene
Quarantine

Dexamethasone:lowere lung inflammation
Remdesivir-inhibit viral RdRp
monoclona antibody against spike
Use several drugs to avoid res

mRNA vaccine

56
Q

HIV

A

HIV latent, spread lots before AIDS recog
From primates

retrovirus
+ ssRNA, like mRNA with 5’cap and polyA tail
genome diploid, has tRNA to prime reverse transcriptase
Inserted into host genome by integrase
Provirus has long terminal repeats at each end
regulatory and evasion proteins made intially
tat and rev switch so capsid and env made later
Vpu-block NF-Kb signalling

transmitted by sex, needles, blood
education, anti retroviral therapy, screen blood

gp120 binds CD4 on T/macrophages as well as co recptor CCR5, CXCR4(Tcell)

Intitially infects CCR5 but as immunodeficiency develops infects T cells

Polymorphism of CCR5, deletion so non functional, decreases risk in caucasian

57
Q

HIV treatment

A

Intially provirus heavily spliced, makes small proteins like tat and rev, later less splicing, bigger proteins

Leaves by budding
goes on for lonf periods
LAtent if provirus not transcribed, reservoir

Initial infection, CD8 T cell kill infected CD4 T cell
Later virus goes asymptomatic, comes back later, less TH cells to maintain toxic T cells, immunodeficiency
Opportunistic infection can kill

Rapid progerssors and long term, long term can control virus for a long time

No vaccine due to error prone reverse transcriptase, rapid variation
Azidothymidine- thymidine analogue, incoroporated by RT, terminates chain
better substrate for HIV pol than DNA pol

ritonavir-inhibit HIV protease so polyprotein not cleaved

Fusion or integrase inhibitors

HIV becomes drug resitance quickly, Highly active anti-retroviral therapy (HAART) where multiple drugs given at once.

58
Q

Virology control

A

Quarantine, slaughter
surveilance
hygiene
vector control
Screen blood
Vacines

59
Q

Antiviral chemotherapy

A

acyclovir for herpes simplex virus
phosphorylated by HSV
thymidine kinase, but not cellular kinases, incoporates into viral DNA by HSV DNA pol and terminates chain

60
Q

Smallpox eradication

A

Variola, 40% Initialy variolation, material from patient who survived smallpox rubbed into arm

Vaccination by using cow pox

Eradication possible due to
no animal reservoir
no latent infection
easily recognizable symptoms
no antigenic variation
Vaccine effective, cheap, heat stable, easy to administer

Rinderpest also eradicated by vaccination

61
Q

Vaccine

A

Live vaccines.
Attenuated mutants or related virus
Self replicating-cheap
Virus may revert to virulence, danger to immunocompromised,
needs cold storage

Dead vaccine
inactivated whole virus
Or subunit of virus
safe
may require mutliple shots to become immune

Passive
Give antibodies
from animal serum or monoclonal antibodies
Maternal antibodies in breast milk
immedtaie protection
serum sickness
short lived

Rational attenuation-delete virulence genes

Live recombinant virus-Put antigen into safer virus, rabies glycoprotein in vaccina

Virus-like particles-capsid can be virus like

Nucleic acid immunization-mRNA encoding antigen

BOD (5 decks)

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