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Medical Microbiology > Day 2: Coronaviruses, Arboviruses, HIV-1 > Flashcards

Day 2: Coronaviruses, Arboviruses, HIV-1 Flashcards

HC03, 04, 05

1
Q

HC03: Types of viral DNA genomes

A

(+) ssDNA
(-) ssDNA
dsDNA

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2
Q

Types of viral RNA genome

A

(+) ssRNA > direct translation
(-) ssRNA > conversion
dsRNA

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3
Q

The central dogma of a virus is dependent on the …

A

host machinery

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4
Q

DNA virus requirement

A

Needs to travel to the nucleus
> all the parts there to make mRNA from viral DNA

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5
Q

(-) ssDNA in host nucleus

A

> directly mRNA made
(-) strand DNA, virus can do a lot

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6
Q

dsDNA viruses

A

Have large battery: large DNA
> large viruses
> go into nucleus as well

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7
Q

(+) ssDNA viruses in humans

A

do not exist in humans

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8
Q

Often, DNA viruses cause … infection

A

chronic
> virus replicates with the host cell

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9
Q

Cell favourite for DNA virus

A

Rapid dividing cell
> highly proliferative progenitor cells
> does not want to infect definitely differentiated cells

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10
Q

Are RNA viruses often chronic?

A

No, do not integrate into genome
> like coronaviruses

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11
Q

(+) ssRNA characteristics

A
  • Directly translated to proteins
  • faster synthesis
  • is the own mRNA
  • like coronaviruses
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12
Q

(-) ssRNA characteristics

A
  • Needs to make mRNA with RNA-dependent RNA polymerase
  • Virus needs to carry its own polymerase
    > human cells do not have RNA-dependent RNA polymerase
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13
Q

dsRNA example

A

rotavirus

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14
Q

Where is the cells do the viral RNA reside?

A

In the cytosol > protein synthesis > make mRNA or be the mRNA
- exception: HIV goes to nucleus

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15
Q

RNA are … chronic except

A

Not, except HIV, which can get inside nucleus or if it is inside regenerative cells like hepatocytes

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16
Q

Which cells preferred by RNA virus: different types

A
  • RNA are Acute viruses: Hit and run: infect, spread (through excretion, sneezing and pooping) and infect again
    > epithelial cells: lung intestine > secretory cells make mucus etc > specialized and differentiated cells preferred
    > acute viruses bind these cells (epithelial cell receptors): cell does not have to divide in order for virus to spread, and close to the excretion sites for more contamination
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17
Q

Coronavirus structural proteins

A
  • Membrane glycoproteins (M) (on envelope membrane)
  • Spike proteins (S) (on the envelope membrane)
  • Envelope protein (E)
  • Nucleocapsid protein (around the RNA to protect it, form the capsid)
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18
Q

Coronavirus genome

A

(+) ssRNA, largest human RNA virus, 30,000 nt
> direct protein synthesis
> S, E, M and N genes on 3’ side of ORF
> at 5’: products which are transcribed first

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19
Q

First steps coronavirus after infection

A

Translate 1a and 1b genes at the 5’ of the ORF only by stopping the translation early
> proteins made for replication
> build a protective ‘house’ around the virus
> polyprotein of 1a and 1b made which is cleaved by virus its own proteases: go into cytosol

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20
Q

Entry coronaviruses: SARS-CoV-2

A

> Use receptor on differentiated cell, the ACE2
only on cilia epithelial cells ACE2
Entry via receptor mediated endocytosis and fusion with endosome membrane

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21
Q

Coronavirus when (+) ssRNA in the cytosol

A

> Make double membrane vesicles to hide from TLRs (Toll like receptors, which look out for pathogens to signal this) inside the cell: protective house made at the ER
ER bulges into double membrane vesicles around the ssRNA > replicase complexes makes more and make (-) ssRNA strands
when enough (-) strands made and (+) strands made from them > make subgenomic messengers

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22
Q

Making subgenomic messengers by corona, what is made

A

RNA-dependent RNA polymerase jumps at the (-) strand to make little parts of (+) strands with just one gene for example > for viral replication and release
> subgenomic messengers needed for spike proteins for example and the E, M and N genes (only the non-structural proteins 1a and 1b are made directly from the primary (+) ssRNA)
> make (-) strand from (+) strand
» you want 5’ UTR (for translation initiation) and not 1a and 1b, not needed for replication and release of new virus

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23
Q

Why not splicing of the RNA genome of coronaviruses?

A

That is only possible in the nucleus, alternative mechanisms required

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24
Q

Coronavirus goal principle of the virus

A

Make new viruses as fast as possible and release before detection and elimination in the host > spread fast

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25
Q

Human coronaviruses types

A

8 types in total, just 5 circulating still
> SARS-CoV-2
> HCoV-HKU1
> HCoV-OC43
> HCoV-NL63
> HCoV-229E

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26
Q

Sarbecoviruses

A

SARS-CoV and SARS-CoV-2
> SARS-CoV is extinct: had a high mortality rate especially at older age > patients isolated fast
» in China and Hongkong

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27
Q

Merbecoviruses

A

MERS-CoV
> in Saoudi-Arabia, not worldwide as well
> From camels to humans
> Deathly, mostly in patients with underlying conditions: septic shock, acute respiratory distress syndrome and organ failures
> fever, cough, chills, sore throat and rapid progress to pneumonia
> also asymptomatic carriers
> Low prevalence now and regulated

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28
Q

Porcine DELTA coronavirus

A

HKU15
> From sea animals which can infect pigs
> can infect humans
> can be dangerous when becoming more infectious, now already vaccinations
> mild disease in children: cough and abdominal pain and fever

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29
Q

Besides SARS-CoV-2, 4 other endemic coronaviruses:

A

Seasonal coronaviruses: causing a cold
> in humans for hundreds of years
> HCoV- HKU1/OC43/NL63/229E

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30
Q

HCoV-229E history

A

Detected long ago and symptoms related to cold
> can be asymptomatic as well and infectious still

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31
Q

First infection with seasonal coronaviruses

A

For all of them > before age of 6 years old

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32
Q

When susceptible for seasonal coronaviruses

A

After maternal antibodies transferred to the child start to disappear

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33
Q

Seasonal coronaviruses acute/chronic

A

Acute > when following adult humans in study > spikes of antibodies (short infections, peaks)
> viruses disappeared
> half-life of antibodies has to do with it as well
> decrease in levels

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34
Q

SARS-CoV-2 progression

A

At start pandemic: highest mortality, lowest amount of positive tests
> later on, spikes in positive test but not that high peaks in mortality as first
» eldery most vulnerable
> Omicron appeared: more infectious, less deadly
» evolution to milder variant with lowered pathogenicity.
» virus does not want the host to die: more favourable to infect other persons when the host is alive and well and goes into public except for isolation in hospital or quarantaine elsewere

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35
Q

HC04: Arboviruses are transmitted through:

A

Vectors

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36
Q

Infections spread on … to reach large area

A

Wings: by insects, birds, bats, (and planes)

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37
Q

Are blood-sucking insects favourable for the virus as vector?

A

Yes > get into the bloodstream immediately.

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38
Q

Requirement arboviruses

A

Adaptations to survive in these different host vector species

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39
Q

Vector

A

Animal between human infections

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40
Q

Arbovirus meaning

A

Arbo: arthropod borne > transmission by stinging insects

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41
Q

Are arboviruses a family of viruses?

A

No, just same infection route

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42
Q

Two types of arboviruses

A
  • Mosquito-borne: Flaviviridae, Bunyaviridae and Togaviridae
  • Tick-borne: Flaviviridae, Bunyaviridae and Reoviridae
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43
Q

Almost all mosquito-borne viruses are transmitted by mosquitos of the subfamily …, mainly genera … and …

A

Culicinae Culex and Aedes (with bend in body)

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44
Q

Culicinae Culex transmitted viruses diseases

A

Mostly derived from birds, most risky for encephalitis

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45
Q

Culicinae Aedes transmitted viruses disease

A
  • can cause haemorrhagic disease
  • life cycle involves water source: diverse sources even glass of tap water is enough
    > remove water sources is important
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46
Q

Why can Aedes mosquitos still spread viruses?

A

Stopped eradication campaigns and human travel
> climate change enables survival in previously inhabitable areas

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47
Q

Tiger mosquito and viruses

A

Culicinae Aedes > Aedes albopictus
> trasmission DENV and CHIKV > can breed in more temperate zones because eggs hatch there due to difference in lipid composition
» differences in ability to transmit virus exists between local mosquito populations: genetics
» can survive Dutch winter now due to climate change
> virus replicates in Aedes mosquito as well
> virus needs multiple host proteins: should replicate in mosquito and human cells

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48
Q

Transmission Chikungunya virus (CHIKV)

A

Through Aedes aegypti and Aedes albopictus > both active at daytime

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49
Q

Yellow fever virus (YFV) genome and family

A

Flavivirus
> (+) ssRNA enveloped virus

50
Q

YFV mosquitos and disease

A

> sting (active) at daytime, protection when sleeping does not work
continuous protective clothing required
fatal in 10-20% of cases
genome, capsid and spike proteins which go through envelope
make one large polyprotein which is cleaved by protease which is mostly made by the virus itself > releases itself first and then releases other proteins

51
Q

Linear ssRNA of YFV, the ends

A

3’ end of genome not polyadenylated but forms loop structure
5’ end has methylated nucleotide cap generated by virus specific methyltransferase

52
Q

Flavivirus life cycle

A

> enter by receptor-mediated endocytosis
release nucleocapsid into cytoplasm by fusion with endosomal membrane
fusion event is triggered by the acidic pH in endosome and mediated by major envelope protein E
translation, polyprotein processing, viral RNA replication on membranes
immature virus assembly into ER
mature, replicate, release

53
Q

Origin YFV and DENV (dengue virus)

A

Non-human primates > transmission cycles viruses in mosquitos and monkeys
> spillover to human

54
Q

Disease symptoms YFV infection

A

clinical spectrum
> subclinical infection
> abortive nonspecific febrile illness without jaundice
> Life-threatening disease with fever, jaundice, renal failure and haemorrhage
» Yellow fever affects all ages, but disease severity and lethality is highest in eldery > onset appears 3-6 days after mosquito bite

55
Q

Live-attenuated vaccine for YFV

A

17D and 17DD vaccines produce high levels of protection, protective immunity occurs in nearly 100% of individuals within 3-4 weeks after vaccination
» benefit of vaccination should first be investigated because serious adverse effects particularly when >60y

56
Q

DENV transmission and family

A
  • Transmission by Aedes mosquitos
  • Flavivirus
    » enveloped (+) ssRNA
57
Q

Clinical problems DENV infection

A
  • Severe complications through repetitive infections: dengue haemorrhagic fever and dengue shock syndrome
    > break-bone fever
    > rash, fever, severe pain in deep tissues
58
Q

Proteins made by DENV

A

Is flavivirus: makes large polyprotein
> from each protein one
> envelope protein at 5’
> More envelope proteins made
> ribosomes do not always make the end of the ORF, then only 5’ parts made with those proteins > more E made than polymerase because there is more needed

59
Q

DENV genome encodes&raquo_space;>

A

Structural proteins
> Capsid (C)
> Membrane (M)
> Envelope (E)
7 nonstructural proteins

60
Q

Chikungunya virus (CHIKV) genome and family

A

Enveloped (+) ssRNA virus family Togoviridae

61
Q

Clinical symptoms CHIKV infection

A

Severe headache, complications at joints, problems with walking

62
Q

How are envelope proteins made by CHIKV and polyprotein made

A

Via subgenomic messengers
> make a lot of E except of 5’ RNA synthesis and polymerase proteins.
> genome is tranlated into non-structural polyprotein which is processed by host and viral proteases, the structural program (polyprotein) is expressed through subgenomic mRNA (jump to the last bit making (+) from the made (-) for replication)

63
Q

Transmission CHIKV

A

From humans/monkeys to Aedes mosquitos to humans

64
Q

CHIKV disease and vaccine

A

> no vaccine available
causes acute febrile polyarthralgia (joint pain) and arthritis
low mortality

65
Q

Zika virus (ZIKV) threat

A

Also arbovirus besides YFV, DENV and CHIKV
> transmitted by Aedes mosquitos

66
Q

Symptoms ZIKV

A

> rash, fatigue, headaches, swollen and painful joints
can affect the unborn child: microcephaly and other birth defects/
sporadic disease
no deaths
also found in semen, sexual transmission is possible
threat has increased because mutations

67
Q

Japanese encephalitis virus (JEV)

A

Arbovirus
> Flavivirus
> leading cause encephalitis in Asia
> severe disease 1 in 250
> amongst survivors: large part have long-term neurologic sequelae
> no specific treatment
> vaccine is available

68
Q

JEV enzootic transmission cycle

A

Natural cycle
> Culex mosquitos (vector) and waterbirds (reservoir host)

> Incidental (dead-end) hosts humans and horses
> do not develop sufficient concentrations of JEV in blood to infect feeding mosquitos (low viral load)
Amplification cycle
Culex mosquitos and Pigs (amplifying hosts)

69
Q

Viral load measurment

A

Via PCR, check the viremia

70
Q

HC05: Kaposi’s sarcomas (KS)

A

Often seen in AIDS (acquired immune defieciency syndrome) patients
> caused by herpesvirus HHV8 > opportunistic
> Replicated when immuncompromised

71
Q

HIV is a retrovirus, name its characteristics

A
  • RNA virus
  • Two copies of the genome per particle
  • Enveloped virion
  • Non-segmented genome
  • Can make DNA from the RNA with reverse transcriptase (1) and insert the DNA into genome host cell in nucleus (2) > impossible to remove when cell alive: 2 exceptional properties
72
Q

Subgenomic messenger mechanism

A

> RNA pol starts at clustering RNA at the 3’ UTR of mRNA and makes copy of all structural proteins and jumps to the 5’ UTR > minus strands made with only 5’ UTR and structural proteins (growing chain 5>3)
> specific jump sequence at jumping site
> RNA-dependent RNA pol will make subgenomic (+) messengers from the (-) strands
specific for coronaviruses

73
Q

8% of the human genome is residual of retroviruses, which mean they partly …

A

drive evolution

74
Q

HIV is from the retrovirus family and in the lentivirus group. What does this entale?

A

That there is a slow progression from infection to disease (with symptoms) (7-10 years)
> HIV can cause AIDS

75
Q

Inside the HIV particle

A
  • 2 copies of the viral RNA genome ((+) ssRNA) complexed with proteins such as reverse transcriptase and integrase
    > these structures are protected by a capsid
76
Q

HIV particle capsid made out of …

A

gag proteins

77
Q

Outside of the HIV particle

A
  • Lipid membrane taken from host cell when budding from cell: covers the viral particle
  • envelope proteins gp120 (glycoprotein) and gp41 form spike-like structures > sugar groups are bound to proteins
78
Q

Polymerase of HIV

A

DNA polymerase > makes DNA but is flexible in template > makes first DNA strand from RNA template (then RNA removed by viral RNase H activity) > then make DNA from DNA template > double stranded proviral DNA
» needs primer to start
» reverse transcriptase
> RNA polymerase needs RNA template

79
Q

Genome HIV and reverse transcription

A

gag-pol-env and a primer binding site (pbs)
> also two R (repeats) at outsides and U5 (unique 5’ site) or U3 within it
> start at PBS > make bit pbs-U5-R
> translocate to R on 3’ end
> make the rest until pbs
> polypurine site before U3 is hybridized > make U3-R-U5-Primer
> translocate to pbs DNA
make the rest
> now: U3, R and U5 at each end!
> proviral DNA is longer than viral RNA with one U3, R and U5

80
Q

The primer for the reverse transcription of HIV genome:

A

3’ of our own tRNAs

81
Q

Life cycle of HIV in the host cell

A

1 Binding
2 Fusion
3 Uncoating
4 cDNA synthesis
5 Integration
6 Transcription
7 Packaging
8 Budding
9 Release of particle

82
Q

Reverse transcriptase of HIV: how does it become functional

A

It is already present in the viral particle of HIV

83
Q

Integration HIV

A

Double strand breaks made > repaired with viral cDNA between it > done by integrase

84
Q

Which enzyme transcribes HIV viral proteins

A

RNA polymerase 2 in the nucleus

85
Q

Viral RNAs of HIV-1 made by transcription contain splice sites. What happens with it?

A

Evasion of splicing in nucleus by viral proteins

86
Q

How does viral proviral DNA make it to the nucleus

A

A pre-integration complex is made around it which can pass the nuclear pores. (unsure how)

87
Q

Viral Rev protein of HIV

A

Limits the number of integrations per cell by binding to and inhibiting the integrase
> unlimited viral integrations result in death of the cell (is detected easier)

88
Q

Are there introns in HIV RNA?

A

No

89
Q

Tat protein of HIV

A

Improve viral protein synthesis by upregulating transcription
> Transcription elongation is stimulated by binding to the TAR loop (early gene product)
> RNA polymerase 2 for transcribing retroviral DNA

90
Q

One fate of provirus of HIV in host genome is the transcription. What is the other possible fate?

A

Provirus can become latent, for unstance due to CpG methylation of the LTR (promoter)

91
Q

Why is it hard to get rid of HIV

A

It is silent > the cells do not appear as being infected, but the virus can become active by re-activating transcription of the provirus

92
Q

Battling silent HIV

A

Induce transcription to expose cells as infected

93
Q

HIV was first identified as a variant of the Human T-lumphotropic virus (HTLV). Is that true?

A

No: HIV is a lentivirus and HTLV is a delta retrovirus

94
Q

One of the genuses of the retroviridae family is the spumaviruses. What is their main transmission route?

A

From apes to human

95
Q

Two types of retroviruses: simple and complex

A
  • Simple encodes only gag-pol-env
  • Complex additionally encode accessory proteins
96
Q

Complex view of HIV-1 genome

A

gag > structural proteins
pol > viral enzymes: protease-RT-Integrase
env > envelope protein binds to target cell
important virus specific proteins: tet and rev
less important accessory proteins

97
Q

The general rule is that 1 mRNA encodes 1 protein: cap-scanning-start-stop, how does HIV-1 encode more than 15 proteins from a single RNA?

A

Multiple open reading frames and code polyproteins

98
Q

Name a polyprotein of HIV-1

A

pol > Protease, reverse transcriptase and Integrase
Gag > multiple structural proteins

99
Q

Ribosomes tend to fall off: how and what is the result

A

More made at 5’ > more gag made than pol
» sometimes frameshift needed to get ribosomes into other reading frame
» capsid proteins needed more

100
Q

Gag and Pol are made as polyproteins, how are they cleaved

A

First auto-cleavage: release Protease from the pol polyprotein
> than remainder of pol, and gag
> gag and pol made as polyproteins that are packaged in the virion (cleavage after infection)

101
Q

The capsid proteins from gag

A

MA (matrix) > associated with viral membrane (p17)
CA (capsid) > condenses to cone shaped core (CA)
NC (nucleocapsid) > coats RNA genome

102
Q

Layers around HIV genome in particle

A

First layer > CA / p24
Second layer > MA / p17
Third payer > viral envelope

103
Q

How is the env protein cleaved?

A

By a cellular protease, not the HIV Protease

104
Q

HIV-1 Protease

A
  • Cuts itself out of pol polyprotein to release others later
  • Inhibited with protease inhibitors
105
Q

HIV-1 RT

A
  • Needs primer with 3’ OH termination
  • Template: RNA or DNA
  • Lacks proofreading: high error rate
  • RNase H activity: nuclease specific for RNA in the RNA:DNA hybrids
106
Q

Drugs against RT

A

NRTI and NNRTIs
> Nucleoside RT inhibitors
> Non-nucleoside RT inhibitors

107
Q

NRTIs

A
  • Resemble nucleosides from primer but lack the 3’OH
    > no extension possible: no dsDNA made
  • phosphorylation NRTIs upon uptake in cell
  • dNTP mimics
    > toxicity: cellular polymerases
    > resistance: RT catalytic core mutations
  • Should have higher affinity for viral polymerase than cellular polymerase
108
Q

NNRTIs

A
  • Discovered by random screening
  • Bind hydrophobic pocket on outside of RT
  • Resistance: in contact amino acids
109
Q

HIV-1 Integrase

A
  • Endonuclease activity
  • Integrated retroviral DNA into host genome (random each chromosome)
  • Gets viral dsDNA in proximity of DNA breaks and hosts repair mechanism ligates it in
110
Q

Integrase inhibitors

A
  • Catalytic inhibitors
  • Allosteric inhibitors
111
Q

HIV-1 envelope proteins

A

Encoded by env
> Gp120 and gp41
- Bind host receptor molecules: CD4 + CCR5
- Target for antivirals
- Major target for vaccine strategies

112
Q

Splicing HIV-1 RNA

A

Full-length HIV viral RNA is spliced and exported from nucleus to be transcribed by host ribosomes in order to generate env and the smaller proteins such as Tat and Rev
> in this way, more env made than pol, even though env is downstream of pol
> splice gag-pol off

113
Q

Disease stages HIV

A
  • Acute infection: massive destruction CD4+ T-cells in mucosal tissues
    > cells from blood go to tissues to replace CD4+ T-cells and CD4 decrease in blood
  • Chronic phase: chronic infection in tissues
  • Acquired Immunodeficiency syndrome (AIDS): almost no CD4+ T-cells: mortality to opportunistic infections which cannot be repressed
114
Q

Prognostic markers HIV

A
  • Viral RNA load in blood (RNA copies/ml)
  • CD4 count (cell/ul)
    » this decreases to virtually zero
115
Q

Effects on patients care for HIV

A
  • New approach to patient monitoring: diagnostic improvement: monitor plasma viral load and CD4+ counts
  • Pharmocology: development antivirals: by realizing that viral proteins can be targeted even though they are inside the cell
116
Q

Origin of HIV

A

From African primate species
> but these rarely get AIDS?
> HIV-1 group M, N, O and P are result of separate transmissions of SIV from apes to humans
> M and N are cross-species transmissions from chimpanzees (SIVcpz)
> O and P been transmitted from gorillas (SIVgor)

117
Q

Which HIV-1 group is responsible for pandemic?

A

The M viruses, the N, O and P groups are rare

118
Q

HIV-2 origin

A

From transmission SIV in West Africa

119
Q

Almost 50% of HIV diagnoses were ..

A

Late-stage

120
Q

HIV-1 group M is still adapting to its new host, with which results?

A
  • Becomes more virulent
  • Newly infected patients have higher viral load and lower CD4 counts
  • Strains are starting to circulate that have escaped from certain HLA-types which used to be protective against AIDS development like HLA-B27 (targets gag epitope)
  • HIV strains of today can be less efficiently inhibited with antibodies

Medical Microbiology (11 decks)

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