Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Viruses > Flashcards

Viruses Flashcards

1
Q

What are the diameters of viruses?

A

20-300nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do we visualise viruses?

A

Most viruses cannot be seen with an optical microscope, so scanning and transmission electron microscopes are used to visualise them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What genome do most viruses have?

A

RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does positive sense mean?

A

Positive-sense viral RNA is in the same sense as viral mRNA and thus at least a part of it can be immediately translated by the host cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does negative sense mean?

A

Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA-dependent RNA polymerase before translation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does each Baltimore group define?

A

Group I: double-stranded DNA viruses

Group II: single-stranded DNA viruses

Group III: double-stranded RNA viruses

Group IV: positive sense single-stranded RNA viruses

Group V: negative sense single-stranded RNA viruses

Group VI: single-stranded RNA viruses with a DNA intermediate in their life cycle (retro)

Group VII: double-stranded DNA viruses with an RNA intermediate in their life cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give an example of a virus in each Baltimore group

A

Group I: Herpes, smallpox, adenovirus

Group II: B19 parvovirus (slapped cheek rash)

Group III: Rotavirus

Group IV: Polio, norovirus, dengue

Group V: influenza, measles, mumps, rabies

Group VI: HIV-1

Group VII: hepatitis B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the protective coat of the nucleic acid?

A

Capsid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the virion lipid envelope derived from?

A

Host cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are proteins associated with nucleic acid known as?

A

Nucleoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Roughly how do DNA viruses replicate?

A

The genome replication of most DNA viruses takes place in the cell’s nucleus. Most DNA viruses are entirely dependent on the host cell’s DNA and RNA synthesising machinery, and RNA processing machinery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Roughly how to RNA viruses replicate - what is it dependent on?

A

Replication of RNA viruses usually takes place in the cytoplasm. The method depends on several further factors.

The polarity (whether or not it can be used directly by ribosomes to make proteins)

Single-stranded or double-stranded genetic material.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Roughly how do reverse transcribing viruses replicate?

A

Reverse transcribing viruses have ssRNA or dsDNA in their particles.

Reverse transcribing viruses with RNA genomes (retroviruses) use a DNA intermediate to replicate, whereas those with DNA genomes (pararetroviruses) use an RNA intermediate during genome replication.

Both types use a reverse transcriptase, or RNA-dependent DNA polymerase enzyme, to carry out the nucleic acid conversion.

Retroviruses integrate the DNA produced by reverse transcription into the host genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a plaque assay?

A

Virus stock is incubated, the spread of the new viruses is restricted to neighbouring cells by the gel.

Consequently, each infectious particle produces a circular zone of infected cells called a plaque.

Eventually the plaque becomes large enough to be visible to the naked eye.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Haemagglutination?

A

Many viruses attach to molecules present on the surface of RBCs.

A consequence of this is that at certain concentrations, a viral suspension may bind together (agglutinate) the RBCs, thus preventing them from settling out of suspension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a plaque assay useful for calculating?

A

Comparing these plates at different viral concentration helps us to calculate the viral load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Haemagglutination requires samples containing whole (live or inactivated) virus

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does convalescent mean?

A

Non-infectious/ recovering phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nose and throat swabs from convalescent phase patients are a good source of samples for qRT-PCR.

A

False, once the patient has recovered the immune system has cleared the virus and therefore there are no virions to detect by qRT-PCR at any sampling site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Serum samples from acute phase patients are usually positive for influenza by qRT-PCR.

A

False, during the course of a normal influenza infection only cells of the upper respiratory tract are infected and these shed viruses from their apical surface, releasing virus back into the respiratory mucus. This means that virions are not generally found within the blood, except (in rare and mostly fatal cases (e.g. a fatal H5N1 avian influenza case).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Serum samples from convalescent patients are a good source of samples for qRT-PCR.

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Haemagglutinin adopts a fusion-promoting conformation at pH values above 8.2

A

False - Once a pH of about 5 is reached (actual pH varies by strain from 4.6 to 6) the HA protein alters its conformation to insert a fusion peptide into the endosomal membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Haemagglutinin binds to sialic acid residues

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Haemagglutinin changes conformation at low pH

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Haemagglutinin cleaves n-acetyl neuraminic acid from oligosaccharides

A

False - N-acetyl neuraminic acid or sialic acid is cleaved from oligosaccarides on glycoproteins by the viral neuraminidase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Haemagglutination can be used to titrate virus concentration

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does haemagglutination work

A

In sufficient concentrations, virions will cross-link red blood cells to each other

If the virus is sequentially diluted eventually there will not be enough present to agglutinate the red blood cells.

By observing how many dilutions are required to lose this haemagglutination response it is possible to provide a standardised measure of viral titre (i.e. the concentration of virus) in an unknown sample.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why are haemagglutination units arbitrary?

A

It is very dependent on experimental conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Haemagglutination is inhibited by antibodies to haemagglutinin

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can a haemagglutination inhibition assay be used to titre anti-HA antibodies?

A

The higher the titre of antibodies, the more the serum will have to be diluted until it no longer inhibits haemagglutination.

This forms the basis of the haemagglutination inhibition (HI) assay, which measures anti-HA antibody titres and can be used to assess seroconversion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Haemagglutination is recognised by the formation of a ‘shield’ in the base of a micro-titre plate

A

True A shield is the product of red blood cells being hindered from forming a pellet by the cross linking of the cells via viruses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

The HAI test involves testing serial dilutions of patient sera

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

The HAI test takes as its end point the first dilution failing to inhibit haemagglutination

A

False, the end point is recorded as the last dilution showing inhibition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

The HAI test produces a ‘button’ as a positive result (presence of antibody)

A

True - A button is produced from settling red blood cells. Enough virus is added to each well to cause haemagglutination (producing a shield), so a button can only result if antibodies are present to neutralise the virus and prevent haemagglutination - thus a button is a positive result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Is the plaque assay qualitative or quantitative?

A

Can be quantitative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How many types of influenza virus are there?

A

Influenza A,B,C,D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What influenza viruses cause seasonal influenza?

A

A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What influenza virus causes pandemics?

A

Influenza A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Why do pandemics have higher death rates?

A

Because of lack of pre-existing immunity in humans more infections and more deaths than usual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Where does the influenza virus infect first?

A

Upper airway then spreads to the ciliated calls in the bronchus and bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the approximate size of influenza virus?

A

120nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What Baltimore type is influenza?

A

Type V negative-sense single-stranded RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Major influenza glycoproteins?

A

HA and NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is antigenic drift?

A

Accumulation of point mutations in the viral haemagglutinin and neuraminidase genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does antigenic drift facilitate?

A

Seasonal epidemics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is antigenic shift?

A

Sporadic event, in which a novel virus strain finds a niche within a human host.

Genetic change is much more stark in antigenic shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How do novel viruses commonly arise?

A

Co-infection of a cell with two viruses, this leads to assortment of the viral DNA within the cell and the generation of new HA/NA genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How is viral cross-infection normally prevented?

A

Differential sialic acid binding

Human influenza viruses preferentially bind to α2,6-linked sialyloligosaccharide receptors, (which predominate in the human upper respiratory tract); whereas avian influenza viruses bind to α2,3-linked sialyloligosaccharide receptors, (which are more prevalent in the lower respiratory tract).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is human sialic acid vs bird sialic acid?

A

Human - 2,6

Avian - 2,3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why are pigs powerful mixing vessels?

A

Pigs are able to bind HA to either sialic linkage - new strains can develop upon co-infection with both a human and avian virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does influenza enter cells?

A

Viral hemagglutinin interacts with sialic acid receptors on cell surface, extracellular proteases then cleave the HA, modifying it to facilitate attachment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What facilitates release of influenza from the endosome?

A

Low pH of the endosome is what facilitates this release, M2 receptors carry protons into the interior of virion and promote uncoating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

When the genetic material enters the nucleus what happens? (influenza)

A

virion RNA polymerase transcribes the eight genome segments into eight mRNAs,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why is RNA transcription limited to the nucleus?

A

5’ guanosine cap must be utilised from the cell (this is called cap snatching).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What must the influenza use from the host cell?

A

5’ guanosine cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where does translation occur?

A

Cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where does mRNA go after it is transcribed? influenza

A

Most mRNA then moves to the cytoplasm for translation to viral proteins

Some remain in the nucleus to act as a template for synthesis of the negative sense strand RNA genomes for progeny virions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does NA release the virus?

A

NA releases the virus by cleaving the sialic acid on the cell surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What TLR responds to ssRNA?

A

TLR7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does RIG-1 respond to?

A

5’-triphosphate RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What Baltimore group is SARS-CoV2?

A

Type IV, positive sense ssRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What three proteins does the COVID membrane contain?

A

Spike (S) type I glycoprotein, forming peplomers on the virion surface

Membrane (M) protein

Small membrane protein (E).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What receptor does spike protein S bind to in humans?

A

ACE-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What cells contain ACE-2 receptors?

A

Type II pneumocytes and resident macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How does COVID associate with and enter host cell?

A

Coronavirus spike protein S1 region associates with ACE-2

S2 protease makes cleavage of S1 domain on spike protein, exposes the binding domain on S2, brings virus much closer for membrane fusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What happens once COVID enters the host cell?

A

Following entry, the release and uncoating of the genomic RNA subject it to immediate translation (ribosomes) into the polyprotein.

Replication of the viral genome occurs alongside some mRNAs from the structural proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What happens to the viral polyprotein? (CoV-2)

A

Polyprotein is cleaved by protease to proteins needed for replication (i.e RNA dependent RNA polymerase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Where does replication occur? (CoV-2)

A

Replication does not occur in the nucleus, instead, biogenesis of viral replication organelles create a protective microenvironment in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What host gene acts to block COVID life cycle?

A

Type 1 interferon stimulating gene 15 (ISG-15), blocks various stages of the viral life cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the hepatitis viruses?

A 
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is hepatitis?

A

Describes the inflammation of the liver tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Signs and symptoms of hepatitis

A 
Generally feel off colour 
Nausea and vomiting 
Hepatomegaly 
Jaundice 
Pale stool/dark urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the biochemical markers of hepatitis?

A

Alanine aminotransferase (ALT), which is derived from hepatocytes.

Later, there is a rise in Bilirubin and also Alkaline Phosphatase (biliary) (accompanied by jaundice).

If very severe (i.e chronic hepatitis) may see changes in synthetic function of the liver (albumin, clotting factors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Are hepatitis viruses cytopathic?

A

Relatively non-cytopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What leads to viral hepatitis?

A

Innate immune response necessary for viral clearance (IFN gamma, TNF alpha), these responses lead to the killing of infected cells and bystander killing.

Increased levels of CD8 cells in the hepatic tissue is thought to play a role in cell mediated immune injury in response to the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What family is hep A part of?

A

Picornavirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the hep A baltimore group/genome?

A

IV, +ssRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Is hep A enveloped?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Where does hep A replicate?

A

Cytoplasm

80
Q

How is Hep A transmitted?

A

Feco-oral route

81
Q

How is hep A diagnosed?

A

Diagnosed by detecting Hepatitis A IgM, there is an effective vaccine

82
Q

Risk of hep A?

A

Mild and transient but can be lethal in pregnancy (20%)

83
Q

What family is hep B?

A

Hepadnavirus

84
Q

What Baltimore group/genome is hep b?

A

Group VII, partially double stranded DNA virus with reverse transcriptase

85
Q

What is the hep B surface antigen?

A

HBsAg

86
Q

What are the genes coded for by hep B?

A

S gene - surface antigen
C gene - core antigen and e antigen
P gene - polymerase
X gene - X protein HBx (activator of viral transcription)

87
Q

How does hep B DNA form completely dsDNA?

A

Virion DNA polymerase synthesizes the missing DNA portion - ds circular DNA formed

88
Q

What happens to the cccDNA hep b?

A

The cccDNA utilizes the cellular transcriptional machinery to produce all viral RNAs necessary for protein production and viral replication.

89
Q

How is hep B genome replicated?

A

cccDNA converted to +RNA - reverse transcriptase then converts to genome DNA

90
Q

How is hep B transmitted?

A

Blood (needle stick injuries, therefore small amounts of blood necessary)

Sexual intercourse

Perinatally from mother to newborn

91
Q

What is the outcome for hep B patients?

A

> 95% of adults resolve infection naturally.

~5% of adults become chronic carriers, and 90% of newborn babies. In this case viral DNA and viral antigen is present in the blood long term

92
Q

What mediates lifelong hep B immunity?

A

Lifelong immunity is mediated by the anti HBsAg antibody - preventing it from interacting with the hepatocyte.

93
Q

What type of virus family is hep C?

A

Flavivirus

94
Q

What is the hep C Baltimore group/genome?

A

+ssRNA, IV

95
Q

Does hep C have polymerase?

A

No

96
Q

Why is hep C difficult to vaccinate?

A

The genetic variability is due to the high mutation rate in the gene and absence of proofreading function.

97
Q

How many cases of hep C lead to chronic infection, why ?

A

More than 50% of cases result in chronic infection (more than HBV), this chronic condition

This high rate is due to the ability of the HCV protease to inactivate a signal protein involved in inducing interferon in hepatocytes.

98
Q

What can hep C lead to?

A

Predisposes to hepatocellular carcinoma.

99
Q

Where is Hep C present?

A

Hepatocytes and blood borne

100
Q

How is hep C transferred?

A

Transmitted primarily in the blood - injection drug use accounts for almost all transmission.

Also mother to child during birth

101
Q

How many patients of hep C can control infection? How?

A

Control of infection can occur after acute infection in about 15% of patients, they soon develop an anti-HCV antibody

85% of patients remain as carriers, despite development of an antibody.

102
Q

What is the lower CD4 limit that distinguishes someone to have AIDS?

A

100 cells per microlitre of blood

103
Q

Common secondary infections in AIDS?

A 
Karposi sarcoma 
Meningitis type infections. 
Cryptococcus neoformans 
Toxoplasma gondii
CMV
Candida (thrush) 
Pneumocystis jirovecii
Mycobacterium tuberculosis
104
Q

What Baltimore group and genome is HIV1?

A

Group VI +ssRNA retrovirus

105
Q

What family is HIV?

A

Lentivirus

106
Q

HIV genome consists of…

A

Three open reading frames:
gag, which codes for core structural proteins
pol, which codes for the important nucleocapsid enzymes, reverse transcriptase, integrase and protease
env, which is the glycoprotein coding gene.

107
Q

What interactions does HIV make with CD4 cells for entry?

A

gp120 envelope protein binds to cell surface CD4 conformational change exposes co-receptor binding site on gp120

Binds chemokine receptor CCR5 (expressed by activated/memory CD4+ T cells, macrophages and dendritic cells - R5 strains) or CXCR4 (naïve CD4+ T cells, X4 strains)

108
Q

What cells express CCR5?

A

Activated/memory CD4+ T cells, macrophages and dendritic cells

109
Q

What cells express CXCR4?

A

Naive CD4+ T cells

110
Q

What does gp41 facilitate?

A

Fusion of viral envelope with cell membrane

111
Q

What happens to HIV ssRNA when inside cell?

A

RT converts to ds proviral DNA

112
Q

What happens to HIV proviral DNA after it is produced in the cytosol?

A

Trafficked to the nucleus where integrase integrates viral DNA into host cell DNA

113
Q

What antivirals are used for influenza (endosome stage)?

A

M2 channel blockers (amantadine and rimantadine) are used as antiviral drugs for influenza.

114
Q

What antivirals are used for influenza (release stage)?

A

Neuraminidase inhibitors (oseltamivir) prevent cleavage and thus, the release of the progeny from the cell.

115
Q

What antiviral is used on HIV entry?

A

Small molecule antagonist Maraviroc (MVC) is the only CCR5 inhibitor currently clinically approved for use - only useful for patients with CCR5+ HIV

116
Q

What antivirals are used at the HIV RT stage - how do they work?

A

NRTIs are incorporated into viral DNA by RT - they lack a 3′ hydoxyl group, thus, their incorporation blocks viral DNA synthesis.

NNRTIs inhibit viral reverse transcriptase but not at the nucleotide binding site

117
Q

What is an NRTI example?

A

AZT

118
Q

Why are viral proteases needed?

A

Viral protease cleaves Gag and Pol polyproteins into functional polypeptides - form mature, infectious virion

119
Q

What antivirals target protein cleavage?

A

Protease inhibitors: ritonavir, amprenavir, saquinavir

120
Q

What facilitates HIV cell-cell spread?

A

A virological synapse is a transient adhesive junction allowing viral spread from an infected to uninfected cell

121
Q

Where does HIV cell-cell spread occur?

A

Cell-cell spread occurs predominantly in densely populated tissues and enhances rate and amount of infection

122
Q

How is HIV transmitted?

A

Transmission of HIV occurs primarily through sexual contact and transfer of infected blood.

Perinatal transmission from infected mother to neonate also occurs (across placenta, at birth, or through breastmilk).

123
Q

When is the early acute stage of HIV, what occurs?

A

Lasts for 2-4 weeks after infection, fever, lethargy, sore throat, maculopapular rash is also seen on the trunk and extremities.

124
Q

What are CD4/WBC counts like in early acute HIV?

A

Leukopenia but CD4 count usually normal

125
Q

What is viraemia like in early acute HIV?

A

High level viraemia, infection is readily transmissible

126
Q

As the early acute phase ends what happens to CD4 count, viral load, CD8?

A

As this phase ends, the viral load and CD4 counts begin to fall, while CD8 count may rise.

127
Q

How long after HIV infection does it take for antibodies to appear?

A

Antibodies appear in around 10-14 days

128
Q

How long does the mid-latent phase of HIV last? What occurs?

A

7-11 year untreated, patient asymptomatic

129
Q

What is viraemia like in mid-latent HIV?

A

Low

130
Q

What occurs in the AIDS stage?

A

Persistent fevers, weight loss, fatigue, common opportunistic commensal infections

131
Q

What is viral load and CD4 count like in AIDS stage?

A

Viral load rises again

CD4 count at critical stage

132
Q

Reverse transcriptase action

A

Hybridises to primer binding site.

RNA primed RT elongates until the 5’ end of the RNA is reached to form a negative strand of DNA.

The DNA hybridizes with repeat sequences at the 3’ end and circularises further elongated by RT.

RT hydrolyses remaining RNA, leaving polypurine tract, which serves as a primer for 2nd DNA strand synthesis.

RT DNA dependant DNA pol activity results in 2nd DNA strand synthesis.

133
Q

Integrase action

A

IN recognises both ends of viral DNA and cleaves the 3’ in a staggered fashion.

Links the 3’ end of viral DNA with 5’ end of target DNA.

134
Q

Integrase inhibitors

A

Raltegravir.

135
Q

Elite controllers of HIV..

A

Have a delta32 CCR5 mutation, therefore gp120 cannot bind.

136
Q

How does HIV induce GALT damage?

A

HIV infects and kills CD4+ T cells

Massive acute inflammation that damages epithelial barrier

Compromised GALT integrity leads to bacterial translocation and systemic immune activation.

137
Q

How does HIV evade the immune response?

A

Escape from antibodies and CTLs: antigenic variation.

Recombination between genomes occurs when there is more than 1 HIV1 genome per cell.

138
Q

What is the main pathogenetic mechanism of HIV?

A

Direct HIV-1 killing of CD4+ cells by apoptosis or pyroptosis.

Killing of infected CD4+ cells by CD8+ cells. Indirect killing of HIV-1 infected T cells by non-specific immune activation.

Slow loss of lymphoid tissue architecture and antigen presentation function.

139
Q

How does HIV Tropism change ?

A

In early infection there is extensive death of CCR5 CD4+ cells= selection pressure against the R5 phenotype.

50% of infected have a switch to X4 dominant HIV - no longer detected by immune cells.

140
Q

What immune response is generated by HIV?

A

Innate

NK cell activation and plasmacytoid DC homing.

T cell adaptive response: CTL specific to HIV arise early and persist.

Very short lived HIV specific CD4+ cells.

Antibody response: get a specific response after months - initially weak and strain specific.

141
Q

How do HIV antibodies act?

A

Bind to env to prevent viral entry

142
Q

What is HART?

A

Antiretroviral therapy to block HIV replication.

Combination to prevent mutations conferring resistance.

Drops viraemia however infection persists as soon as come off the therapy viraemia rebounds

143
Q

How is HBV targeted? (antivirals and vaccine)

A

Target viral weakpoints with tenofovir, Entecavir (RT antagonists), treat with interferon alpha.

Vaccine provides effective protection through antibody to HBV surface antigen

144
Q

How long is HBV incubation?

A

2-6months

145
Q

What antivirals are used against HCV?

A

Use RNAdepRNA polymerase inhibitors, ribavirin, protease inhibitors and interferon alpha.

146
Q

What specific CD4 T cells are affected by HIV?

A

Th17 important mediators of mucosal immunity (especially in the GI tract).

Acute inflammatory tissue damage is mediated by viral replication and cell death

147
Q

Symptoms of poliomyelitis?

A

Typically asymptomatic or with minor symptoms such as fever, headache and sore throat when there is viraemia.

Paralytic poliomyelitis occurs in less that 1% of polio

148
Q

What causes paralytic polio?

A

Virus enters the CNS and replicates in motor neurone within the spinal cord, brainstem or motor cortex, resulting in destruction - temporary or permanent paralysis. In rare cases, can lead to respiratory arrest and death.

149
Q

What virus family is polio part of?

A

Picornovirus

150
Q

Polio Baltimore group/ genome?

A

Single stranded positive linear RNA genome, so RNA can associate directly with the ribosome, IV

151
Q

What surrounds the polio genome?

A

Covered by a capsid composed of 4 virion proteins arranged in icosahedral symmetry.

152
Q

What is the polio cell entry mechanism?

A

Binds to Ig-like receptor, CD155, on the surface of the cell, leads to irreversible conformational change of the viral particle necessary for viral entry.

Thought to occur via receptor mediated endocytosis: Immediately released from the endosome into the cytoplasm.

153
Q

Why is polio such a simple virus?

A

Only RNA and a nonenveloped icosahedral protein coat that encapsulates it

154
Q

Why is polio such a simple virus?

A

Only RNA, and a nonenveloped icosahedral protein coat which encapsulates it

155
Q

What part of polio mRNA is cleaved by host to initiate translation?

A

VPg protein at the 5’end is cleaved by cellular phosphodiesterase to initiate translation within the cytoplasm.

156
Q

How is polio mRNA translated

A

Translated as one long peptide, then cleaved by internal proteases.

157
Q

How is polio genome replicated?

A

RNA-dependent RNA polymerase uses +ssRNA genome as a pattern, for synthesis of the negative-strand antigenomic RNA. Then used as templates ofr positive RNA synthesis

158
Q

Polio route of infection?

A

Feco-oral

159
Q

What is HHV3?

A

Varicella Zoster causes chickenpox, reactivation = shingles

160
Q

Are all herpes viruses structurally similar?

A

Yes

161
Q

What is the Baltimore group/genome of herpes virus?

A

dsDNA genome (Baltimore group 1)

162
Q

What is the size of herpes viruses?

A

120-200nm

163
Q

What do herpes simplex viruses cause, which viruses?

A

HHV-1, causes cold sores HHV-2, causes genital herpes

164
Q

Where do HSVs assert their latency?

A

Sensory ganglia

165
Q

Where is HSVs DNA during latency?

A

Most (if not all) the viral DNA is present in the cytoplasm rather than the nuclear DNA.

166
Q

What herpesvirus is EBV? What does it cause?

A

HHV-4, infectious mononucleosis, glandular fever. It is associated with Burkitt’s Lymphoma and nasopharyngeal carcinomas.

Infection in infancy is normally asymptomatic

90% of adults worldwide are chronic carriers

167
Q

How can EBV be diagnosed?

A

Unique antigen viral capsid antigen (VCA)

168
Q

What cells can EBV infect?

A

B cells and epithelial cells

169
Q

How does EBV enter B cell?

A

gp350 binds to cellular receptor CD21, and gp42 interacts with MHC II to trigger fusion of the viral envelope with the cell membrane.

170
Q

How does EBV enter epithelial cells?

A

To enter epithelial cells, BMRF-2 interacts with cellular integrins to trigger viral fusion.

171
Q

What happens when EBV enters the cell?

A

Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus.

172
Q

What is latency defined by on a genetic level?

A

Less genes expressed in latency

173
Q

What does EBV cause infected B cells to do?

A

Infected B- cells are stimulated to divide in the absence of B-cell antigen. Virus mimics the signals of replication and reactivation.

174
Q

Why is it beneficial for EBV to stimulate B cell replication?

A

Viral genome is copied alongside the B cells.

175
Q

What gives rise to the pathology of glandular fever?

A

EBV viral proteins produced inside B cells - expressed on MHC II receptors

CTL (CD8) cells then react against the infected B cells. This gives rise to the pathology and inflammation of glandular fever (IM).

176
Q

Is emergence from latency dependent on antigen? (EBV)

A

Reactivation is antigen independent.

177
Q

What occurs in EBV emergence from latency?

A

Plasma cells produced from the activated memory (latent) B-cell

Memory B-cell reservoir also maintained

Differentiation to a plasma cell acts as a trigger for lytic replication, (more genes expressed) virus can infect the epithelia, and B cell clones (previously not infected)

B-cells divide but T-cell response often primed and larger due to immunity.

178
Q

What is the lytic replication (EBV)?

A

Rapid B cell replication and EBV replication

179
Q

Why do B cells replicate when infected with EBV?

A

EBV influences gene expression inside the B cell- B cell behaves as if it has been stimulated by an antigen

180
Q

Why is EBV associated with Burkitt’s Lymphoma?

A

Translocation of cMYC gene from chromosome 8 to chromosome 14 is characteristic of Burkitt Lymphoma

Translocation brings MYC gene under control of immunoglobulin heavy chain enhancer

MYC potently drives B cell proliferation and apoptosis

181
Q

What are papillomaviruses?

A

Small, non-enveloped viruses, 55 nm capsid

182
Q

Papillomavirus genome and Baltimore group?

A

Circular dsDNA, circular, supercoiled genome (Baltimore group 1).

183
Q

What can papillomaviruses cause?

A

Papilloma’s (benign skin tumours that can lead to malignancies)

Cervical carcinoma

184
Q

How are new HBV genomes generated

A

DNA repair to form cccDNA

Transcription of cccDNA to RNA by RNA pol II

Reverse transcription of RNA to form +DNA strand

185
Q

What vaccine, if any, is available for HBV?

A

Hepatitis B vaccine: Recombinant vaccine containing HBsAg (grown in yeast)

186
Q

Does RNA polymerase have proof reading?

A

No

187
Q

Does DNA polymerase have proof reading?

A

Yes

188
Q

What is the initial site of EBV infection?

A

Oropharynx

189
Q

Which infectious agent can be transmitted by a blood transfusion but does not contain nucleic acid?

A

Prions

190
Q

What host genetic factors influence rate of progression to AIDS?

A

HLAB27, B57 good, HLAB35 bad

191
Q

The virus genome is a 7500base long positive sense RNA which is translated into a single long “polyprotein”. This large protein then cleaves itself into subsections and finally into the separate proteins involved in replication and packaging, including the virus capsid proteins.

A

Polio

192
Q

99% of cervical carcinomas contain DNA sequences of this virus. Often in cervical carcinoma the viral genome is integrated into the host genome resulting in unregulated expression of the viral transforming proteins E6 and E7.

A

HPV

193
Q

Which virus has a small circular DNA genome that is partially double stranded? The virus is relatively resilient and, in some instances, has been shown to remain infectious on environmental surfaces for at least a month at room temperature?

A

HBV

194
Q

Which virus has a 172 kb linear double stranded DNA genome that becomes circular for replication and latency? This virus is associated with the development of B-cell lymphoma and nasopharyngeal carcinoma.

A

Epstein Barr

195
Q

What does the term “eclipse phase” mean with regard to virus replication?

A

Corresponds to the period during which the input virus becomes uncoated. As a result, no infectious virus can detected during this time

196
Q

EBV transferred by

A

Saliva

Pathology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions