Viruses Flashcards
1
Q
What are the diameters of viruses?
A
20-300nm
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.
3
Q
What genome do most viruses have?
A
RNA
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.
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.
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
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
8
Q
What is the protective coat of the nucleic acid?
A
Capsid
9
Q
What is the virion lipid envelope derived from?
A
Host cell membrane
10
Q
What are proteins associated with nucleic acid known as?
A
Nucleoproteins
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.
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.
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
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.
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.
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
17
Q
Haemagglutination requires samples containing whole (live or inactivated) virus
A
True
18
Q
What does convalescent mean?
A
Non-infectious/ recovering phase
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.
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).
21
Q
Serum samples from convalescent patients are a good source of samples for qRT-PCR.
A
False
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.
23
Q
Haemagglutinin binds to sialic acid residues
A
True
24
Q
Haemagglutinin changes conformation at low pH
A
True
25
Haemagglutinin cleaves n-acetyl neuraminic acid from oligosaccharides
False - N-acetyl neuraminic acid or sialic acid is cleaved from oligosaccarides on glycoproteins by the viral neuraminidase.
26
Haemagglutination can be used to titrate virus concentration
True
27
How does haemagglutination work
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.
28
Why are haemagglutination units arbitrary?
It is very dependent on experimental conditions
29
Haemagglutination is inhibited by antibodies to haemagglutinin
True
30
How can a haemagglutination inhibition assay be used to titre anti-HA antibodies?
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.
31
Haemagglutination is recognised by the formation of a 'shield' in the base of a micro-titre plate
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.
32
The HAI test involves testing serial dilutions of patient sera
True
33
The HAI test takes as its end point the first dilution failing to inhibit haemagglutination
False, the end point is recorded as the last dilution showing inhibition.
34
The HAI test produces a 'button' as a positive result (presence of antibody)
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.
35
Is the plaque assay qualitative or quantitative?
Can be quantitative
36
How many types of influenza virus are there?
Influenza A,B,C,D
37
What influenza viruses cause seasonal influenza?
A and B
38
What influenza virus causes pandemics?
Influenza A
39
Why do pandemics have higher death rates?
Because of lack of pre-existing immunity in humans more infections and more deaths than usual
40
Where does the influenza virus infect first?
Upper airway then spreads to the ciliated calls in the bronchus and bronchioles
41
What is the approximate size of influenza virus?
120nm
42
What Baltimore type is influenza?
Type V negative-sense single-stranded RNA
43
Major influenza glycoproteins?
HA and NA
44
What is antigenic drift?
Accumulation of point mutations in the viral haemagglutinin and neuraminidase genes.
45
What does antigenic drift facilitate?
Seasonal epidemics
46
What is antigenic shift?
Sporadic event, in which a novel virus strain finds a niche within a human host.
Genetic change is much more stark in antigenic shift
47
How do novel viruses commonly arise?
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.
48
How is viral cross-infection normally prevented?
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).
49
What is human sialic acid vs bird sialic acid?
Human - 2,6
| Avian - 2,3
50
Why are pigs powerful mixing vessels?
Pigs are able to bind HA to either sialic linkage - new strains can develop upon co-infection with both a human and avian virus.
51
How does influenza enter cells?
Viral hemagglutinin interacts with sialic acid receptors on cell surface, extracellular proteases then cleave the HA, modifying it to facilitate attachment.
52
What facilitates release of influenza from the endosome?
Low pH of the endosome is what facilitates this release, M2 receptors carry protons into the interior of virion and promote uncoating.
53
When the genetic material enters the nucleus what happens? (influenza)
virion RNA polymerase transcribes the eight genome segments into eight mRNAs,
54
Why is RNA transcription limited to the nucleus?
5’ guanosine cap must be utilised from the cell (this is called cap snatching).
55
What must the influenza use from the host cell?
5' guanosine cap
56
Where does translation occur?
Cytoplasm
57
Where does mRNA go after it is transcribed? influenza
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
58
How does NA release the virus?
NA releases the virus by cleaving the sialic acid on the cell surface.
59
What TLR responds to ssRNA?
TLR7
60
What does RIG-1 respond to?
5’-triphosphate RNA
61
What Baltimore group is SARS-CoV2?
Type IV, positive sense ssRNA
62
What three proteins does the COVID membrane contain?
Spike (S) type I glycoprotein, forming peplomers on the virion surface
Membrane (M) protein
Small membrane protein (E).
63
What receptor does spike protein S bind to in humans?
ACE-2
64
What cells contain ACE-2 receptors?
Type II pneumocytes and resident macrophages
65
How does COVID associate with and enter host cell?
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.
66
What happens once COVID enters the host cell?
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
67
What happens to the viral polyprotein? (CoV-2)
Polyprotein is cleaved by protease to proteins needed for replication (i.e RNA dependent RNA polymerase)
68
Where does replication occur? (CoV-2)
Replication does not occur in the nucleus, instead, biogenesis of viral replication organelles create a protective microenvironment in the cytosol
69
What host gene acts to block COVID life cycle?
Type 1 interferon stimulating gene 15 (ISG-15), blocks various stages of the viral life cycle.
70
What are the hepatitis viruses?
```
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)
```
71
What is hepatitis?
Describes the inflammation of the liver tissue.
72
Signs and symptoms of hepatitis
```
Generally feel off colour
Nausea and vomiting
Hepatomegaly
Jaundice
Pale stool/dark urine
```
73
What are the biochemical markers of hepatitis?
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)
74
Are hepatitis viruses cytopathic?
Relatively non-cytopathic
75
What leads to viral hepatitis?
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
76
What family is hep A part of?
Picornavirus
77
What is the hep A baltimore group/genome?
IV, +ssRNA
78
Is hep A enveloped?
No
79
Where does hep A replicate?
Cytoplasm
80
How is Hep A transmitted?
Feco-oral route
81
How is hep A diagnosed?
Diagnosed by detecting Hepatitis A IgM, there is an effective vaccine
82
Risk of hep A?
Mild and transient but can be lethal in pregnancy (20%)
83
What family is hep B?
Hepadnavirus
84
What Baltimore group/genome is hep b?
Group VII, partially double stranded DNA virus with reverse transcriptase
85
What is the hep B surface antigen?
HBsAg
86
What are the genes coded for by hep B?
S gene - surface antigen
C gene - core antigen and e antigen
P gene - polymerase
X gene - X protein HBx (activator of viral transcription)
87
How does hep B DNA form completely dsDNA?
Virion DNA polymerase synthesizes the missing DNA portion - ds circular DNA formed
88
What happens to the cccDNA hep b?
The cccDNA utilizes the cellular transcriptional machinery to produce all viral RNAs necessary for protein production and viral replication.
89
How is hep B genome replicated?
cccDNA converted to +RNA - reverse transcriptase then converts to genome DNA
90
How is hep B transmitted?
Blood (needle stick injuries, therefore small amounts of blood necessary)
Sexual intercourse
Perinatally from mother to newborn
91
What is the outcome for hep B patients?
>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
What mediates lifelong hep B immunity?
Lifelong immunity is mediated by the anti HBsAg antibody - preventing it from interacting with the hepatocyte.
93
What type of virus family is hep C?
Flavivirus
94
What is the hep C Baltimore group/genome?
+ssRNA, IV
95
Does hep C have polymerase?
No
96
Why is hep C difficult to vaccinate?
The genetic variability is due to the high mutation rate in the gene and absence of proofreading function.
97
How many cases of hep C lead to chronic infection, why ?
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
What can hep C lead to?
Predisposes to hepatocellular carcinoma.
99
Where is Hep C present?
Hepatocytes and blood borne
100
How is hep C transferred?
Transmitted primarily in the blood - injection drug use accounts for almost all transmission.
Also mother to child during birth
101
How many patients of hep C can control infection? How?
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
What is the lower CD4 limit that distinguishes someone to have AIDS?
100 cells per microlitre of blood
103
Common secondary infections in AIDS?
```
Karposi sarcoma
Meningitis type infections.
Cryptococcus neoformans
Toxoplasma gondii
CMV
Candida (thrush)
Pneumocystis jirovecii
Mycobacterium tuberculosis
```
104
What Baltimore group and genome is HIV1?
Group VI +ssRNA retrovirus
105
What family is HIV?
Lentivirus
106
HIV genome consists of...
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
What interactions does HIV make with CD4 cells for entry?
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
What cells express CCR5?
Activated/memory CD4+ T cells, macrophages and dendritic cells
109
What cells express CXCR4?
Naive CD4+ T cells
110
What does gp41 facilitate?
Fusion of viral envelope with cell membrane
111
What happens to HIV ssRNA when inside cell?
RT converts to ds proviral DNA
112
What happens to HIV proviral DNA after it is produced in the cytosol?
Trafficked to the nucleus where integrase integrates viral DNA into host cell DNA
113
What antivirals are used for influenza (endosome stage)?
M2 channel blockers (amantadine and rimantadine) are used as antiviral drugs for influenza.
114
What antivirals are used for influenza (release stage)?
Neuraminidase inhibitors (oseltamivir) prevent cleavage and thus, the release of the progeny from the cell.
115
What antiviral is used on HIV entry?
Small molecule antagonist Maraviroc (MVC) is the only CCR5 inhibitor currently clinically approved for use - only useful for patients with CCR5+ HIV
116
What antivirals are used at the HIV RT stage - how do they work?
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
What is an NRTI example?
AZT
118
Why are viral proteases needed?
Viral protease cleaves Gag and Pol polyproteins into functional polypeptides - form mature, infectious virion
119
What antivirals target protein cleavage?
Protease inhibitors: ritonavir, amprenavir, saquinavir
120
What facilitates HIV cell-cell spread?
A virological synapse is a transient adhesive junction allowing viral spread from an infected to uninfected cell
121
Where does HIV cell-cell spread occur?
Cell-cell spread occurs predominantly in densely populated tissues and enhances rate and amount of infection
122
How is HIV transmitted?
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
When is the early acute stage of HIV, what occurs?
Lasts for 2-4 weeks after infection, fever, lethargy, sore throat, maculopapular rash is also seen on the trunk and extremities.
124
What are CD4/WBC counts like in early acute HIV?
Leukopenia but CD4 count usually normal
125
What is viraemia like in early acute HIV?
High level viraemia, infection is readily transmissible
126
As the early acute phase ends what happens to CD4 count, viral load, CD8?
As this phase ends, the viral load and CD4 counts begin to fall, while CD8 count may rise.
127
How long after HIV infection does it take for antibodies to appear?
Antibodies appear in around 10-14 days
128
How long does the mid-latent phase of HIV last? What occurs?
7-11 year untreated, patient asymptomatic
129
What is viraemia like in mid-latent HIV?
Low
130
What occurs in the AIDS stage?
Persistent fevers, weight loss, fatigue, common opportunistic commensal infections
131
What is viral load and CD4 count like in AIDS stage?
Viral load rises again
CD4 count at critical stage
132
Reverse transcriptase action
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
Integrase action
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
Integrase inhibitors
Raltegravir.
135
Elite controllers of HIV..
Have a delta32 CCR5 mutation, therefore gp120 cannot bind.
136
How does HIV induce GALT damage?
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
How does HIV evade the immune response?
Escape from antibodies and CTLs: antigenic variation.
Recombination between genomes occurs when there is more than 1 HIV1 genome per cell.
138
What is the main pathogenetic mechanism of HIV?
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
How does HIV Tropism change ?
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
What immune response is generated by HIV?
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
How do HIV antibodies act?
Bind to env to prevent viral entry
142
What is HART?
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
How is HBV targeted? (antivirals and vaccine)
Target viral weakpoints with tenofovir, Entecavir (RT antagonists), treat with interferon alpha.
Vaccine provides effective protection through antibody to HBV surface antigen
144
How long is HBV incubation?
2-6months
145
What antivirals are used against HCV?
Use RNAdepRNA polymerase inhibitors, ribavirin, protease inhibitors and interferon alpha.
146
What specific CD4 T cells are affected by HIV?
Th17 important mediators of mucosal immunity (especially in the GI tract).
Acute inflammatory tissue damage is mediated by viral replication and cell death
147
Symptoms of poliomyelitis?
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
What causes paralytic polio?
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
What virus family is polio part of?
Picornovirus
150
Polio Baltimore group/ genome?
Single stranded positive linear RNA genome, so RNA can associate directly with the ribosome, IV
151
What surrounds the polio genome?
Covered by a capsid composed of 4 virion proteins arranged in icosahedral symmetry.
152
What is the polio cell entry mechanism?
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
Why is polio such a simple virus?
Only RNA and a nonenveloped icosahedral protein coat that encapsulates it
154
Why is polio such a simple virus?
Only RNA, and a nonenveloped icosahedral protein coat which encapsulates it
155
What part of polio mRNA is cleaved by host to initiate translation?
VPg protein at the 5’end is cleaved by cellular phosphodiesterase to initiate translation within the cytoplasm.
156
How is polio mRNA translated
Translated as one long peptide, then cleaved by internal proteases.
157
How is polio genome replicated?
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
Polio route of infection?
Feco-oral
159
What is HHV3?
Varicella Zoster causes chickenpox, reactivation = shingles
160
Are all herpes viruses structurally similar?
Yes
161
What is the Baltimore group/genome of herpes virus?
dsDNA genome (Baltimore group 1)
162
What is the size of herpes viruses?
120-200nm
163
What do herpes simplex viruses cause, which viruses?
HHV-1, causes cold sores HHV-2, causes genital herpes
164
Where do HSVs assert their latency?
Sensory ganglia
165
Where is HSVs DNA during latency?
Most (if not all) the viral DNA is present in the cytoplasm rather than the nuclear DNA.
166
What herpesvirus is EBV? What does it cause?
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
How can EBV be diagnosed?
Unique antigen viral capsid antigen (VCA)
168
What cells can EBV infect?
B cells and epithelial cells
169
How does EBV enter B cell?
gp350 binds to cellular receptor CD21, and gp42 interacts with MHC II to trigger fusion of the viral envelope with the cell membrane.
170
How does EBV enter epithelial cells?
To enter epithelial cells, BMRF-2 interacts with cellular integrins to trigger viral fusion.
171
What happens when EBV enters the cell?
Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus.
172
What is latency defined by on a genetic level?
Less genes expressed in latency
173
What does EBV cause infected B cells to do?
Infected B- cells are stimulated to divide in the absence of B-cell antigen. Virus mimics the signals of replication and reactivation.
174
Why is it beneficial for EBV to stimulate B cell replication?
Viral genome is copied alongside the B cells.
175
What gives rise to the pathology of glandular fever?
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
Is emergence from latency dependent on antigen? (EBV)
Reactivation is antigen independent.
177
What occurs in EBV emergence from latency?
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
What is the lytic replication (EBV)?
Rapid B cell replication and EBV replication
179
Why do B cells replicate when infected with EBV?
EBV influences gene expression inside the B cell- B cell behaves as if it has been stimulated by an antigen
180
Why is EBV associated with Burkitt's Lymphoma?
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
What are papillomaviruses?
Small, non-enveloped viruses, 55 nm capsid
182
Papillomavirus genome and Baltimore group?
Circular dsDNA, circular, supercoiled genome (Baltimore group 1).
183
What can papillomaviruses cause?
Papilloma's (benign skin tumours that can lead to malignancies)
Cervical carcinoma
184
How are new HBV genomes generated
DNA repair to form cccDNA
Transcription of cccDNA to RNA by RNA pol II
Reverse transcription of RNA to form +DNA strand
185
What vaccine, if any, is available for HBV?
Hepatitis B vaccine: Recombinant vaccine containing HBsAg (grown in yeast)
186
Does RNA polymerase have proof reading?
No
187
Does DNA polymerase have proof reading?
Yes
188
What is the initial site of EBV infection?
Oropharynx
189
Which infectious agent can be transmitted by a blood transfusion but does not contain nucleic acid?
Prions
190
What host genetic factors influence rate of progression to AIDS?
HLAB27, B57 good, HLAB35 bad
191
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.
Polio
192
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.
HPV
193
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?
HBV
194
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.
Epstein Barr
195
What does the term "eclipse phase" mean with regard to virus replication?
Corresponds to the period during which the input virus becomes uncoated. As a result, no infectious virus can detected during this time
196
EBV transferred by
Saliva
