Module 11 - Viral Pathogenesis Flashcards

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1
Q

What is viral pathogenesis?

A

The mechanisms where viruses cause disease in target hosts

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2
Q

What must viruses do to reproduce?

A
  1. Get into permissive host
  2. Acquire resources needed for replication
  3. Evade host defenses
  4. Spread to new hosts
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3
Q

What feature of viruses makes pathogenesis more complicated compared to bacteria?

A

They must replicate intracellularly

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4
Q

For viruses, what is infection?

A

Entry of a virus into a host cell

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5
Q

What is a productive infection?

A

New infectious viral particles are produced (viral replication occurs)

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6
Q

Which cell leads to productive infection?

A

A permissive cell

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7
Q

What is an abortive infection?

A

Few, if any, new viral particles are produced (viral replication does not occur)

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8
Q

Which cell leads to abortive infection?

A

A non-permissive cell

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9
Q

What are the different types of viral infections?

A

Acute, latent, and persistent

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10
Q

What is an acute infection?

A

An infection with a short duration

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11
Q

What are some characteristics of an acute infection?

A

Signs/symptoms observed, infection is cleared, usually results in immunity

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12
Q

What is an example of an acute infection?

A

Rhinovirus infection (common cold)

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13
Q

What is a latent infection?

A

A period of acute infection is followed by latency

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14
Q

What causes an infection to be latent?

A

The virus is still present, but replication is shut down

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15
Q

What does reactivation mean in a latent infection?

A

Reactivation can lead to the recurrence of acute infection signs and symptoms

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16
Q

What are some examples of latent infections?

A

Lambda phages and herpesviruses

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17
Q

How do lambda phages remain latent?

A

Via repression by the cI repressor

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18
Q

How do herpesviruses remain latent?

A

Through LATs

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19
Q

What does LAT stand for?

A

Latency associated transcripts

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20
Q

What do herpesviruses maintain during latency?

A

A circular episome

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21
Q

What does HHV-1 lead to?

A

Cold sores and genital sores

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22
Q

What does HHV-2 lead to?

A

Cold sores and genital sores

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23
Q

What does HHV stand for?

A

Herpesvirus

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24
Q

What does HHV-3 lead to?

A

Chicken pox rash and shingles

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25
Q

What does HHV-4 lead to?

A

Burkitt lymphoma, mononucleosis

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26
Q

What does HHV-8 lead to?

A

Kaposi sarcoma lesions

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27
Q

What is another name for persistent infections?

A

Chronic infections

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28
Q

What is a persistent infection?

A

New viral particles are continuously produced

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29
Q

What are some characteristics of a persistent infection?

A

The host does not clear the virus, but signs and symptoms may cease

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30
Q

How come the host may not clear the virus in a persistent infection?

A

Either targeted weakening of the immune system, or mutational changes in the virus and/or host target cells

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31
Q

What are some examples of persistent infections?

A

Hepatitis B and C

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32
Q

True or false: hepatitis B and C are always persistent

A

False: they are not always persistent, but they can be in some individuals

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33
Q

What are the basic types of viral transmission?

A

Horizontal, vertical, zootonic, and mechanical

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34
Q

What is horizontal transmission?

A

Transfer from individual to individual within the same species

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35
Q

What does horizontal transmission require?

A

A mode of exit and mode of entry

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36
Q

When someone says they “caught” a cold from someone, what type of transmission is this?

A

Horizontal transmission

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37
Q

What are some examples of horizontal transmission?

A

Respiratory, fecal/oral, and sexual

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38
Q

What are some examples of respiratory horizontal transmission?

A

Rhinoviruses, influenza

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39
Q

What are some examples of fecal/oral horizontal transmission?

A

Polioviruses, hepatitis A

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40
Q

What are some examples of sexual horizontal transmission?

A

HIV, human papillomaviruses

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41
Q

What is vertical transmission?

A

Transmission within the same species, from mother to fetus or newborn

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42
Q

What are some mechanisms of vertical transmission?

A

Via placenta/during birth, via breast milk, or via germ cells

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43
Q

What are some examples of vertical transmission via placenta/during birth?

A

Rubella, hepatitis B and C, HIV

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44
Q

What are some examples of vertical transmission via breast milk?

A

HIV

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45
Q

What are some examples of vertical transmission via germ cells?

A

Spermatocytes/oocytes infected with mouse mammary tumor virus (MMTV)

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46
Q

What does MMTV stand for?

A

Mouse mammary tumor virus

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47
Q

Which vertical transmission is intensely studied?

A

HIV vertical transmission

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48
Q

How come rates of HIV vertical transmission have dropped in the US?

A

Antiretroviral drug therapies and C-sections

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49
Q

What is zootonic transmission?

A

Transfer between individuals of different species (from animals to humans)

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50
Q

What are some examples of zootonic transmission?

A

Rabies, West Nile, and Ebola

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51
Q

What may zootonic transmission lead to?

A

More widespread horizontal transmission events

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52
Q

What is an example of zootonic transmission leading to more widespread horizontal transmission events?

A

HIV arising from SIV

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53
Q

What is mechanical transmission?

A

Facilitated transfer of virus from host between individuals in the same species

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54
Q

How can viruses travel in mechanical transmission?

A

Via vectors like mosquitoes, or contaminated medical equipment

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55
Q

What are some examples of mechanical transmission?

A

Myxoma virus and yellow fever in mosquitoes, Ebola in contaminated medical equipment, plant viruses

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56
Q

What is viral exposure?

A

Simply coming into contact with a virus

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57
Q

When does an infectious disease occur?

A

During a productive infection

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58
Q

What do almost all viral infections activate?

A

The host immune system

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59
Q

What does the overall outcome of viral infection depend on?

A

The interplay between viral replication and immune response of the host

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60
Q

What type of infection is the majority of viral infections?

A

Acute infections

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61
Q

In acute infections, what does the severity of symptoms depend on?

A

The rate that the virus replicates, and the strength of the individual immune response

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62
Q

What are the best studied human viruses that exhibit latency?

A

Herpes viruses

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63
Q

What happens after acute infection of HSV-1?

A

It enters the nuclei of neurons

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64
Q

What happens after HSV-1 enters the nuclei of neurons?

A

It exists as an episome

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65
Q

What is an episome?

A

A non-integrated extra chromosomal closed circular DNA molecule that can be replicated in the nucleus

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66
Q

What genes are expressed in the HSV-1 episome?

A

LATs

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67
Q

What happens when HSV-1 is reactivated from latency?

A

The viral particles travel back down the neuron to the periphery to cause disease symptoms

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68
Q

How might a virus maintain a chronic infection?

A

By weakening the immune system, or suppressing apoptotic signals

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69
Q

True or false: Ebola virus can be transmitted in various ways

A

True: it has multiple mechanisms of transmission

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70
Q

Why do rhinoviruses cause sneezing and coughing?

A

They allow the virus to leave the infected individual and find a new host

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71
Q

How can Ebola virus be transmitted horizontally?

A

By direct contact with contaminated bodily fluids

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72
Q

Why might a virus only be transmitted zootonically and not horizontally?

A

The virus is dead in the human host, and thus cannot spread

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73
Q

How can rabies be transmitted to humans?

A

Through the saliva of an infected animal

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74
Q

How is Ebola transmitted zootonically to humans?

A

Either directly through bats, or indirectly from primates

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75
Q

What does SIV stand for?

A

Simian immunodeficient virus

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76
Q

What is HIV to SIV an example of?

A

A zootonic virus mutating to become more infectious to humans

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77
Q

How does the myxoma virus gets transmitted?

A

By rabbit to rabbit via mosquitos or fleas (mechanical transmission)

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78
Q

True or false: the myxoma virus replicates in the mosquitoes or fleas

A

False: they just act as passive vectors

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79
Q

True or false: yellow fever virus replicates in the insect vector

A

True: unlike myxoma virus, it can replicate in the insect vector

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80
Q

How can Ebola virus be transmitted mechanically?

A

Through medical devices contaminated with the blood of an infected individual

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81
Q

How do some viruses cause cytopathology?

A

By inhibiting host cell transcription and translation processes, or avoiding immune responses

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82
Q

How can viruses induce cellular damage?

A

Through necrosis, apoptosis, or inclusion body formation

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83
Q

Why might a virus induce necrosis or apoptosis?

A

It gives it access to more resources for translating its own proteins

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84
Q

How does poliovirus lead to necrosis?

A

It inhibits host cell mRNA translation

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85
Q

How does poliovirus inhibit host cell mRNA translation?

A

It cleaves an essential translation initiation factor (eIF-4G)

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86
Q

What happens when eIF-4G is cleaved by poliovirus?

A

Rapid inhibition of host cell translation, and initiates translation of viral mRNA

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87
Q

How does cleaved eIF-4G lead to translation of viral mRNA?

A

It is moved to internal ribosome entry segment of the viral mRNA to initiate translation

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88
Q

What does IRES stand for?

A

Internal ribosome entry site

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89
Q

What does an IRES do?

A

An RNA element that allows for translation in a cap-independent manner

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90
Q

What is needed for the initiation of the translation complex in eukaryotic cells?

A

A 5’ cap

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91
Q

How does bunyavirus lead to necrosis?

A

Through a cap snatching process

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92
Q

What happens when the cap is stolen from mRNA?

A

It is promptly degraded

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93
Q

Besides bunyaviruses, what other viruses cleave the 5’ cap off of mRNA?

A

Automyxo viruses

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94
Q

What do cap-snatching viruses do with the 5’ cap?

A

Use it to prime synthesis of viral mRNA

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95
Q

What is apoptosis?

A

Programmed cell death

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96
Q

What type of organisms undergo apoptosis?

A

Multicellular organisms

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97
Q

How does apoptosis work?

A

Biochemical processes lead to characteristic cell changes

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98
Q

What are some characteristic cell changes during apoptosis?

A

Blebbing, global mRNA decay, and chromosomal DNA fragmentation

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99
Q

When might induction of the apoptosis pathway be useful?

A

To prevent the production of more virus particles and limit the spread of virus within the host

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100
Q

Why might a virus want to inhibit apoptosis?

A

So it can multiply and produce more virions

101
Q

How do herpesviruses and adenoviruses interact with the apoptosis pathway?

A

They produce proteins that mimic anti-apoptotic proteins to inhibit apoptosis

102
Q

True or false: apoptosis induces inflammation

A

False: it is usually safer for surrounding cells

103
Q

How does the immune system use apoptosis?

A

It can induce apoptosis to safely kill virally infected cells

104
Q

Which viruses form syncytia?

A

HIV and measles virus

105
Q

How do syncytia form?

A

Infected cells fuse with adjoining infected or uninfected cell

106
Q

What is the result of a syncytia?

A

The formation of a multinucleated giant cell that ultimately dies

107
Q

What do rabies virus, adenovirus, and reovirus do to cells?

A

They form nuclear of cytoplasmic inclusion bodies to kill cells

108
Q

What are inclusion bodies?

A

Clumps of virus/proteins inside host cells

109
Q

What do inclusion bodies do?

A

They lead to disruptions in cellular morphology and cellular function

110
Q

What is the viral advantage of a syncytia?

A

They can avoid extracellular immune responses

111
Q

What can cause the symptoms of a viral infection?

A

The virus itself, or the actions of the host immune response

112
Q

How do rhinoviruses affect cells of the upper respiratory tract?

A

There is not much pathology

113
Q

How do rhinoviruses lead to the clinical symptoms?

A

They lead to elevated levels of inflammatory cytokines IL-6 and IL-8

114
Q

What does IL-6 and IL-8 lead to?

A

Vasodilation and a buildup of fluid in the respiratory tract

115
Q

What is the sneezing and coughing of a rhinovirus infection a direct result of?

A

A buildup of fluid in the upper respiratory tract

116
Q

What do invading microbes usually trigger?

A

The release of various cytokines

117
Q

What do cytokines do?

A

Facilitate communication between cells of the immune system and initiate inflammatory response

118
Q

What does the clinical outcome of HBV infection depend on?

A

The particular immune response

119
Q

In most cases, what is the clinical outcome of HBV infection?

A

They are cleared by the immune response with no significant site of pathology

120
Q

What does hepatitis result from?

A

Cytotoxic T-lymphocyte mediated destruction of infected hepatocytes

121
Q

What are hepatocytes?

A

Liver cells

122
Q

What does accumulation of HBV antigen - antibody complexes lead to?

A

It can cause kidney damage in kidneys

123
Q

What can chronic HBV infection of the liver lead to?

A

Liver cancer

124
Q

How might viruses cause disease indirectly?

A

Through auto-immunity

125
Q

How do auto-immune diseases occur?

A

When the immune system incorrectly targets normal cellular components

126
Q

How can auto-immune diseases be triggered by viral infections?

A

Through molecular mimicry

127
Q

How does molecular mimicry lead to auto-immune diseases?

A

If viral antigens are structurally similar to host cell proteins, immune cells may target both the virus and the host cells

128
Q

How is multiple sclerosis an auto-immune disease?

A

Myelin is similar to a viral antigen, so it is attacked by T cells

129
Q

When was the tumor causing virus in chicken discovered?

A

1911

130
Q

What is tumorigenesis?

A

The formation of a tumor

131
Q

What is a tumor?

A

An abnormal growth of tissue

132
Q

How can transformation make a cell cancer-like?

A

It can make the cell immortal or grow uncontrollably

133
Q

What may cancer transformed cells exhibit?

A

Reduced growth factor requirements and chromosomal aberrations

134
Q

What type of cancer does HPV 16 and 18 lead to?

A

Cervical, anal, penile

135
Q

What are some notes on HPV 16 and 18?

A

Oncogenic HPV strains may cause up to 10% of all human cancers

136
Q

What percentage of cervical cancers are caused by HPV 16 and 18?

A

70%

137
Q

What virus family is HPV 16 and 18 a part of?

A

Papillomaviridae

138
Q

What type of cancer does SV40 lead to?

A

Sarcomas in rodents

139
Q

What are some notes on SV40?

A

It can transform some human cell lines

140
Q

What virus family is SV40 part of?

A

Polyomaviridae

141
Q

What type of cancer does Adenovirus lead to?

A

Transformation of cells in culture

142
Q

What are some notes on Adenovirus?

A

Both E1A and E1B proteins are needed for transformation

143
Q

What type of cancer does HHV-8 lead to?

A

Kaposi sarcoma

144
Q

What are some notes on HHV-8?

A

It transforms endothelial cells, and it is a defining cancer of people with HIV/AIDS

145
Q

What virus family is HHV-8 part of?

A

Herpesviridae

146
Q

What type of cancer does HHV-4 lead to?

A

Burkitt lymphoma

147
Q

What is another name for HHV-4?

A

Epstein-Barr virus

148
Q

What are some notes on HHV-4?

A

It also causes infectious mononucleosis

149
Q

What virus family is HHV-4 part of?

A

Herpesviridae

150
Q

What type of cancer does HBV lead to?

A

Hepatocellular carcinoma

151
Q

What are some notes on HBV?

A

An effective vaccine is available

152
Q

What virus family is HBV part of?

A

Hepadnaviridae

153
Q

What type of cancer does HCV lead to?

A

Hepatocellular carcinoma

154
Q

What are some notes on HCV?

A

60-85% of people infected with HCV develop a chronic infection

155
Q

What virus family is HCV a part of?

A

Falviviridae

156
Q

What type of cancer does Rous sarcoma virus lead to?

A

Sarcoma in chickens

157
Q

What are some notes on Rous sarcoma virus?

A

Led to the identification of proto-oncogenes

158
Q

What virus family is Rous sarcoma virus a part of?

A

Retroviridae

159
Q

What is an oncogene?

A

Genetic material capable of inducing a transforming event in host cells

160
Q

What have almost all mammalian DNA virus been shown to cause?

A

Transformation of cells in culture or tumor formation in animals

161
Q

What types of genes do mammalian DNA viruses usually contain?

A

Oncogenes

162
Q

What is similar between mammalian DNA viruses?

A

The mechanisms by which they transform cells

163
Q

What do strains of papillomaviruses lead to?

A

Genital warts and cervical cancer

164
Q

What do papillomaviruses typically infect?

A

Certain mucosal surfaces and keratinocytes

165
Q

What are keratinocytes?

A

Cells that form the outer layer of skin

166
Q

How come keratinocytes are quiescent cells?

A

They do not actively divide

167
Q

What is the consequence of keratinocytes being quiescent?

A

They have very few nucleotides and enzymes needed for DNA replication

168
Q

How do viruses overcome the lack of resources in quiescent cells?

A

They stimulate the cell to enter S phase of the cell cycle

169
Q

What happens when a cell enters S phase?

A

It prepares the resources needed for DNA synthesis

170
Q

What happens to epithelium infected with papillomavirus?

A

The cells proliferate rather than differentiate

171
Q

What is the structure of papillomavirus?

A

Non-enveloped icosahedral dsDNA (8 kb) virus

172
Q

What proteins are used by papillomavirus to transform the cell?

A

E6 and E7

173
Q

What vaccines for papillomaviruses exist?

A

Those for the most common E6/E7 carrying strains

174
Q

What does Rb stand for?

A

Retinoblastoma

175
Q

What do Rb and p53 do?

A

They act as tumor suppressors to stop the cell cycle

176
Q

What does Rb do?

A

It binds to E2f transcription factors to prevent entry into S phase

177
Q

What happens when Rb is phosphorylated?

A

It cannot bind to E2f, so E2f can stimulate the transcription of genes needed for entry into S phase

178
Q

When is p53 activated?

A

In the event of DNA damage or cell stress, it is phosphorylated

179
Q

What happens when p53 is phosphorylated?

A

It acts as an active transcription factor for p21

180
Q

What does p21 do?

A

It prevents the cell from entering into S phase

181
Q

What does accumulated phosphorylated p53 lead to?

A

It induces apoptosis

182
Q

How does E6 interfere with cell cycle control?

A

In the presence of E6AP, it targets p53 for destruction

183
Q

What happens when p53 is degraded in proteosomes?

A

p21 is not transcribed, so the cell is free to enter S phase

184
Q

How does E7 interfere with cell cycle control?

A

It binds to Rb and prevents Rb from binding to E2f

185
Q

What happens when there is no Rb-E2f complex?

A

The cell is free to enter S phase

186
Q

True or false: cells infected with papillomavirus die

A

True: the virus triggers apoptosis

187
Q

What happens if the papillomavirus genome is inserted into the host genome, without the production of viral particles?

A

The host cells are not killed, but they are transformed

188
Q

What happens if E6 and E7 genes are inserted into the host genome?

A

They continue to inactivate p53 and Rb, leading to more division of the cells

189
Q

How does papillomavirus lead to cancer?

A

The continuously dividing cells acquire mutations over time, and thus become cancer

190
Q

True or false: very few RNA viruses seem to cause cancer

A

True: many DNA viruses, but not many RNA viruses, seem to cause cancer

191
Q

What type of RNA viruses usually cause cancer?

A

Retroviruses

192
Q

What is the only non-retrovirus RNA virus associated with cancer?

A

Hepatitis C

193
Q

How does hepatitis C lead to cancer?

A

Via constant attempts to replace damaged liver cells in chronic hepatitis C, altering the genetic material (not through direct transformation)

194
Q

What have several retroviruses been associated with?

A

Tumorigenesis

195
Q

How do retroviruses cause cancer?

A

They can insert their cDNA into the genome to alter proto-oncogenes

196
Q

What are the two ways in which a proto-oncogene can become an oncogene?

A
  1. The pro-viral DNA may integrate near a proto-oncogene and alter its expression
  2. The retrovirus may acquire a cellular oncogene and transform another cell
197
Q

What do cis-acting retroviruses do?

A

They integrate cDNA into the genome to convert a proto-oncogene into an oncogene

198
Q

How come a retrovirus is called “cis-acting”?

A

It only affects the portion of DNA near it

199
Q

What is the best studied cis-acting retrovirus?

A

MMTV

200
Q

What does MMTV stand for?

A

Mouse mammary tumor virus

201
Q

What does MMTV do to infected animals?

A

It causes tumors of the breast tissue

202
Q

True or false: the MMTV genome contains an oncogene

A

False: it does not contain an oncogene, but it can lead to tumor formation

203
Q

How does MMTV lead to tumorigenesis?

A

It integrated near Wnt1 to increase its expression

204
Q

What does increased Wnt1 lead to?

A

Increased proliferation and tumor formation of the cell

205
Q

Where is the cis-acting enhancer element found in MMTV?

A

In the pro-viral long-terminal repeat (LTR) transcriptional regulatory region

206
Q

What do trans-acting retroviruses do?

A

They transform a cell with an oncogene from a different cell

207
Q

How does a retrovirus obtain an oncogene?

A

It integrates near a cellular proto-oncogene, where it can be copied into the RNA genome

208
Q

How come trans-acting retroviruses are not a major cause of cancer?

A

They are fairly rare

209
Q

What are some examples of trans-acting retroviruses?

A

Avian leukosis virus, Rous sarcoma virus, and Avian myelocytoma virus

210
Q

What is the structure of Avian leukosis virus?

A

LTRs with three genes

211
Q

What is the structure of Rous sarcoma virus?

A

It has the Rous proto-oncogene src in addition to the normal retrovirus genome

212
Q

What is the structure of Avian myelocytoma virus?

A

It has the proto-oncogene myc but missing the entire pol and other two genes

213
Q

What genes are in a normal retrovirus genome?

A

gag, pol, and env

214
Q

How can a proto-oncogene become an oncogene?

A

By being overexpressed or altered in some way

215
Q

How are proto-oncogenes usually altered to become oncogenes?

A

They become truncated

216
Q

What is an example of a proto-oncogene becoming truncated to become an oncogene?

A

EGFR

217
Q

What does EGFR do?

A

It is a transmembrane protein that binds to EGF to stimulate growth

218
Q

What does EGF stand for?

A

Epidermal growth factor

219
Q

What gene encodes for EGFR?

A

ERBB

220
Q

What happens when normal EGFR binds to EGF?

A

It becomes phosphorylated to continue the pathway

221
Q

What does the mutant EGFR do?

A

It is truncated, so it can become phosphorylated without EGF present

222
Q

What has study of cis and trans acting retroviruses led to?

A

The understanding of many cell cycle control genes

223
Q

What are three ways in which viral genomes can change?

A

Mutations, recombinations, and assortments

224
Q

How can mutations, recombinations, and assortments lead to virulence?

A

They can change the structure of proteins to make them more pathogenic

225
Q

How come a 1 in a billion chance is not improbable for a virus over time?

A

They have a high replication rate

226
Q

What type of genome is needed for evolution?

A

A mutating genome

227
Q

What type of genome is desired in the short term?

A

A stable genome

228
Q

How come the mutation rate in viruses is very high?

A

The mechanisms to reduce the mutation rate are not present

229
Q

What does DNA polymerase have that RNA polymerase does not?

A

Proofreading ability

230
Q

How come new RNA viruses will be geneticallly heterogeneous?

A

RNA polymerase lacks proofreading ability, so there are more mutations during replication

231
Q

What does a high mutation rate imply?

A

The viruses are evolving at a fast rate

232
Q

What is the mutation rate of influenza virus?

A

10^-5

233
Q

What is antigenic drift?

A

The change in the protein structures of the surface proteins HA and NA on influenza virus due to mutations

234
Q

How come mutations in HA and NA are significant?

A

They are the primary targets of the immune system, so if they change, the immune system will not recognize the influenza virus

235
Q

What is the consequence of mutations in HA and NA?

A

A new influenza vaccine needs to be given every year

236
Q

How come a person with HIV can have multiple viral alleles?

A

HIV has a high mutation rate inside the host

237
Q

What switch can occur due to HIV mutations?

A

A switch from monocytes and macrophages to CD4+ T cells for recognition

238
Q

How con HIV can switch host range?

A

Due to mutations in the gp120 protein

239
Q

What receptors can gp120 bind to (before and after mutations)?

A

CCR5 on monocytes and macrophages, and CXCR4 on CD4+ T cells

240
Q

When does viral recombination occur?

A

When a cell is infected by two different strains of a virus simultaneously

241
Q

What is the result of viral recombination?

A

Progeny viruses that have part of each genome

242
Q

What does RNA synthesis in coronaviruses appear to be?

A

Discontinuous

243
Q

What is the consequence of RNA synthesis in coronaviruses being discontinous?

A

An RNA polymerase can jump from one RNA strand to another to produce recombinant RNA genomes

244
Q

What is viral reassortment?

A

Combining of gene segments from two or more parental viruses

245
Q

What types of viruses undergo viral reassortment?

A

Segmented viruses, such as influenza

246
Q

What does each segment in a segmented genome encode for?

A

One or two polypeptides

247
Q

How is viral reassortment similar to viral recombination?

A

It requires coinfection with two different strains of a virus

248
Q

How is viral reassortment different to viral recombination?

A

Genome molecules do not undergo recombination to form a hybrid molecule

249
Q

What does each progeny virus receive in viral reassortment?

A

One copy of each segment from either parental virus