Micro Final1 Flashcards
(500 cards)
1
Q
What was the first virus discovered?
A
Tobacco mosaic virus
2
Q
What was the first animal virus isolated?
A
Foot and mouth disease virus, in 1898
3
Q
What is a major structural categorization for viruses based on the outer layer of the virus?
A
Enveloped viruses (with a lipid bilayer) and non-enveloped viruses
4
Q
Are GI viruses usually enveloped or non-enveloped?
A
Non-enveloped
5
Q
Is HIV an enveloped or a non-enveloped virus?
A
Enveloped
6
Q
How many genomic groups of viruses are there? How many are based on DNA? How many are based on RNA?
A
Six; two DNA; four RNA
7
Q
Viral genomic groups IV and V are both based on single-stranded RNA. What is the distinction between them?
A
Polarity: whether the genome as it enters the cell is the right orientation for translation in the protein, or needs to create an antisense RNA template that will be translated
8
Q
How is a virus grown in a laboratory if they are obligate parasites?
A
On a host cell culture
9
Q
Can you directly visualize viruses on an agar plate?
A
No, you can only see signs of virus infection, like cytopathic effect, inclusion bodies or hemadsorption
10
Q
How are viruses being visualized in this assay?
A
By the number of plaques of killed cells
11
Q
What is the eclipse period of viral growth? What is the latent period?
A
Eclipse: when you have a low, undetectable level of the virus, because it is within cells but not yet replicating; Latent: when there is a detectable level of virus but it has not yet reached the level of the infectious dose
12
Q
Routes of viral infection include: […], respiratory, transcutaneous, sexual, and contact with infectious bodily fluid.
A
Routes of viral infection include: oral/fecal, respiratory, transcutaneous, sexual, and contact with infectious bodily fluid.
13
Q
Routes of viral infection include: oral/fecal, respiratory, […], sexual, and contact with infectious bodily fluid.
A
Routes of viral infection include: oral/fecal, respiratory, transcutaneous, sexual, and contact with infectious bodily fluid.
14
Q
Routes of viral infection include: oral/fecal, respiratory, transcutaneous, sexual, and contact with infectious […].
A
Routes of viral infection include: oral/fecal, respiratory, transcutaneous, sexual, and contact with infectious bodily fluid.
15
Q
What percent of human cancers are thought to have a viral etiology?
A
15%
16
Q
What general disease have HTLV-1, HBV, HCV, HPV, HHV-8, and EBV all been linked to?
A
Cancer
17
Q
Historically, what has been the most effective way of combatting viral illness?
A
Vaccines
18
Q
What effect is used here to assess the presence of viruses on the right?
A
The cytopathic effect: damaged cells are visible on the right
19
Q
What shows a positive result in a hemagglutination test?
A
The virus spreads over the surface of a drop of hematies, and spreads it over a well
20
Q
Herpes viruses include: the Herpes […] viruses, the Varicella Zoster virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
A
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
21
Q
Herpes viruses include: the Herpes Simplex viruses, the […] virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
A
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
22
Q
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, […] virus, cytomegalovirus, and Human Herpes viruses.
A
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
23
Q
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, Epstein-Barr virus, […], and Human Herpes viruses.
A
Herpes viruses include: the Herpes Simplex viruses, the Varicella Zoster virus, Epstein-Barr virus, cytomegalovirus, and Human Herpes viruses.
24
Q
What is the genomic content and structure of herpes viruses?
A
Large, enveloped dsDNA viruses (group I)
25
What timecourse of infection is caused by herpes viruses?
Chronic and latent infection
26
Where is the Herpes virus assembled during replication?
In the ER and Golgi
27
What is the mechanism of acyclovir? What class of viruses does it inhibit?
First it is phosphorylated by a viral thymidine kinase, and then when it is incorporated into the replicating DNA chain, replication is terminated
28
How do HSV I and II enter the body?
Abraded skin or mucosa
29
Where do HSV I and II lie latent after primary infection?
Sensory ganglia
30
What histological diagnosis is possible from this slide?
This is a giant cell with intranuclear inclusions (Tzanck test), indicating a herpesvirus infection
31
What is the prevalence of HSV-1 in adults? What is the prevalence of HSV-2?
50-70% for HSV-1; 20-50% for HSV-2
32
What is the appearance of herpetic lesions?
Crops of painful small blisters and ulcers in skin and mucous membranes
33
What is a herpetic infection of the finger called?
Herpetic Whitlow
34
What viral infection depicted here can cause painful swallowing?
HSV esophagitis
35
Besides the skin and mucous membranes, what are other common targets for HSV infection?
Conjunctiva, encephalitis, esophagus
36
What are presenting symptoms for a neonatal CNS infection by HSV?
Seizures, lethargy, irritability, fever with an onset at 14-21 days
37
Can HSV be cultured from CSF for a CNS infection? What lab technique is most appropriate for finding HSV in CSF?
No; PCR is more appropriate
38
Besides culturing and Tzanck smear, what other lab findings can be used to diagnose HSV?
Direct fluorescence antibodies of skin lesions and PCR of CSF
39
Is acyclovir available in IV form? What is the typical oral formulation?
Yes, IV acyclovir is used for serious disease; valacyclovir is the oral formulation, a prodrug that is better absorbed than acyclovir
40
How is resistance to acyclovir generated? Are they seen in typical patients?
Mutations in the viral thymidine kinase, or the DNA polymerase; no, resistance is mostly seen in immunocompromised patients
41
What can be used to treat acyclovir resistant HSV? What are its side effects?
Foscarnet, an inorganic pyrophosphate that inhibits the viral DNA polymerase; nephrotoxicity and calcium/phosphate dysregulation
42
What is Foscarnet used to treat? Does it have an oral formulation?
Acyclovir resistant HSV; no
43
What can be used to prevent HSV transmission from a pregnant woman with genital lesions to her infant?
C-section
44
In what cases might long term acyclovir be administered?
Pregnant women at risk of transmitting to their infant; transplant recipients; AIDS patients
45
What skin condition is seen here? What virus causes it?
Chicken pox; varicella zoster virus
46
What is the most contagious mode of transmission for varicella zoster virus?
Aerosolization from the respiratory tract
47
What is the time period of chicken pox infection? Which period is the contagious period?
2-3 weeks; 9-21 days
48
Where does the varicella zoster virus establish latency after an episode of chicken pox? If it reactivates, what does it cause?
Dorsal root ganglia; shingles
49
What percentage of shingles patients can recall that they were exposed to the virus in the past (e.g., had chickenpox)?
\>90%
50
Can shingles be spread by respiratory droplets?
No, only during an initial exposure via the respiratory tract will the varicella virus be contagious via aerosolization, during shingles the latent virus in the dorsal root ganglia is reactivated
51
Do adults have more or less symptomatic reactions to varicella infection?
More symptomatic
52
What is a significant adverse neurological outcome for herpes zoster (shingles)?
Post-herpetic neuralgia, where pain or lack of sensitivity manifests in a nerve affected by the virus
53
How is shingles treated?
Acyclovir and valacyclovir, at higher doses than for HSV
54
Parainfluenza, coronavirus, and adenovirus are all viruses that affect which system?
Respiratory
55
What family of viruses do parainfluza viruses belong to?
Paramyxoviridae
56
Which family of viruses do respiratory syncytial virus and metapneumovirus belong to?
Pneumoviruses
57
What is the genomic makeup of a paramyxovirus?
Negative-sense, single stranded RNA
58
What is transcribed from the negative sense RNA paramyxovirus genome?
Individual mRNAs and a full length positive-sense RNA template
59
What is the "barking cough" a sign of? What is the typical infectious agent?
Croup, or laryngotracheitis; parainfluenza virus
60
Which HPIV viruses cause croup?
HPIV-1, -2, and -3
61
What is the steeple sign?
An anatomical hallmark of croup, which is the narrowing of the trachea in the subglottic region
62
What is the course of treatment for parainfluenza virus?
Usually supportive: IV/IM/oral dexamethasone, and nebulized racemic epinephrine
63
What is the clinical syndrome caused by RSV virus?
Bronchiolitis or pneumonia
64
Does the immune response to RSV appear to play a role in the pathogenesis and severity of bronchiolitis?
Yes
65
When are the usual seasons for RSV virus infection in temperate climates?
Winter and early spring
66
What treatment can be used for severe infections by RSV? What is its mechanism?
Ribavarin; nucleoside analog that inhibits nucleic acid synthesis
67
What antibody is used to prevent RSV infection in high risk infants? How often is it adminstered and via which route?
Palivizumab; monthly, IM
68
What virus is the 2nd leading cause of bronchiolitis after RSV? What percentage of common colds in children is caused by it?
Human metapneumovirus; 15%
69
Can human metapneumovirus and RSV be transmitted by close contact? In a nosocomial setting?
Yes to both
70
How is human metapneumovirus treated?
Supportive
71
What is the structure and genomic makeup of coronavirus?
Enveloped, single stranded, and positive sense RNA virus
72
Does paramyxovirus have a lipid envelope?
Yes
73
Where does the coronavirus assemble?
The rough endoplasmic reticulum
74
Besides the common cold, what can coronavirus manifest as clinically?
Gastroenteritis and SARS (Severe Acute Respiratory Syndrome)
75
What are the hallmarks of SARS? What is the mortality rate?
Fever, pneumonia/respiratory distress, diarrhea, and leukopenia; 10% out of 8000 infected individuals
76
What is the reservoir for coronavirus?
Common in many animals
77
How can coronavirus be diagnosed? When would these tests be needed?
PCR on respiratory secretions or stool, or EM; if SARS caused by coronavirus is suspected
78
Is there a proven effective antiviral therapy for coronavirus?
No
79
Are DNA viruses generally more or less complex than RNA viruses?
DNA viruses are more complex
80
What is the structure and genomic makeup of adenovirus?
Non-enveloped icosadeltahedral virus with linear, dsDNA genome
81
What membrane protein does adenovirus co-opt to enter the cell?
Integrin
82
Is the DNA genome of adenovirus delivered to the nucleus?
Yes
83
Does adenovirus replication lead to cell lysis?
Yes
84
What sort of patients can be suspected for adenovirus?
Young (\<10yo) patients with pink-eye, sore throat, or fever and generalized rash
85
What patient populations are likely to have severe infections of adenovirus manifest (e.g. pneumonia, meningitis, and encephalitis)?
Young infants and the immunocompromised
86
What virus can cause all of these syndromes?
– URI/LRI
– Pharyngo-conjunctivitis
– Gastroenteritis
– Hemorrhagic cystitis
Adenovirus
87
How is adenovirus spread?
Aerosol, close contact, or fecal-oral
88
What is the typical first site of infection for adenovirus spread by aerosol?
Pharyngeal infection
89
Which cell type is infected by adenovirus in the respiratory and GI tract?
Mucoepithelial cells
90
Can adenovirus spread to visceral organs? In which tissue can it persist longest?
Yes; lymphoid tissue
91
What drug can be used to treat severe cases of adenovirus, e.g. in the immunocompromised? What is the mechanism? What toxicity results?
Cidofovir; it is a cytosine analog that blocks viral DNA synthesis; nephrotoxicity
92
What is the most frequent cause of the common cold?
Rhinovirus
93
What is the major vector for transmission of rhinovirus?
Hands
94
Does measles infect immune cells, epithelial cells, or both?
Both
95
What virus causes measles and from what family? What is its genomic structure? Is it enveloped?
Morbillivirus, from paramyxovirus family; negative strand nonsegmented RNA; enveloped
96
What are the three proteins in the envelop of the measles virus?
Hemagglutinin (H), fusion (F) and matrix (M)
97
Which protein on morbillivirus mediates fusion between the viral envelope and the host cell?
F protein
98
Which two proteins in morbillivirus drive RNA-dependent RNA polymerization? Where does this occur in the host cell?
L and P; in the cytoplasm
99
What receptor is used by morbillivirus to target epithelial cells?
Nectin 4, an epithelial cell receptor
100
What is the route of spread of measles?
Respiratory droplets
101
What is the latent period for measles? What symptoms characterize the prodrome?
10-14 days; 2-3 day prodrome of fever, coryza (cold symptoms), cough, and conjunctivitis
102
What visible sign of measles infection correlates with the initiation of viral clearance?
Maculopapular rash
103
What are the first cell types to be invaded by morbillivirus?
Macrophages and dendritic cells of the respiratory tract
104
What happens when the morbillivirus replicates in lymphoid tissue?
Formation of multinucleated giant cells as the envelope fusion proteins exert effects on the cell membrane, or "syncytium"
105
What initiates viremia from a measles infection?
Amplication of the virus in lymph nodes
106
Which cell in the blood is infected by the morbillivirus?
Lymphocyte
107
What is the average infection spread caused by one measles patient?
1 will infect ~10 without isolation
108
What viral infection is characterized by this rash?
Measles: it is a maculopapular, semi-confluent rash
109
What day of infection does the characteristic measles rash manifest?
~13 days
110
What bacterial complication is common in 5-15% of measles cases?
Superinfection involving otitis media, mastoiditis, sinusitis, etc.
111
What rare neurological disease beginning 2-10 years after infection is associated with measles?
Subacute sclerosing panencephalitis
112
What infection can cause a rare neurological disorder characterized by personality changes, intellectual deterioration, and possibly death about 2-10 years afterward?
Measles
113
How is measles diagnosed—clinically, or by lab tests?
Usually clinically (in atypical cases, measles antigen can be visualized with direct fluorescent antibody)
114
When does production of IgG begin after exposure to morbillivirus?
Around ~20 days afterward
115
How long can maternal antibodies suppress morbillivirus infection?
6 months
116
What is the treatment for measles?
None is available, so supportive
117
What kind of vaccine is the measles vaccine? What combination vaccine is it given with?
Live attenuated virus; measles mumps and rubella (MMR)
118
When are the MMR vaccines administered to children?
Between 12-15 months with a booster at 4-6 years
119
When was the measles vaccine introduced in the US?
1963
120
What is the reason for sporadic outbreaks of measles in select populations of the US?
Refusal of vaccination
121
Where is measles still common?
Africa and Asia
122
What viral infection is characterized by this presentation?
Mumps (from the british to "mump", which means to grimace or grin)
123
Which gland swells in the presentation of rubulavirus (which causes mumps)?
The parotid gland
124
Which virus causes mumps, and what family does it belong to?
Rubulavirus, from the paramyxovirus family
125
On what day of infection does mumps spread to the spleen and lymphoid tissue?
7-10 days
126
What fraction of mumps cases results in meningitis?
10%
127
What fraction of mumps cases are subclinical?
30%
128
What is the type of vaccine used for mumps? What vaccine is it included with?
Live attenuated virus; MMR
129
What disease causes this rash?
Rubella
130
What is the genomic makeup of the rubella virus? What family does it belong to? Does it have an envelope?
Positive strand RNA virus; Togavirus; enveloped
131
What happens if a pregnant mother is infected with rubella in the early months of pregnancy?
Congenital rubella syndrome, which causes birth defects such as deafness, cataracts, heart defects, and mental retardation (\>20% chance)
132
What is the type of vaccine used to counter rubella?
Live attenuated virus
133
What kind of drug is azidothymidine (AZT)?
A nucleoside reverse transcription inhibitor (NRTI), used to treat HIV by blocking the reverse transcriptase
134
Which class of HIV drugs is most similar in mechanism to acyclovir?
Nucleoside reverse transcriptase inhibitors: molecules that are similar to nucleosides, are incorporated into the chain by viral reverse transcriptase and terminate transcription
135
What are two major adverse effects of NRTIs as a class of drugs?
Mitochondrial toxicity (muscle weakness, mental status changes, pancreatitis, lactic acidosis) and dyslipidemia
136
What is the common name for azidothymidine?
Zidovudine
137
Which NRTIs have minimal toxicity outside of the mitochondrial toxicity and dyslipidemia caused by all NRTIs?
Lamivudine (3TC) and emtricitabine (FTC)
138
Which NRTI can cause a hypersensitivity reaction in certain HLA genotypes?
Abacavir (ABC)
139
Which NRTI has a high probability of renal toxicity or osteopenia?
Tenofovir (TDF)
140
Which two NRTIs have a particularly high risk of mitochondrial toxicity and insulin resistance?
Didanosine (ddI) and stavudine (d4T)
141
When did the era of combination anti-retroviral therapy for HIV begin?
1995-6
142
Does resistance develop faster with NRTIs or NNRTIs?
Generally, NNRTIs
143
What class of drugs do nevirapine, efavirenz, etravirine, and riplivirine belong to?
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
144
What adverse effect is common to efavirenz, etravirine, and rilpivirine?
Rash
145
Which NNRTI can cause a hypersensitivity reaction that is more common in women and in patients with high CD4+ cell counts?
Nevirapine (NVP)
146
How do NNRTIs inhibit viral reverse transcriptase?
Binding to an outside allosteric pocket: they do not target the active site of DNA synthesis directly
147
What liver enzyme is affected by NNRTIs that crease toxicity across the entire class of drugs?
Cytochrome P450
148
What class of drugs do atazanvir, darunavir, fosamprenavir, and lopinavir/ritonavir belong to? What infection are they a first-line agent for, assuming the infectious agent has not been exposed to drugs previously?
Protease inhibitors; HIV
149
Can ritonavir be used for its antiretroviral effect?
No, it is a potent CP450 inhibitor, it is only used as a pharmacokinetics booster at a low dose (since it allows another drug, e.g. lopinavir, to maintain effective plasma concentrations for longer)
150
What are adverse effects of all protease inhibitors?
Dyslipidemia, lipohypertrophy, and cytochrome P450 interactions
151
What class of drugs do nelfinavir, indinavir, and saquinavir all belong to? What are they used to treat?
Protease inhibitors; HIV
152
Do we still use the "treat early, treat hard" mantra for HIV?
No, treatment is now based on CD4+ counts, VL, and symptoms
153
By how much has mortality decreased for HIV in the US since the introduction of protease inhibitors and NNRTIs?
42%
154
What class of drugs do raltegravir and elvitegravir belong to? What is their function?
Integrase strand transfer inhibitors; they inhibit the enzyme that integrates the HIV genome into the host cell
155
What CCR5 antagonist is used to treat HIV? Does it work on all strains of the virus?
Maraviroc; no, it requires the CCR5 tropic virus
156
What happens during periods when HIV patients are not taking their medications properly?
Populations of drug resistant virus will replicate and re-infect cells, leading to a potentially very resistant infection
157
Can a sample of HIV from a patient be measured for resistance to various antiretrovirals?
Yes
158
What is being performed by this kind of assay?
Phenotypic resistance testing on a patient's strain of a virus
159
What kind of prophylaxis is common for opportunistic infections of *Pneumocystis jiroveci* and *Mycobacterium avium-complex* in HIV patients?
TMP-SMX for *P. jiroveci* and Azithromycin for *M. avium-complex*
160
What percentage of HIV infected people in the US are estimated to be diagnosed? How many are retained in active HIV care?
80% diagnosed; 40% receiving ongoing care
161
Can antiretroviral therapy be given to prevent mother to infant transmission of HIV or infection post-exposure to contaminated fluids?
Yes
162
Does an efficacious AIDS vaccine currently exist? When was the last clinical trial for them performed?
No; 2012 ALVAC/AIDSVAX trial in Thailand
163
Has the number of people infected with HIV declined or increased since 1996? Are deaths stable, rising, or decreasing?
Infections have declined; deaths are decreasing slightly
164
What is the current first-line regimen for HIV?
Tenofovir and emtricitabine (NNRTIs) with either efavirenz (NNRTI), darunavir+ritonavir (PI), atazanavir+ritonavir (PI), or raltegravir (INSTI)
165
Which class of MHCs is responsible for presenting viral peptides?
MHC class I
166
Which kind of cells participate in cell mediated immunity against viruses?
Cytotoxic T-cells specific for immunogenic viral peptides
167
What cell types are involved in the humoral immunity response to a virus?
Helper (CD4+) T cells and B cells
168
What type of vaccines are the MMR and VZV vaccines?
Live-attenuated virus vaccines
169
When was the last case of paralytic poliomyelitis in the US?
1999
170
What are the current flu vaccines composed of? What phenomenon is responsible for the need for a new vaccine every year?
Two prevalent strains of influenza A (one H1N1 and one H3N2) and the single most prevalent strain of influenza B from the past year; antigenic drift requires updating of the vaccine
171
How many deaths are still attributable to measles worldwide per year?
~140k
172
Why can't the Rubella vaccine be given during pregnancy?
Concerns for congenital rubella
173
Is the mumps vaccine 100% effective?
Some recent cases of mumps have occurred in vaccinees
174
What is an adverse effect of the varicella vaccine?
It may occasionally produce mild vaccine-associated disease
175
What is the difference between Varivax and Zostivax?
Zostivax is a zoster vaccine (same virus as varivax) but at a 10x higher dose intended for ≥60 yo patients
176
Should live virus vaccines be given to patients with defective cell-mediated immunity?
No, because they could contract the disease
177
What is the composition of the human papillomavirus vaccine? Does it contain nucleic acids
Reassambed virus-like particles; no
178
How is HPV typically transmitted
By direct (sexual) contact
179
What are common adverse reactions to viral vaccines?
Fever, injection site reactions and a mild rash after MMR
180
What was a risk of the live oral vaccine for polio? What change in the polio vaccine was introduced to prevent it?
Small chance of developing paralytic polio; an inactivated whole virus viaccine is now used
181
What would be a contraindication to administering any vaccine?
A prior anaphylactic reation
182
What allergy is checked before administering the influenza vaccine?
Eggs, since the vaccine is cultured in eggs
183
What happened to the paper published in the Lancet by Wakefield et al. claiming vaccines could cause autism?
It was retracted 10 years later
184
What are the top three cancers attributable to HPV?
Cervix, oral cavity and larynx
185
Which type of cancer caused by HPV represents 10% of female cancers worldwide?
Cervical cancer
186
Is HPV infection common or rare? How many types or strains are there?
Very common; \>140 types/strains
187
What are the symptoms of infection with a low-risk HPV type?
Ano-genital condyloma (genital wart) and low-grade dysplasia
188
Which are the HPV types that are most prevalently associated with high grade dysplasia and cervical cancer?
16 and 18
189
What proportion of cervical cancers are associated with HPV infections?
\>99%
190
What proportion of anal, vaginal, and penile cancers are attributable to high-risk HPV infection?
70-85% of anal cancers and 40-50% of vaginal and penile cancers
191
What is the outcome for most HPV infections?
Spontaneous clearance
192
What are suspected coexisting risk factors for cervical cancer post HPV infection?
Smoking, host polymorphisms, oral contraception, and other STDs
193
What is the structure and genomic makeup of HPV?
Non-enveloped dsDNA virus with a circular genome (7.9kbp)
194
Why are HPV proteins named either by E or L?
E is the early region of the genome that codes for replication proteins and oncogenic proteins, and L is the late region that codes for capsid proteins
195
Are keratinocytes easier or harder for cytotoxic lymphocytes to kill than most other cell types? How does this affect HPV infection?
Harder; HPV can survive more easily
196
Does HPV infect the bloodstream?
No
197
Both commercial vaccines for HPV contain VLPs. What are they?
Virus-like particles, or "shells" of the virus without the nucleic acid portion
198
HPV vaccines contain adjuvants. What is their purpose?
To stimulate a stronger immune response
199
What are the commercial names for the HPV vaccines?
Gardasil and Cervarix
200
Which HPV strains are covered by the HPV4 or quadrivalent (Gardasil) vaccine? Which are covered by the HPV2 or bivalent (Cervarix) vaccine?
Quadrivalent: 6,11,16,18;
Bivalent: 16,18
201
Is there a correlation between states with higher HPV vaccine uptake and lower cervical cancer rates?
Yes
202
When should HPV vaccines be first administered?
Boys and girls ~11-12 yo, before onset of sexual activity
203
Where do most anal cancers related to HPV infection develop?
The anal T-zone, where there is a transition from stratified squamous to columnar epithelium similar to the cervical T-zone
204
How many new infecitons of HPV occur per year in the US?
6.2 million
205
Do ACIP recommendations for the HPV vaccine address patients with a history of cervical dysplasia?
No, only women with a positive HPV screen or genital warts
206
Do people necessarily develop antibodies after HPV infection? Would thise cause serology studies to underestimate or overestimate the prevalance of infection?
No, less than 70% of people develop antibodies to an HPV type after infection; this causes underestimation of prevalence
207
What does aseptic meningitis means?
CSF is cultured and no bacteria grows, but the WBC count is elevated
208
What family of viruses do enteroviruses, rhinoviruses, and Hep A belong to?
Picornaviruses, small RNA viruses
209
How many enteroviruses are there?
At least 71 serotypes
210
Are enteroviruses seasonal?
Yes, summer and fall
211
Between May and September, what is the most common viral etiology of aseptic CNS infection?
Enterovirus
212
Can enterovirus survive in harsh environments?
Yes it can survive in sewage, the GI tract, and detergents
213
How does enterovirus conceal its receptor binding sites from antibodies?
They are contained within canyons formed by VP1
214
Is enterovirus cytolytic? What is its effect on host cell RNA synthesis?
Yes; it inhibits host cell RNA synthesis
215
How does Poliovirus enter the CNS?
It travels via motor neurons from muscle to the brain
216
How do echovirus, Coxsackie virus, Hep A, and poliovirus enter the body? How do they get to the target tissue?
Via the oropharynx; after entering the bloodstream
217
What is the mechanism of tissue injury of enteroviruses?
Cytolysis, except for Hep A, which is immune mediated
218
What two antibody types combat enterovirus infection?
IgA inhibits establishment of initial infection, while serum IgG prevents and controls viremia
219
What countries are still endemic for polio?
Afghanistan, Nigeria, and Pakistan
220
In what percentage of polio infections does paralytic disease result?
2%
221
Are asymptomatic polio carriers able to transmit the disease?
Yes, they can shed it in the stool and nasal secretions
222
What is the difference between the Salk and the Sabin vaccines? Which has a very low risk of causing an infection? What is that vaccine's advantage?
Salk's vaccine is inactivated, while Sabin's is attenuated; Sabin's has the potential to cause infection; Sabin's is easier to administer (it can be given orally)
223
Is the Sabin vaccine for polio used in the US?
No, the inactivated Salk vaccine is used
224
What class of virus related to Hep A can cause these symptoms?
Enteroviruses
225
What condition is this, and which virus causes it?
Herpangina caused by Coxsackie A
226
What disease is this and what virus causes it? 
Hand, foot, and mouth disease caused by Coxsackie A
227
What are possible manifestations of Coxsackie B virus?
Pleurodynia, myocarditis, pericarditis, and overwhelming neonatal disease
228
What enterovirus besides Coxsackie B can cause overwhelming neonatal disease?
Echovirus
229
What is the glucose and level in typical viral meningitis? What would they more likely be in bacterial meningitis?
Both are normal viral; they tend to be low with bacterial meningitis
230
What is the treatment for viral meningitis?
Usually supportive
231
Why is CSF glucose usually lowered in bacterial meningitis?
The bacteria consumes the glucose in the CSF
232
What infectious agent causes mad cow disease?
Prions
233
What disease are these histological findings in brain tissue common for?
Prion disease (mad cow): on the left, amyloid plaques, on the right, vacuoles
234
What is the prognosis for prion disease?
It is uniformly fatal over a period of months
235
What is the structure of a prion?
It is an infectious protein that lacks nucleic acid or a virus like structure
236
How do prions cause disease within brain tissue?
They are a conformational isomer of a normal host protein that seems to trigger a conformational change in the normal host protein, which spreads this misformed conformation to other instances of the protein
237
What human diseases (not transmitted by animals) are caused by prions?
Kuru disease, Creutzfeldt-Jacob disease (CJD) mostly in older patients, and variant CJD which can manifest at a younger age
238
What is the full name for Mad Cow disease?
Bovine spongiform encephalopathy
239
What led to this decline in mad cow disease seen in the UK?
Regulations on feeding cows animal products (e.g., the brains of other cows)
240
How long can infected individuals shed enteroviruses in the stool?
Weeks
241
How common are prion diseases?
Not at all
242
What is the most common viral cause of severe diarrhea in young children?
Rotavirus
243
What is the distribution of rotaviruses? How many children are infected by age five?
Worldwide; almost all
244
What is the percentage of childhood gastroenteritis hospitalizations that is attributable to rotavirus in first world infants? Is mortality common?
34%-52%; no
245
Which is the most common cause of gastroenteritis: rotavirus, adenovirus or bacteria?
Rotavirus
246
What are presenting symptoms for rotavirus?
Fever, vomiting, watery diarrhea, and dehydration
247
Are subsequent infections of rotavirus more severe or less severe?
Less severe
248
What is the transmission route of rotavirus?
Fecal-oral
249
Can rotavirus be cell cultured?
Yes
250
What family does rotavirus belong to?
*Reoviridae*
251
Which serotype group of rotavirus is most important clinically?
Group A
252
Why was rotavirus named with rota-?
It appears like a wheel on EM
253
What is the genomic structure of rotavirus? Does it have an envelope?
It is a segmented dsRNA virus; no envelope
254
What are the outermost proteins of rotavirus, participating in cell attachment?
VP4, also called the P antigen
255
How many segments does the rotavirus have? How many proteins are produced by each segment?
11; about 1 protein per segment
256
Does the dsRNA genome of rotavirus get transcribed into DNA during the life cycle of the virus?
No, it is replicated using an RNA-dependent RNA polymerase
257
Which protein in rotavirus induces secretory diarrhea?
NSP4
258
What viral proteins to rotavirus are the basis for humoral immunity following the first infection?
VP4 and VP7 which are on the surface of the virus
259
How many serotypes of rotavirus are included in the RotaTeq vaccine? What is the route of administration? What is the most important contraindication?
5 serotypes; 3 liquid doses at 2, 4, and 6 months of age; cannot be given to immunodeficient infants
260
What can happen to the genome of rotavirus after coinfection?
Shuffling or reassortment of the genomic fragments
261
How many serotypes was RotaShield able to protect against? Is it still on the market?
4 serotypes; no, because it was linked to intussusception (invagination of the intestine)
262
What is the valency of the Rotarix vaccine? Is it still used in infants?
1 serotype of rotavirus; yes, and it provides some cross-protection against other serotypes
263
What concern was raised with the Rotateq vaccine after highly sensitive nucleic acid sequencing?
PCV-1 and PCV-2 (a porcine virus) sequences were found in it, but the FDA cleared it
264
Has the rotavirus vaccines been shown to reduce incidence of rotavirus infection in infants?
Yes
265
What is the most common cause of outbreaks (e.g. isolated clusters) of nonbacterial acute gastroenteritis?
Norovirus
266
Are noroviruses easily grown in culture?
No
267
What family does norovirus belong to? What is their genomic structure? Do they have an envelope?
Calciviridae; + sense, ssRNA genome; no envelope
268
What are presenting symptoms for norovirus infection?
Mild febrile illness of watery diarrhea and fever, with more severe illnesses of fever, vomiting, headache, and constitutional symptoms
269
What proportion of the population is susceptible to norovirus? What mutation do 20% of humans have that confers resistance?
About 45%; 20% of people are resistant do to a mutation in FUT2 that alters the carbohydrates found on epithelial cells
270
Is norovirus usually diagnosed in the clinical setting?
No, but it can be identified for epidemiological purposes
271
Besides norovirus and rotaviruses, what other viruses can cause GI illness?
Enteric adenoviruses and astroviruses
272
Are all cases of viral hepatitis symptomatic?
No
273
How many kinds of hepatitis viruses are known to exist currently? Which one depends on another virus to successfully infect a patient?
Four: Hep A, B, C, and E; Hepatitis δ virus (delta agent) relies on Hep B for infection
274
What virus was originally called hepatitis G? Why was it renamed?
GB virus-C; it does not appear to replicate primarily in the liver
275
Which hepatitis viruses cause insidious (as opposed to abrupt) infection? What is their incubation period?
Hepatitis B and C; 45-160 days
276
What family of virus does Hep A belong to?
Picorna virus
277
What family of viruses does Hep B belong to?
Hepadnavirus
278
What family of viruses does Hep C belong to?
Flavivirus
279
Between Hepatitis B and Hepatitis C, which one usually causes subclinical infections?
Hepatitis C
280
Can Hepatitis A produce a chronic infection?
No
281
Which hepatitis viruses are transmitted via sexual contact? What about perinatal transmission?
B, C, D and commonly transmitted sexually and from mother to child, but A and E can also be transmitted sexually depending on specific acts
282
Is there a therapy for Hepatitis A?
No
283
Is there a vaccine for Hepatitis B? What about Hepatitis C?
Yes for B; no for C
284
How many people are chronically infected with HBV worldwide? What about in the US?
350M worldwide; ~1M in the US
285
Are vaccines for Hep B given routinely to US children?
Yes, since 1991
286
What is the genomic structure of Hepatitis B? Is it enveloped?
Partially double-stranded DNA, circular; Enveloped
287
Which antigen is on the surface of HBV? What are collections of this antigen without viral proteins called?
HBsAg; subviral particles
288
What proportion of acute infections of HBV result in subclinical disease?
60-65%
289
Is death due to acute Hepatitis B virus infection common?
No
290
What are the two serological proteins that differentiate between acute and chronic hepatitis B infection?
HBsAg is eliminated in acute infection, but remains in the plasma for chronic infections—also, acute infection with HBV results in production of anti-HBsAg antibodies
291
If you have been vaccinated for HBV, how can you be serologically differentiated from somebody who resolved an acute HBV infection?
You will not have anti-HBc IgG, since your immune system was never exposed to HBc (the HBV core protein)
292
With acute and early acute HBV infection, which class of Ig to HBc is not yet present against HBc? What class of antibody for HBc develops during acute HBV infection?
IgG is not present during acute infection; IgM antibodies for HBc are released during acute HBV infection
293
Does chronic HBV infection increase the risk of liver cancer? Why or why not?
Yes; there are two theories, where either virus is activating oncogenes, or the chronic hepatic injury leads to genetic changes in hepatocytes that disrupts growth regulation
294
What are the two therapies available for HBV?
Pegylated interferon α and reverse transcriptase inhibitors
295
When would you treat for HBV as opposed to letting an acute infection running its course?
If the patient is positve for HBsAg for a long time (\> 6mo), has a very high viral load, or evidence of liver disease (e.g. elevated ALT)
296
Are all the HBV antivirals available NRTIs or NNRTIs?
NRTIs (nucleoside analog reverse transcriptase inhibitor)
297
Which antiviral has HBV developed widespread resistance to?
Lamivudine
298
Which antiviral for HBV is the most expensive? Why is it used anyway?
Entecavir; because resistance has developed to the cheapest drug, lamivudine
299
Does Hepatitis δ virus infection alter the prognosis for HBV infection?
Yes, it increases the likelihood of death from fulminant hepatitis, and the chance of cirrhosis and hepatocellular carcinoma from chronic HBV
300
How many people in the US have a chronic HCV infection?
~3.2 million
301
What is the leading indication for liver transplants in the US?
Chronic HCV infection
302
What is the most common source of HCV infection?
IV drug use
303
What is the genomic structure of HCV? Is it enveloped?
It is a single stranded, positive sense RNA virus; yes it is enveloped
304
How many ORFs does HCV have? How can it produce more proteins than it has ORFs?
It has only one; polyprotein self-cleavage
305
What is significant about the evolutionary dynamics of HCV?
It has a high mutation rate do to an error-prone RNA polymerase, and therefore it can escape immune responses and interferon treatment
306
What is the most clinically significant genotype of HCV seen in the US?
Genotype 1
307
Which areas of the world do not have a prevalence for genotype 1 of HCV?
Central Africa and the Arabian peninsula have predominantly genotype 4; South Africa has predominantly genotype 6
308
What serological quantities differentiate between acute and chronic HCV infeiton?
Acute HCV infection has no HCV RNA detectable after several years, and ALT levels remain low, while chronic HCV infection results in spiky ALT levels and recurrently detectable HCV RNA
**Acute:**
**Chronic:**
****
309
What causes some individuals to retain latent HCV while it is cleared in others?
It is not entirely understood, but co-infection with HIV, evasion of immune responses, impaired NK or dendritic cells, or the glycosylated envelope are thought to play significant roles
310
How long does it take for antibodies to HCV proteins to be detected after exposure?
6-8 weeks
311
What is the standard of care for HCV?
Pegylated interferon, ribavarin and a protease inhibitor
312
How does a protease inhibitor contribute to the treatment regimen for HCV?
It prevents breakdown of the polyprotein into the 10 constituent proteins that make up the virus
313
Do all people respond to HCV therapy?
No, some have a sustained virologic response (success), but others have viral load drop to undetectable levels and still return later
314
Which genotype of HCV responds worst to interferon + ribavarin therapy? What variable can be adjusted to maximize that genotype's response?
HCV genotype 1 responds most poorly; with a higher dose and longer treatment course, there is a greater chance of sustained virologic response
315
What are the two protease inhibitors used in HCV therapy?
Telaprevir and boceprevir
316
Which genotype of HCV are telaprevir and boceprevir approved to treat?
Genotype 1
317
How is hepatitis A virus transmitted? What is the usual timecourse of disease?
Fecal-oral; about 3 weeks
318
When is hepatitis A virus infection a risk for fulminant hepatic failure?
Previous infection with HBV or HCV
319
How many acute cases of hepatitis A are estimated to occur within the US each year?
\<20k, as it has dropped since the licensing of the vaccine
320
During what week of hepatitis A infection might a spike in ALT levels be seen?
Between week 1 and week 2
321
Is Hepatitis E virus commonly found in the US?
No, it is predominantly in developing countries where fecal contamination of drinking water occurs
322
What is a risk factor for fulminant hepatitis in women that are infected with hepatitis E?
Pregnancy, with a mortality rate of 20% in the third trimester
323
Is Hepatitis B or Hepatitis C virus more genetically heterogenous?
Hepatitis C virus
324
Do patients with chronic HBV infection ever develop antibodies to the HBV S antigen?
No
325
How many people are estimated to have HIV in North America?
~1.5 million
326
How is the HIV genome integrated into the host cell genome if it is an RNA virus?
A RNA-dependant DNA polymerase (reverse transcriptase)
327
What is the evolutionary origin of HIV?
SIV, a simian virus that jumped to humans
328
Which group of HIV-1 causes the most human disease?
The M group
329
What are the two surface proteins on HIV involved in fusion?
gp41 and gp120
330
Does HIV have a lipid bilayer?
Yes
331
What is the genomic structure of HIV?
Double-stranded positive sense RNA
332
Is HIV enveloped?
Yes, by *env *proteins
333
What is the function of the LTR of the HIV genome?
Regulates transcription of the genome
334
Which gene product of HIV codes for matrix and capsid proteins?
*Gag*
335
Which gene product of HIV codes for the reverse transcriptase, protease, and integrase?
*Pol*
336
Which does regulatory or accessory genes are absolutely required for HIV infectivity? How many are there in total?
*Tat* and *Rev *are necessary; six in total
337
Which HIV protein attaches to CD4 and CCR5 or CXCR4 to initiate fusion into the T cell? What other viral protein mediates this?
gp120 attaches to the receptors; gp41 mediates it
338
What T cell mutation can produce resistance to HIV infection? What is the phenotype for heterozygous individuals?
A homozygous deletion of 32 basepairs in CCR5; heterozygous individuals can be infected but it progresses slowly
339
Why does HIV mutate so rapidly within the host?
The reverse transcriptase is very error prone, misreading a base every 2000 bases
340
What allows HIV to remain latent within T cells for years and constitutes a major barrier to curing HIV with small molecule therapies alone?
It is integrated into the host cell genome of T cells as a pro-virus
341
What feature of mRNA is used to produce many proteins from the small genome of HIV?
Alternate splicing
342
When immature polyproteins in HIV are cleaved by PR to generate infectious viral particles, where are the immature viral particles—intracellular or extracellular?
They have budded and so are extracellular
343
How do Vif and Vpu increase the virulence of HIV?
They block host cell proteins that counter viral replication
344
What is the transmission rate of HIV from mother to child *in utero*, at birth, or through breastfeeding without intervention?
25%
345
Does male to male transmission increase the risk of HIV transmission over other gender pairings? Do STIs increase the risk of HIV acquisition?
Yes to both
346
In a stratified epithelium (e.g. of the rectal or vaginal canals), how do viral particles get to T cells?
An abrasion allows presentation of particles to dendritic cells that migrate to T cells
347
Why is the rectal epithelium more susceptible to HIV transmission than the vaginal epithelium?
It is more susceptible to trauma, and vaginal secretions form a strong barrier to HIV transmission
348
Can HIV be found in the gut within days of infection? What about the CNS?
Yes to the gut, in its lymphoid tissues; yes it can also be found in the CNS
349
At approximately how many weeks following primary infection does HIV load drop to initiate the latent or chronic period?
9 weeks
350
What are the symptoms of acute HIV syndrome?
Similar to mononucleosis or flu-like illness: fever, sore throat, and malaise
351
What is the fastest lab test for determining acute HIV infection?
RNA PCR, which is faster than detecting antibodies
352
During latency, does HIV still replicate?
Yes, billions of viral particles are produced per day
353
If there is no viral load of HIV detectable in plasma, does that mean that an HIV patient has been cleared of the virus?
No, it is likely still in the lymph nodes
354
Why do CD4 T-cell counts drop following HIV infection?
The virus can kill cells or trigger apoptotic pathways, and infected cells are also killed by the immune system or experience anergy due to inappropriate signalling
355
Can an HIV patient have high IgG levels? Why or why not?
Yes, because they often are in a state of hyperactivation of T cells and B cells, which make more antibodies and cytokines
356
Does HIV cause direct neuronal damage?
Yes, possibly because of direct infection of microglia, or because shed gp120 activates microglia to produce neurotoxins
357
What is the main line of defense against HIV? Why can HIV evade them so easily?
Cytotoxic T lymphocytes; HIV infects CD4 T cells which would normally activate these lymphocytes, but cannot following infection
358
What three properties of the surface proteins of HIV make it hard for the immune system to develop a response?
They are glycosylated, making it difficult to develop antibodies against them. They mutate quickly. Conserved regions are recessed or hidden.
359
When the rate of loss of CD4 T cells increases steadily, what stage of HIV has been reached? What clinical symptoms are present?
AIDS; opportunistic infections begin to appear
360
When extracellular bacteria elicit an adaptive response, what effector mechanisms are used to rid the body of the bacteria?
Phagocytosis via opsonization by antibodies, concurrent with neutralization of the microbes and their toxins by the antibodies
361
How do superantigens like SEB trigger a hyperactive systemic inflammatory response?
They grip the TCR-HLA interaction and lock them together, causing uncontrolled hyperactivation of T cells and release of cytokines
362
What class of bacteria carry lipoteichoic acid? What serious inflammatory condition can it cause?
Gram positive; septic shock
363
What does *S. epidermidis* form to evade the immune system?
Biofilms
364
Why does *S. aureus* have coagulase?
It encourages clot formation, which allows immune evasion
365
Staphylococci are catalase positive. Why does this enzyme make them more virulent?
Catalase allows them to neutralize ROS released by immune cells attempting to kill them during phagocytosis
366
How are the number of intracellular bacteria controlled during the innate immunity phase of infection?
Macrophages release IL-12, which activates NK cells, killing infected macrophages
367
How are infected cells killed during the adaptive immunity phase of infection by intracellular bacteria?
CD4+ T helper cells activated by IFNγ from macrophages activate CD8+ cytotoxic T lymphocytes, which find the infected macrophages and kill them
368
If intracellular bacteria cannot be eliminated and chronically stimulate the immune system, what do lymphocytes form in response?
Granulomas
369
What is the first immune cell type to respond to a viral infection?
NK cells
370
What cytokine upregulates the cytotoxicity of NK cells?
Type 1 interferons
371
When an RNA virus has a segmented genome like influenza does, what can happen in a coinfected host?
The virus can swap segments producing a differently virulent strain
372
Which five steps of the Class I MHC pathway are obstructed by viruses to obscure the infected state of the cells they enter?
The proteasomes, the TAP transport, MHC synthesis, MHC survival in the ER, and CTL recognition of the MHC
373
Why might viruses produce cytokines or cytokine receptor decoys?
They may release cytokines that downregulate immune responses or decoy receptors to absorb inflammatory cytokines
374
What pathway is blocked by all infectious human viruses?
Type 1 interferon
375
What do dengue virus, yellow fever, West Nile, and hantaviruses have in common?
They are significant zoonotic viruses (transmitted by animals)
376
What does "arbovirus" mean?
Borned by arthropod, e.g., mosquitos
377
What virus family do denguevirus, West Nile, and yellow fever all belong to?
Flaviviridae
378
What is the genomic structure of flaviviridae?
Single stranded positive sense RNA
379
What prevents flaviviruses from generally causing viremia and then encephalitis?
Antibody block by the immune system
380
How do alpha and flavivurses enter the host cell?
Receptor-mediated endocytosis
381
Does denguevirus have an envelope?
Yes
382
How much of the world's population is at risk for denguevirus infection?
About half
383
Which mosquito species transmits denguevirus?
* Aedes aegypti*
* *
384
How can the mosquito that spreads denguevirus be identified visually?
*Aedes aegypti* has white bands or scale patterns on its legs
385
Can the *Aedes albopictus* mosquito transmit denguevirus? Can humans transmit it to each other?
Yes, this mosquito can; no, humans do not transmit to each other
386
Can a patient be infected with multiple serotypes of denguevirus within a few weeks of exposure?
Typically no, because they provide short-term cross-immunity
387
What serious complications of denguevirus can occur during the second phase of illness?
Dengue hemorrhagic fever and dengue shock syndrome
388
Between the primary and secondary infection phases of denguevirus, is the virus detectable? What about IgG to denguevirus antigens?
The virus is not detectable, but IgG is
389
What proportion of denguevirus cases cause hospitalization?
10%
390
Is there a vaccine for denguevirus?
No, but three are undergoing trials
391
Does a treatment for denguevirus exist?
Not yet, but a novel antiviral is being developed
392
How can denguevirus be detected via laboratory testing?
Anti-DENV IgM in serum, or PCR
393
What is the most effective currently available method for denguevirus control in a population?
Controlling (eliminating) the vector, which is the mosquitos
394
Why are scientists introducing *Wolbachia pipientis* bacteria into *A. aegypti* mosquitos?
It is a benign bacterium for mosquitos but reduces the chance that they can carry denguevirus, and this strategy is being tried in Australia
395
What happened to the Sanofi Pasteur vaccine for dengue virus?
There was only 30% efficacy and no enhancement of immune response, hence it is being redesigned
396
What is the natural reservoir for yellow fever?
Monkeys
397
What vector is used by yellow fever virus to move from monkeys to humans (typically)?
Mosquitos
398
Is a vaccine available for yellow fever?
Yes, a live virus vaccine is available and mandatory in some YF affected countries
399
How do arboviruses enter the body in the course of eventually manifesting as encephalitis?
Via subcutaneous tissue (puncture wound, mosquito)
400
What is the seasonality of arborvirus-caused encephalitis? What other viral encephalitis tracks this seasonality?
Most common in late summer to early fall; Enterovirus
401
What is the genomic structure of West Nile virus? Is it enveloped?
Single stranded positive sense RNA; yes it is enveloped
402
Approximately how many cases of West Nile occur in New York State per year, based on 2009 data?
~6
403
Is an animal model for West Nile available?
Yes, in mice
404
What mutation confers resistance to HIV infection but increased risk for West Nile infection?
A deletion in CCR5
405
Can West Nile be spread by exposures other than the mosquito vector?
Yes, via transfusion, transplant, or mother → child via placenta or breast milk
406
Out of eastern equine encephalitis, western equine encephalitis, St. Louis, and La Crosse, which infection has the greatest mortality rate?
Eastern equine encephalitis
407
Where is Hantaanvirus endemic? What vector do they use? What is the presenting symptom?
Russia, China, and Korea; the striped field mouse; hemorrhagic fever with renal syndrome
408
What two types of hantavirus are significant in the US and Canada? What do both cause?
Sin Nombre and New York hantavirus; hantavirus pulmonary syndrome
409
How do hantaviruses infect a human host?
Via the pulmonary tract, upon inhalation of virus-contaminated aerosols of rodent excretions
410
What is the genomic structure of Rhabdoviruses? Is it enveloped? What is notable about the viral shape?
single-strand negative-sense RNA; yes; it is bullet-shaped
411
How many cases of rabies present per year in the US? How much is spent on rabies post-exposure prophylaxis?
2 cases per year; $300 million per year on prophylaxis, since many patients are bitten by animals
412
What cell types are infected and locations of replication for rhabdovirus?
Muscle and nerve cells
413
Does rabies cause neuronal necrosis?
No, but it still injures the CNS somehow
414
What infection characteristically produces Negri bodies in the brain?
Rhabdovirus (rabies)
415
What are presenting symptoms of rabies that has infected the CNS? How quickly can death occur?
Personality changes, parathesis, pain at the site of exposure, and other neurologic symptoms; 18 days after viral prodome
416
How can rabies be diagnosed?
Biopsy and immunofluorescence from skin on the nape of the neck, and PCR on CSF, saliva, and tissue
417
What are these indicated features in a pathology study of Rabies infection of the CNS?
Negri bodies
418
What family do Epstein-Barr virus and Cytomegaloviruses belong to?
Herpes viruses
419
What herpes viruses are latent, is there synthesis of viral particles?
No
420
What is the genomic makeup of all herpes viruses? Are they enveloped?
Large double stranded DNA viruses; yes, enveloped
421
What cell type does EBV infect and remain latent in?
B lymphocytes
422
What happens to life cycle of B cells infected by Epstein-Barr virus?
They become immortalized
423
What cancer can immunocompromised hosts of Epstein-Barr virus develop?
Lymphoma
424
Can the Monospot test be used in patients of all ages? What virus is it used to detect?
No, it is not sensitive in young children; Epstein-Barr
425
Which serological protein steadily rises and plateaus during convalescence of Epstein-Barr?
EBNA
426
What proportion of early childhood infections by Epstein-Barr are asymptomatic?
50%
427
What proportion of the US population is infected with Epstein-Barr by age 30?
70%
428
What virus causes infectious mononucleosis?
Epstein-Barr virus
429
What viral infection is consistent with fever, pharyngitis, lymphadenopathy, hepatosplenomegaly and rash that gets worse with ampicillin or amoxicillin?
Mononucleosis (Epstein-Barr)
430
How long does it take for infectious mononucleosis to resolve?
2-3 weeks
431
Which virus is associated with Burkitt's, Hodgkin's and CNS lymphoma in AIDS? What other cancer is associated with this virus?
Epstein-Barr virus; nasopharyngeal carcinoma
432
What is this condition? Is it malignant? What virus(es) is it associated with?
Oral hairy leukoplakia; it is non-malignant; Epstein-Barr in the context of HIV infection
433
What is the level of association between post-transplant lymphoproliferative disease and Epsteinn-Barr virus?
Very high (90%)
434
What serological protein level characterizes chronic active Epstein-Barr virus?
A lack of EBNA response and high titers of acute phase antibodies (EA and VCA)
435
How Epstein-Barr treated?
Supportively
436
Why might rituximab be given to somebody that previously had an Epstein-Barr virus infection?
It is used to treat certain EBV-related malignancies by controlling B cell proliferation
437
What is the mechanism of rituximab?
It is an antibody to CD20, a B-cell marker, which initiates antibody-dependent cellular cytotoxicity, complement activation, and apoptosis in malignant B cell lymphomas
438
What proportion of the young population is infected with CMV?
70-90%
439
What bodily fluids contain CMV?
Saliva, vaginal fluid, semen, and urine
440
How does cytomegalovirus downregulate the immune system?
It downregulates MHC I expression
441
What is the function of UL97 in cytomegalovirus and how does it relate to the drug Gancyclovir?
It is a viral kinase that phosphorylates Gancyclovir, a viral polymerase inhibitor
442
Is mononucleosis always caused by Epstein-Barr virus?
No, there is an EBV-negative mononucleosis that is usually milder and caused by cytomegalovirus (CMV)
443
What is the number one cause of congenital hearing loss in the US?
Cytomegalovirus infection
444
What is the most common patient population with cytomegalovirus seen in hospitals?
Immunocompromised patients
445
What are some complications of congenital cytomegalovirus infection?
Hepatitis, thrombocytopenia, CNS disease, retinitis, and hearing loss
446
How can CMV be diagnosed in newborns? Why is this technique less useful in an adult?
Urine culture; Infection and reactivation are so common in adults that such assays would not be specific or sensitive
447
What is the first line treatment for cytomegalovirus infection in a newborn or the immunocompromised? What is its mechanism?
Ganciclovir; it is a nucleoside analogue that inhibits the viral polymerase
448
What is the difference between ganciclovir and valganciclovir?
Valganciclovir is a better orally absorbed version of ganciclovir
449
What are cidofovir and foscarnet second line treatments for?
Cytomegalovirus infection
450
What are two second line treatments for CMV infection?
Cidofovir and foscarnet
451
What virus is this rash and timecourse typical of?
Roseola
452
Which virus causes roseola?
Human herpes virus 6 (HHV-6)
453
What is the genomic structure of cytomegalovirus? It is enveloped?
It is a double-stranded DNA virus; yes it is enveloped
454
What cell types are infected by HHV-6?
Lymphocytes, monocytes, and macrophages
455
What virus is most closely related to HHV-6 that infects nearly all children by age 5?
Human herpes virus 7 (HHV-7)
456
What is another name for HHV 8, which causes the following skin presentation?
Kaposi's sarcoma associated herpesvirus
457
Which herpesvirus is not widely distributed in the population? Who does it infect?
HHV 8 or Kaposi's sarcoma associated herpesvirus; immunocompromised
458
How is HHV-8 typically transmitted in the US?
Sexual contact (more often seen in MSM)
459
Are gastrointestinal symptoms possible with an influenza infection?
Yes, but they are rare
460
Besides pneumonia, what are three other serious complications of influenza?
Otitis media, Reye's syndrome, and encephalitis
461
What happened in 1918 that caused life expectancy in the US to drop by more then 12 years?
The Spanish Flu epidemic
462
What is the most frequently isolated type of influenza? Which causes the most severe disease?
Type A for both
463
Which type of influenza has an animal reservoir?
Influenza type A
464
What are the black blobs within these EM images of influenza?
Individual RNA strands
465
How many different influenza A virus hemagglutin subtypes are there?
17
466
What does the H in e.g. H1N1 refer to?
Hemagglutinin subtype
467
What is the difference between antigenic drift and antigenic shift?
Drift is the change in the hemagglutinin from year to year, caused by point mutations, while shift is the occasional change that results from a *reassortment event* between human and avian influenza strains
468
What does the N in H1N1 stand for?
Neuraminidase
469
Which strain of influenza is more deadly once the case is discovered: swine H1N1 influenza, or avian H5N1 influenza?
Avian H5N1 is more deadly
470
What are the two classes of FDA-approved influenza antivirals? Which are approved against type B influenza?
Ion channel blockers and neuraminidase inhibitors; only the latter is effective against type B
471
What are two ion-channel blockers approved for use against influenza? Which type(s) of influenza can they treat?
Amantadine and rimantadine; only type A
472
What are two neuraminidase inhibitors approved for use against influenza? Which type(s) of influenza can they treat?
Zanamivir and oseltamivir; both A and B type influenza
473
Which ion channel on influenza is blocked by amantadine?
M2
474
Which stage of influenza replication is inhibited by ion channel inhibitors? Which stage is inhibited by neuraminidase inhibitors?
Uncoating is prevented by ion channel (M2) inhibitors; release of the virus from the cell membrane is inhibited by neuraminidase inhibitors
475
What is another name for Tamiflu? What kind of drug is it? What types of influenza can it treat?
Oseltamivir; neuraminidase inhibitor; type A and B
476
Are killed virus (inactivated), live virus (attenuated) or both types of vaccine used against influenza?
Both types are used
477
What is the formulation strategy for the influenza vaccine?
The most prevalent strain of H1N1 (type A), H3N2 (type A), and type B influenza are selected for the vaccine
478
What is the field of mycology about?
Fungi
479
What is the differentiation between yeasts and molds?
Yeasts are budding unicellular organisms that look sort of like bacteria, while molds have a long fluffy appearance and are multicellular
480
What does it mean for a fungus to be dimorphic?
It acts as a yeast in the body, but as a mold in the environment
481
What is a hypha?
A long branching structure of a fungus
482
Of the following, which are systemic dimorphic endemic fungi, and which are opportunistic?
– Histoplasma
– Candida
– Cryptococcus
– Blastomyces
– Aspergillus
– Histoplasma - systemic dimorphic endemic
– Candida - opportunistic
– Cryptococcus - opportunistic
– Blastomyces - systemic dimorphic endemic
– Aspergillus - opportunistic
483
Of the following, which are systemic dimorphic endemic fungi, and which are opportunistic?
– Coccidiodes
– Paracoccidioides
– Mucorales
– Penicillium
– Coccidiodes - systemic dimorphic endemic
– Paracoccidioides - systemic dimorphic endemic
– Mucorales - opportunistic
– Penicillium - systemic dimorphic endemic
484
Where do *Trichophyton* and *Malassezia* infect the body? What kind of organism are they?
Skin; they are superficial dermatophytic fungi
485
Are all fungi eukaryotic?
Yes
486
What is the analog of cholesterol used in the cell membrane of fungi?
Ergosterol
487
A 30 year old patient on total parental nutrition with this organism growing on culture of peripheral blood likely has ...?
*Candida albicans—*recall that patients on total parenteral nutrition are at risk for bloodstream infections, and that *C. albicans* can grow in a hyphae form
488
Does *Candida albicans* grow on blood cultures?
Yes
489
What are pseudohyphae?
Chains of individual budding cells with constrictions seen in some fungi
490
What are these structures? What kind of organisms would form it?
Pseudohyphae; fungi like *C. albicans*
491
Can C. albicans grow as a unicellular yeast, pseudohyphae, or hyphae forms within the body (or some combination of them)? Can it form chlamydospores?
Yes to all forms; yes, it can form chlamydospores
492
What is this fungal infection?
Oral thrush or candidiasis
493
What is a pharmacological risk factor for vulvovaginal candidiasis in patients with normal immune systems?
Taking antibiotics, which eliminates the normal flora
494
What fungal infection can cause these skin manifestations?
*C. albicans*
495
What organism causes diaper rash?
*C. albicans*
496
Which *Candida* species is most significant in bloodstream infections?
*C. albicans*
497
If this infection on the liver is seen during surgery, with the following features seen in pathology, what is suspected?
*Candida albicans*
498
What are four risk factors for systemic candidiasis?
Neutropenia, catheters, parenteral nutrition, and broad-spectrum antibiotics
499
Can this infection be found in an immunocompetent host?
Yes, but it is much more common in AIDS patients (oral thrush)
500
How is a *C. albicans* infection treated?
Amphotericin, fluconazole, or echinocandins
