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MHD2 > Block 11 - L6-L9 > Flashcards

Block 11 - L6-L9 Flashcards

1
Q

Describe the distinctive morphology of restroviral particles on EM.

A

Membrane bilayer, bullet-shaped, electron dense core, hazy extensions of glycoproteins

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2
Q

What are the 4 enzymes present in the core of HIV?

A

Reverse transcriptase (RT), RNase H, integrase, protease

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3
Q

Describe the RNA contained in the core of HIV.

A

2 single-stranded positive sense RNA

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4
Q

What are the two important glycoproteins on the surface of HIV?

A

GP120 (receptor-binding protein) and GP41 (transmembrane protein)

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5
Q

What enzymatic activity signifies the presence of retroviruses?

A

RT activity

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6
Q

How does HIV enter a cell?

A

One of the three GP41 binds CD4. Structural changes occur in GP120, exposing a binding site, which binds to CCR5 (co-receptor) on the cell.
The virus and cell are brought into close proximity, such that the membrane bilayers coalesce and open a portal for the virus to infect.

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7
Q

What is the target immunogen for an HIV vaccine?

A

GP120/GP41

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8
Q

What happens to people who do not express the CCR5 co-receptor?

A

They do not get infected by HIV

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9
Q

Once the viral core is in the cytoplasm, what happens?

A

Uncoating, reverse transcription, and trafficking of the DNA form into the nucleus.

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10
Q

Virion RNA genomes are ___.

A

Diploid

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11
Q

What are LTRs seen on the ends of the provirus DNA?

A

Long terminal repeats that promote transcription of the DNA form of the virus

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12
Q

Once the viral DNA is in the nucleus of the cell, what are the possible outcomes?

A
  1. Proviral integration, but no transcription - latent infection
  2. Proviral integration into germ line cells - endogenous (vertical) transmission
  3. Proviral integration into an essential cellular gene - cell may die
  4. Proviral integration near a cellular oncogene - cell may transform and cancer may develop
  5. Proviral integration followed by DNA transcription - production of progeny viruses
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13
Q

What happens after integration?

A

Transcription, nuclear export, translation, assembly, budding, and maturation

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14
Q

What happens in maturation of HIV?

A

Immature HIV condenses gag proteins into a conical shape; done via a viral protease

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15
Q

Current HIV-1 is related to what original virus?

A

HIV-cpz, a chimpanzee lentivirus

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16
Q

How is HIV transmitted?

A

Plasma, semen, vagina/cervical fluid, breast milk

NOT saliva, sweat, tears, bronchial fluid, urine feces

HIV is not a particularly infectious virus and is not contagious like measles (can be reduced/killed by air drying, heating, bleach, alcohol, pH extremes, detergents)

Not spread by respiratory, alimentary, or vector routes

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17
Q

HIV has evolved into what two groups? One of these groups has evolved into ___.

A

Groups - M (main) and O (outlier)

M group has evolved into clades

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18
Q

Which clade predominates in the US and Europe? In Thailand?

A

US/Europe - B

Thailand - E

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19
Q

Evolution of variability of HIV is largely in ___.

A

Surface glycoproteins GP120 and 41

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20
Q

Evolution and variability in HIV GP120 determines virus tropism for which cells?

A

Macrophages and CD4+ T cells

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21
Q

Discuss the pathology of HIV infection?

A

Robust, cytotoxic infection causing death of CD4+ T cells and syncytia formation in lymph nodes

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22
Q

What are the 3 stages of HIV-induced disease?

A
  1. Acute (4-8 weeks)
  2. Latent (up to 12 years)
  3. AIDS (2-3 years)
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23
Q

Describe the infection of CD4+ T cells over the course of these stages.

A

Infection occurs and a large drop in T-cells occurs during the acute phase; this rebounds somewhat (not to pre-infection levels), and decreases slowly over the latent period. It drops completely in AIDS, leading to death

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24
Q

Describe the Ab over the course of the stages of HIV.

A

The acute phase has a peak and drop in viremia, which then remains fairly low during the latent period. It increases without stopping in AIDS.

Antibodies to HIV-specific CTL appear first, followed by Ab to the HIV envelope and to p24. These stay high during the latent period and drop in AIDS.

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25
Q

What are the symptoms of acute infection with HIV?

A

Monolike syndrome (fever, fatigue, swollen lymph nodes), observed ~3 weeks after initial infection

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26
Q

What are the symptoms of clinical latency and what does this mean for the virologic latency?

A

Few if any clinical manifestations, typically lasts 8-12 years

NOT virologic latency - continued, high levels of viral replication, easily detectable in blood of patients

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27
Q

When CD4+ T cell counts fall below 350 cells/microliter, what AIDS-related symptoms appear?

A

Oral lesions
Basal cell carcinomas
Activation of latent herpes
Mycobacteria infections

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28
Q

When CD4+ T cell counts fall below 200 cells/microliter, what more severe AIDS-related symptoms appear?

A

Protozoal, bacterial, and fungal infections (pneumonia with Pneumocystis carnii, CMV retinitis, oral leukoplakia due to candida)
Viral infections and malignancies (Kaposi sarcoma due to HSV8)
Neurological disorders (AIDS dementia)

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29
Q

What is the goal of HAART (Highly active antiretroviral therapy)?

A

Lower the virologic set point, which slows disease progression

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30
Q

What is the indication to start HAART?

A

Definitive laboratory evidence of HIV

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31
Q

What types of drugs are used in HAART?

A

RT inhibitors (block reverse transcriptase) and protease inhibitors (prevent virion capsid morphogenesis), used concomitantly

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32
Q

What are the AE of long-term HAART?

A

Heart disease, diabetes, liver disease, certain cancer, anemia

Clinical AE - diarrhea, N/V, weakness, lipodystrophy

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33
Q

Why must HAART be prolonged?

A

Drug-resistant viruses are easily formed, as HIV is mutable

HIV provirus can stay in latently-infected cells for a long time

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34
Q

Compare HTLV (lymphotropic retrovirus) with HIV lentivirus.

A

Similar patterns of transmission, both are common

HTLV has lower disease penetrance than HIV

HTLV clinical latency period is longer than HIV (20+ years from infection to clinical disease)

HTLV causes T cell leukemia, which HIV causes T cell death and immunosuppression

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35
Q

How does HTLV cause T cell leukemia?

A

Encodes tax, an accessory protein which induces cell proliferation

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36
Q

Which cell type is most important for disseminating HIV into the central nervous system?

A

Macrophages

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37
Q

What is the genome and family of HIV?

A

Positive strand RNA lentivirus

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38
Q

What method for detection of HIV infection is the most rapid and now widely used?

A

RT-PCR for detection of viral genetic information

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39
Q

What is the current method of detection of HIV?

A

Serology and confirmation by Western blot

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40
Q

What is the mechanism of pathogenesis of HIV?

A

HIV targets CD4+ T cells and macrophages, causing a flu-like syndrome

Chronic viral replication results in a depletion of CD4+ T cells during a period of clinical latency

Low T cell count results in susceptibility to opportunistic infections and clinical AIDS

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41
Q

Are there any available anti-virals to treat patients with HIV?

A

Yes, triple drug therapy is required to prevent drug resistant mutants from arising during treatment. Antivirals are a combination of reverse-transcriptase inhibitors, protease inhibitors and integrase inhibitors

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42
Q

Is there a vaccine available against HIV?

A

No

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43
Q

Are there long-term consequences to HIV infection?

A

Progression to Acquired Immunodeficiency Syndrome (AIDS)

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44
Q

List the major viruses that can cause CNS disease.

A
  1. Herpes
  2. Enterovirus
  3. Arbovirus
  4. Measles
  5. Rabies
  6. Prions
  7. HIV
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45
Q

Of the 7 major viruses that can cause CNS disease, which are present in a specific geographic location?

A

Arbovirus (tropics)

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46
Q

Of the 7 major viruses that can cause CNS disease, which are predominantly found in children?

A

Enterovirus and measles

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47
Q

Of the 7 major viruses that can cause CNS disease, which are predominantly found in the elderly?

A

Arbovirus

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48
Q

Of the 7 major viruses that can cause CNS disease, which are predominantly found in adults?

A

HIV

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49
Q

Of the 7 major viruses that can cause CNS disease, which present in the summer?

A

Enterovirus and arbovirus

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50
Q

What are the steps required for neuronal virus infection?

A
  1. Enter the neuron at the axon, sensory terminal, or cell body, depending on the site of infection
  2. Transport the virus particle or subviral particle to the neuronal cell body where the virus replication occurs
  3. Replicate the virus genome
  4. Assemble virus particles that egress from the infected neuron in a directional manner
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51
Q

What are the manifestations of HSV infection?

A

Primary oropharyngeal herpes and recurrent labialis
Genital herpes - primary and recurrent
Also - encephalitis, keratitis, mucocutaneous disease (immunocompromised), neonatal herpes

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52
Q

How does herpes infect the CNS (rare)?

A

Via olfactory neurons (dendrites are exposed in the olfactory epithelia)

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53
Q

What is unique about the neuronal transport of herpes viruses?

A

Bidirectional

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54
Q

How is herpes encephalitis diagnosed?

A

PCR of CSF

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55
Q

What is the most common cause of sporadic viral encephalitis?

A

HSV

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56
Q

What are the neurological sequelae of enterovirus infection?

A

Meningitis (primarily), sometimes SC involvement, leading to myelitis and paralysis

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57
Q

What are two common arbovirus (flavivirus) infections?

A

West Nile Virus and Dengue fever

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58
Q

How are flavivirus infections transmitted?

A

Skin inoculation by an insect; infect dendritic cells of the skin -> lymph node -> viremia and CNS infection

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59
Q

Describe the transmission cycle of West Nile Virus.

A

Endemic in insects and birds, enters humans (but not transmitted to other humans)

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60
Q

What does WNV cause?

A

Meningitis

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61
Q

___ is associated with microcephaly in infants.

A

Zika virus

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62
Q

What is the rare CNS sequelae of measles infection?

A

SSPE - develops many years after acute disease

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63
Q

Describe the rabies virus particle structure.

A

Bullet shaped, RNA in the center, lipid envelope, trimeric G glycoprotein trees (bind rabies to neurons)

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64
Q

How is rabies transmitted?

A

Enters tissue from saliva of a biting animal, replicates in muscle near the bite, moves up the PNS to the CNS via the spinal cord (binds to ACh receptors), reaches brain (fatal encephalitis) and salivary glands (can be transmitted)

Uni-directional retrograde transport; fast axonal transport

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65
Q

What is the incubation period of rabies infection?

A

20-90 days

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66
Q

How can rabies be treated prophylactically?

A

Eliminate the virus prior to invasion of the neurons (wash wound, IgG)

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67
Q

What are 4 infectious encephalopathies in humans?

A

Kuru, CJD, GSS disease, FFI

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68
Q

How do prions differ from viruses?

A

No nucleic acid, no defined morphology, no disinfection, no cytopathologic effect, no immune response, no interferon production, no inflammatory response

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69
Q

What is seen in the brain in kuru?

A

Plaques

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70
Q

How are prion plaques formed?

A

Formation of a catalyst (altered form of an endogenous protein), altered proteins form aggregates and accumulate in neurons

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71
Q

What is a common prion protein?

A

Phosphatidylinositol glycan

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72
Q

What is the most common cause of epidemic encephalitis in the USA?

A

WNV

73
Q

How is West Nile virus usually transmitted?

A

Mosquito vector with marsh bird reservoir

74
Q

How is West Nile Virus typically diagnosed?

A

RT-PCR and serology

75
Q

What is the pathogenesis of West Nile Virus?

A

Viremia leading to infection of the CNS

76
Q

Are there any effective therapies against West Nile Virus?

A

No

77
Q

Is there a vaccine currently available for West Nile virus?

A

No

78
Q

What population is most likely to exhibit severe disease after West Nile virus infections?

A

Adults over 60 y/o

79
Q

What are the 8 human herpesviruses?

A 
HSV1
HSV2
VZV
EBV
CMV
HHV6
HHV7
HHV8
80
Q

What is caused by acute infection and reactivation of HSV1?

A

Acute - cold sores

Reactivation - cold sores

81
Q

What is caused by acute infection and reactivation of HSV2?

A

Acute - genital herpes

Reactivation - genital herpes

82
Q

What is caused by acute infection and reactivation of VZV?

A

Acute - chicken pox

Reactivation - shingles

83
Q

What is caused by acute infection and reactivation of EBV?

A

Acute - infectious mononucleosis

Reactivation - lymphoma/cancer

84
Q

What is caused by acute infection and reactivation of CMV?

A

Acute - broad spectrum

Reactivation - pneumonia

85
Q

What is caused by acute infection and reactivation of HHV6 and HHV7?

A

Acute - roseola

No evidence of reactivation

86
Q

What is caused by acute infection and reactivation of HSV8?

A

No evidence of acute infection

Reactivation - Kaposi’s sarcoma

87
Q

What is the general structure of herpesvirus?

A

dsDNA, enveloped virus
Lots of glycoproteins (gB-gN)
Tegument (proteins in the layer between the envelope and capsid)
Capsid with DNA

88
Q

Describe the sequence of transcription events in herpesvirus infection.

A

Immediate (peaks and declines in 3 hours)
Early (peaks and declines in 8 hours) - DNA synthesis proteins
Late (peaks beginning at 4 hours, stays elevated) - virion proteins
DNA production (begins at 3 hours, stays elevated)

89
Q

Where is the viral capsid assembled in a cell infected with herpesvirus?

A

In the nucleus

90
Q

What is the primary infection caused by HSV type 1?

A

Usually cold sores, sore throat, fever, and rarely, encephalitis; less frequently found as a genital infection

91
Q

Describe the infection and pathogenesis of HSV type 1.

A

Primary lytic infection of epithelial cells

Virus infects sensory neurons (latency-associated transcripts - LATs - are the only vmRNA present)

Reactivation - virus travels back to epithelial cells and causes lesions and shedding

92
Q

Latent infection with HSV1 is asymptomatic and no virus is produced. Where does the viral DNA reside?

A

Sensory cells of the trigeminal nerve ganglion

93
Q

What is the primary infection caused by HSV type 2?

A

Vesicular eruptions on the genitalia spread by sexual contact; affects both sexes, less frequently found as herpes labialis (cold sores)

94
Q

Where does latent HSV2 reside?

A

Sensory cells of the sacral ganglion

95
Q

What can be used to treat HSV?

A

Acyclovir

96
Q

What is the MOA of acyclovir?

A

Viral thymidine kinase converts acyclovir to acycloGMP; cellular kinases convert this to acycloGTP, which is a chain terminator when incorporated into DNA

97
Q

What causes resistance to acyclovir?

A

Mutations in the gene encoding the viral thymidine kinase (needed to activate the drug) and/or the viral polymerase (no longer efficiently binds the drug)

98
Q

What is the MOA of pritelivir?

A

Inhibits the herpesvirus helicase-primase

99
Q

Describe the primary infection with varicella zoster.

A

Infection occurs in seasonal epidemics as chicken pox, contracted from another infected individual, results in generalized vesicular rash

100
Q

What are the clinical features of VZV infection?

A

Mild prodrome (fever, malaise) for 1-2 days
Successive crops of pruritic vesicles (2-4 days) - vesicles will be in all stages
Appear first on head, most concentrated on trunk
Generally mild in healthy children

101
Q

What are complications of VZV infection?

A

Bacterial infection of lesions, CNS manifestations, pneumonia, hospitalization, death

102
Q

What is the peak incidence of VZV?

A

4-9 y/o

103
Q

Who dies most often from VZV in healthy people?

A

<1 y/o, >30 y/o

104
Q

Describe the Varicella vaccine.

A

Live-attenuated virus, 95% effective, probably long-lasting, 1 dose + booster, administered with MMRV

105
Q

Where is VZV latent?

A

Cells of the dorsal root ganglia

106
Q

How does reactivated VZV present?

A

Shingles - unilateral painful vesicular eruptions localized to a dermatome, usually in the head or upper trunk

107
Q

What provides passive immunity to VZV?

A

VZIG

108
Q

What is the most common primary manifestation of HSV1?

A

Cold sores

109
Q

How is HSV1 usually transmitted?

A

Close contact such as kissing, wrestling or sex

110
Q

How is HSV1 typically diagnosed?

A

Clinical presentation

111
Q

What is the pathogenesis of HSV1?

A

Primary lytic infection of epithelial cells followed by infection of sensory neurons of the trigeminal ganglia where the virus can become latent, and reactivation can occur.

112
Q

Are there any anti-virals available against HSV1?

A

Acyclovir and Pritelivir

113
Q

Is there a vaccine available for HSV1?

A

No

114
Q

Are there any possible consequences of HSV1?

A

Latent infection with the possibility for recurrence

115
Q

What is the most common primary manifestation of HSV2?

A

Vesicular eruptions on the genitalia

116
Q

How is HSV2 usually transmitted?

A

Close contact such as kissing, wrestling, or sex

Mother to newborn

117
Q

How is HSV2 diagnosed?

A

PCR of viral DNA from the lesion

118
Q

What is the pathogenesis of HSV2?

A

Primary lytic infection of epithelium of genitalia followed by latent infection of sensory cells of the sacral ganglion. Recurrent infection can occur, usually at the same sight as the primary infection.

119
Q

Are there any anti-virals available against HSV2?

A

Acyclovir and Pritelivir

120
Q

Is there a vaccine available for HSV2?

A

No

121
Q

Are there any consequences of HSV2 infection?

A

Latent infection/recurrence

Neonatal infections leading to recovery, neurological impairment, or death

122
Q

What is the most common primary manifestation of Varicella-zoster infection?

A

Chicken pox

123
Q

How is Varicella-zoster usually transmitted?

A

Respiratory

124
Q

How is infection with Varicella-zoster typically diagnosed?

A

Clinical presentation

125
Q

What is the pathogenesis of Varicella-zoster infection?

A

Primary systemic infection with generalized, vesicular rash that results in latent infection that can reactivate as shingles.

126
Q

Are there any anti-virals available to treat Varicella-zoster infection?

A

Acyclovir

127
Q

Is there a vaccine available for Varicella-zoster?

A

Live-attenuated vaccine

128
Q

Are there any possible consequences of Varicella-zoster?

A

Latent infection with the possibility for recurrence as shingles

129
Q

What is caused by primary infection with EBV?

A

Asymptomatic infection

Infectious mononucleosis

130
Q

Discuss the epidemiology of EBV infection.

A

Causes lifelong infection, asymptomatic shedding of virus
Transmitted via saliva
Teens and adults at highest risk for infectious mononucleosis
Worldwide distribution, no seasonal incidence

131
Q

What is the disease mechanism of EBV?

A

Virus in saliva infects epithelia and spreads to B cells. Infection promotes growth of B cells. T cells kill/control B-cell outgrowth, promoting latency in B cells. Severe disease occurs in T-cell deficient patients

132
Q

What is seen on blood smear in EBV?

A

Atypical lymphocytes (Downey cells)

133
Q

How is EBV infection detected?

A 
Monospot test (detects heterophile Ab)
Ab to EBV VCA (viral capsid Ag)
134
Q

In addition to infectious mono, what clinical syndromes can be caused by EBV?

A

Post-transplant lymphoproliferative disorder (PTLD)
Hairy oral leukoplakia (w/AIDS)
African Burkitt’s Lymphoma (w/malaria as a co-factor)
Nasopharyngeal carcinoma (China)

135
Q

What does primary infection with CMV cause?

A

Asymptomatic infection
Mononucleosis
Fetal/neonatal infection (cytomegalic inclusion disease)

136
Q

What does persistent infection/carrier state with CMV cause?

A

Asymptomatic shedding, serious complications in immunocompromised patients (multisite symptomatic disease)

137
Q

How can you distinguish between mono caused by CMV or EBV?

A

CMV - negative heterophile Ab

EBV - positive heterophile Ab

138
Q

How is CMV transmitted?

A

Blood, secretions (breast milk and semen are included)

139
Q

Discuss the pathogenesis of CMV.

A

Acquired from blood/secretions, causes productive infection of epithelium, establishes latency in T-cells, macrophages, and other cells; suppression of CMI allows recurrence

140
Q

How is CMV infection diagnosed?

A

PCR (detect CMV DNA), serology (CMV IgM and IgG), cytology/histology (owl eye inclusion body)

141
Q

How is CMV treated?

A

Ganciclovir (activated in CMV-infected cells)

Letermovir (prophylaxis in hematopoietic-cell transplant)

142
Q

What is the major AE of ganciclovir?

A

Bone marrow toxicity

143
Q

What is the MOA of letermovir?

A

Targets CMV terminase complex (normally allows for packaging of DNA into capsid)

144
Q

What are the symptoms of HHV-6 and 7 infection?

A

Roseola - incubation 4-7days) rapid onset of high fever (103-105 degrees F for 2-4 days), generalized rash 24-48 hours later + no fever, T-cells resolve the infection

145
Q

Where is HHV6 and 7 latent?

A

T cells

146
Q

How is roseola diagnosed and treated?

A

No rapid diagnostic currently available, no specific therapy

147
Q

What is the most common neoplasm in patients with AIDS?

A

Kaposi’s sarcoma

148
Q

What is seen on H&E in Kaposi’s sarcoma?

A

Spindle-shaped tumor cells, neovascularization, inflammatory infiltrate

149
Q

What causes Kaposi’s sarcoma in patients with AIDS?

A

HHV-8 - transmitted sexually, resolved by T-cells, reactivated during immunosuppression

150
Q

What is the most common primary manifestation of infection with CMV?

A

Aysymptomatic
Severe disease in neonates
Infectious mono (~10% of cases in young children)

151
Q

How is CMV most commonly transmitted?

A

Saliva, secretions and mother to newborn

152
Q

How can infection with CMV be diagnosed?

A

PCR of viral DNA from newborn patient sample, serology for CMV specific Ab from patients with infectious mono, owl eye inclusion bodies on histology in CMV pneumonia

153
Q

What is the pathogenesis of CMV?

A

Virus infects epithelium and establishes latency in T cells, macrophages, and other cell types. Virus shedding from saliva and secretions occurs sporadically throughout life

154
Q

Are there any anti-virals available to treat infection with CMV?

A

Ganciclovir

155
Q

Is there a vaccine available against CMV?

A

No

156
Q

Are there any possible consequences of CMV infection?

A

Life-long sporadic shedding of virus

157
Q

What is the most common clinical primary manifestation of infection with EBV?

A

Infectious mononucleosis

158
Q

How is EBV most commonly transmitted?

A

Contact with saliva

159
Q

How can infection with EBV be diagnosed?

A

Monospot test for heterophile Ab and/or serology for Ab against VCA

160
Q

What is the pathogenesis of EBV?

A

Virus infects epithelia spreading to B cells where it replicates. Virus becomes latent in B cells with sporadic recurrence

161
Q

Are there any anti-virals available to treat infection with EBV?

A

No

162
Q

Is there a vaccine available against EBV?

A

No

163
Q

Are there any possible long term consequences of EBV infection?

A 
Burkitts lymphoma (malaria co-factor)
Nasopharyngeal carcinoma (Chinese herb co-factor)
latent infection with sporadic virus reactivation and shedding
164
Q

What is the most common clinical presentation of Roseola?

A

Sudden onset of fever for 2 days, followed by rash in infants

165
Q

What infectious agent causes Roseola?

A

HHV6 and 7

166
Q

How is Roseola most commonly transmitted?

A

Respiratory

167
Q

How can infection with Roseola be diagnosed?

A

Clinical presentation

168
Q

What is the pathogenesis of Roseola?

A

Virus incubation for 4 to 7 days, followed by high fever. When the fever ends a rash will appear. Latency is established in T cells with no known reactivation

169
Q

Are there any anti-virals available to treat infection with Roseola?

A

No

170
Q

Is there a vaccine available against Roseola?

A

No

171
Q

Are there any possible consequences of Roseola infection?

A

Latent infection with no known clinical recurrence

172
Q

In what subset of patients would you normally see Kaposi’s sarcoma?

A

Patients with HIV/AIDS

173
Q

How is HHV-8 most commonly transmitted?

A

Sexual contact

174
Q

How can infection with HHV-8 be diagnosed?

A

Clinical presentation and PCR for viral DNA

175
Q

What is the pathogenesis of HHV-8?

A

T cells control and resolve infection, but activation of Kaposi’s lesions occurs during immunosuppression

176
Q

Are there any anti-virals available to treat infection with HHV-8?

A

No, but treating patients with AIDs with HAART will restore T cells that will control the HHV-8 infection.

177
Q

Is there a vaccine available against HHV-8?

A

No

178
Q

Are there any possible consequences of HHV-8 infection?

A

Kaposi’s sarcoma in immunocompromise

MHD2 (34 decks)

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