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Viruses Flashcards

antiviral I - BRUSH antiviral II - BRUSH infection cont - BRUSH leftover viruses - BRUSH

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1
Q

• That viruses are composed of

A

protein with DNA or RNA, and sometimes a lipid membrane

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2
Q

Criteria for classifying viruses: (7)

A
  1. RNA or DNA
  2. ss or ds
  3. +/- strand (+: same sense as viral mRNA)
  4. symmetry of capsid: helical, icosahedral, complex
  5. presence of envelope
  6. mode of replication
  7. tropism
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3
Q

• The diversity of viral genome structures

A

DNA, RNA, ss, ds, +/-

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4
Q

• That viruses must make_______ to code for new viral proteins and so to replicate

A

positive stranded messenger RNA

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5
Q

• The different methods for detecting viruses

A

EM, viral-specific Ab, PCR

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6
Q

• The general steps in viral replication (8)

A

binding, entry, uncoating, transcription of mRNA, translation of viral proteins, replication of the input genome, assembly of progeny viral particles, and egress

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7
Q

• The mechanisms by which virus enter cells

A

fusion, endocytosis

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8
Q

• What viral inclusion bodies are, and their significance in diagnostic testing

A

endocytosed viruses actively replicating inside of the host cell

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9
Q

• The steps a virus goes through to infect a host (7)

A
  1. Entry into host.
  2. Replication at primary site of infection.
    3.Spread within the host.
    Blood (viremia) versus nervous system.
  3. Replication at secondary site(s) of infection.
  4. Clearance by host immune response or persistence.
  5. Release from host.
  6. Transmission to new host organism.
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10
Q

• What step in the process above is blocked by virus-specific antibodies

A

entry into cells can be blocked

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11
Q

T-cell response to viral infection

A

T-cells recognize host cells infected with virus, rather than the extracellular, intact virus

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12
Q

general mechanisms of viral injury

A

by killing or damaging cells/tissues/organs or by the resulting immune response

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13
Q

The sources of respiratory viruses

A

zoonotic (mammals, birds), P2P

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14
Q

The common means of transmission of respiratory viruses from person to person

A

droplet, contact, fomites
entry thru mucosa or conjunctiva
Exit the host in respiratory secretions

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15
Q

• How respiratory viruses spread within the host, and the usual extent of the spread

A

cillia move mucus and carry virus over other cells

Invasion beyond respiratory epithelium is rare (but happens: SARS)

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16
Q

• Why people get so many respiratory infections

A

many different species
serotype variation
immune response to respiratory viruses is not long lasting
Escape from the antibody response allows the same species of respiratory virus to repeatedly infect an individual

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17
Q

• The general mechanisms by which respiratory viruses damage the host

A

cytopathic effect, inflamation -> damage to epithelium -> impaired function, bacterial infection
(occasionally shock, DIC)

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18
Q

• How the site and manifestations of respiratory virus infection are related

A

tropism of specific viruses for certain locations in the resp tract

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19
Q

• What virus is the most common cause of the common cold

and morphology

A

rhinovirus - Family Picornaviridae

non-enveloped, icosahedral viruses with non-segmented, plus-strand RNA (like polio)

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20
Q

• Why rhinoviruses are tropic for the upper respiratory tract

A

tropism determined by optimum temperature of its replication: 33-34°C

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21
Q

• The mechanism by which rhinoviruses evade the immune response

A

ICAM-1 binding site is in a “canyon” on the surface of the virus

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22
Q

• The symptoms and most common infectious cause of bronchiolitis
and morphology

A

Fever and rhinorrhea -> cough and wheezing (1-2 wk)

RSV, Family Paramyxoviridae, which are enveloped, helical viruses with non-segmented, minus-strand RNA (like measles)

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23
Q

The pathophysiology of bronchiolitis

A

Inflammation of the bronchioles, usually caused by viral infection
inc. mucous and damage to epithel -> constricted airway -> gas trapping

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24
Q

The efficacy of the immune response against respiratory syncytial virus

A

*Stimulates only partially effective response even though only 1 serotype of F, 2 serotypes of G
IgG - wane quickly
IgA - weak or absent
Th2 - response may cause increased pathology (wheezing)

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25
Q

The manifestations of influenza virus infection

A

Severe constitutional symptoms
headache
myalgias

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26
Q

The differences between influenza A, B and C viruses in
Severity of human disease
Type of hosts infected
ocurance of antigenic shift/drift

A

Type|Hosts|Disease|RNA Segments
A|Mammals and Birds|Mild to Severe|8
B|Humans (& Seals)|Mild, rarely severe|8
C|Humans|Very mild, children|7

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27
Q

Relevant structural and functional details of influenza virus

A

the genome of influenza is segmented, negative stranded RNA

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28
Q

The role of a segmented genome in genetic recombination and antigenic shift of influenza A viruses

A

reassortment - when 2 viruses infect same cell and the progeny contains a mix of RNA segments from both parental viruses

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29
Q

The role of M2 protein in viral uncoating and release of viral RNA into the host cell cytoplasm

A

M2 allows H+ into the virus as pH of endosome drops -> release of ribonucleoprotein & fusion of membranes -> release into cytoplasm

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30
Q

How adamantane anti-virals work

A

block the M2 ion channel and prevent release of RNP. They are effective only against influenza A.

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31
Q

The functions of hemagglutinin (H) and neuraminidase (N) in viral entry and exit from cells and in the antibody response against the influenza virus

A
  • hemagglutinin protein on the surface of the virus binds to sialic acid on the host cell-surface, leading to endocytosis of the virus.
  • neuraminidase cleaves sialic acid from the surface of the host cell, preventing the virus from getting stuck to the dying host cell.
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32
Q

How neuraminidase inhibitors work

A

block the action of neuramindase, inhibiting release of the virus.
They are effective against both influenza A and influenza B

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33
Q

The meaning, mechanism and significance of “antigenic shift” and “antigenic drift”

A

sloppy RNA polymerase -> mistake 1/10K bases
drift: point mutation in H or N (but has been previously encountered by humans)
shift: mutation causes a new never before seen strain
(influenza A only)

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34
Q

The importance of zoonotic influenza in human disease

A

source for new flu is usually an animal

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35
Q

The pathogenesis of influenza

A

kills cilliated epithelial cells that it infects -> dec in mucous clearance -> potential for bacterial pneumonia

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36
Q

The composition of the influenza vaccine (in general – not this years vaccine!)

A
  • IM - inactivated influenza
  • nasally - live attenuated virus
  • 2A, 1B
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37
Q

The definition of an arbovirus

A

viruses transmitted by arthopod (insect) vectors

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38
Q

arboviruses belong to several families, commonality =

A

enveloped RNA viruses

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39
Q

How West Nile virus (WNV) is transmitted (including the kind of mosquito), its usual hosts and the seasons that human cases occur

A
  • Aedes (most common)
  • bird = usual host
  • humans & horses = dead end hosts
  • summer
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40
Q

where WNV is found

A
  • TX = hardest hit state

- in many parts of the world and throughout the continental U.S., where the number of cases is rising

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41
Q

• The manifestations of WNV infection (note that it is usually asymptomatic)

A

WN Fever

  • abrupt fever, headache, myalgia, fatigue
  • nausea, vomiting
  • transient macular rash (usually when fever subsides & getting better)

WN meningitis

  • fever, headache, stiff neck, photophobia
  • CSF: generally lymphocytes, neutrophils early

WN Encephalitis

  • alteration of mental status, focal neurologic findings
  • mild confusion to coma
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42
Q

• The risk factors for neuroinvasive infection with WNV

A
  • increasing age
  • immune deficiency
  • males
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43
Q

• The manifestations and pathogenesis of WNV “poliomyelitis”

A
  • anterior horn cell invasion

- asymmetric paralysis

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44
Q

• How Eastern Equine encephalitis (EEE), Western Equine encephalitis (WEE), St. Louis encephalitis (SLE) and Japanese encephalitis viruses are transmitted and the approximate geographic distributions of these viruses

A
  • mosquitoes
  • EEE: East of Mississippi River
  • WEE: west of Mississippi R
  • SLE: MW, but all over US except NE
  • Japanese encephalitis: E Asia w/increase in India, Nepal, n SE asia
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45
Q

• The important body site of infection and consequent manifestations of EEE, WEE, SLE and Japanese encephalitis virus infections

A
  • headache, fever, vomiting, malaise, disorientation, somnolence
  • meningitis or encephalitis
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46
Q

of Dengue virus serotypes

A

4

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47
Q

• The geographic distribution of Dengue virus

A
  • tropical areas
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48
Q

• How Dengue virus is transmitted (including species of mosquito) and its usual host

A
  • female Aedes aegypti - replicate in midgut & then get into salivary glands
  • humans
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49
Q

• The four clinical syndromes caused by Dengue virus, including the manifestations of each

A
  • undifferentiated fever (most common)
  • classic dengue fever: fever, headache, muscle & joint pn, n/v, rash, hemorrhagic manifestations
  • dengue hemorrhagic fever: skin, gum, nasal, GI, urine, increased menstrual flow; low platelet count; elevated hematocrit, low albumin, pleural or other effusion
  • dengue shock syndrome: abd pn, persistent vomiting, fever to hypothermia; circulatory failure (rapid & weak pulse, hypotension, cold clammy skin, AMS)
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50
Q

• The current model of pathogenesis of Dengue hemorrhagic fever

A
  • Ab that can neutralize same serotype
  • in subsequent infection, preexisting Ab form complexes w/infecting serotype (diff) but don’t neutralize new virus
  • increase uptake by macrophages via Fc receptor of Ab in complex - Ab-dependent enhancement
  • infected monocytes release vasoactive mediators, increased vasc permiability & hemorrhagic manifestations
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51
Q

• Factors which contribute to the spread of Dengue virus and the measures that can be taken to reduce spread

A
  • declining vector cont - unchecked vecotrs
  • unreliable water supply
  • increase pop density - pop growth, urbanization
  • poverty
  • increase air travel - migration
  • global warming
  • environmental cont (ie. eliminate habitats, not just insecticides)
  • biolgoical cont (genetically engineered mosqitoes)
  • blood transfusion screening
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52
Q

• How yellow fever virus is transmitted and its geographic distribution

A
  • Aedes mosquitoes
  • long rainy season in forested areas w/monkeys & mosquitoes
  • equatorial areas in Africa & S America
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53
Q

• The important body site of infection and consequent manifestations of yellow fever virus infection

A
  • liver
  • hepatitis, jaundice, hemorrhage, multi-organ failure
  • symptoms for 3 days (viremia), improvement, & then fever & symptoms return w/vomiting, epigastric pn, prostration, jaundice
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54
Q

poliovirus morphology

(how is the lack of an envelope significant in the transmission of this virus?)

A

nonenveloped, RNA virus

no envelope means it can survive desication

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55
Q

• The manifestations of poliovirus infection (including post-polio syndrome)

A
  • inflammation of gray matter of the spinal cord & brain due to infection w/poliovirus
  • inapparent or subclinical (90-95%)
  • abortive polio: fever, sore throat, headache
  • aseptic meningitis or non-paralytic polio: more headache, fever, stiff neck, PMN & then lymphocyte in CSF
  • paralytic polio: sore throat, headache, vomiting, meningitis followed by flaccid paralysis of limb muscles & resp muscles
  • post-polio syndrome: fatigue, muscle weakness & pn, develops 30-40 yrs after recovery from polio, may involve muscle atrophy
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56
Q

• The significance of the multiple serotypes of poliovirus in antibody protection against the virus

A
  • each serotype of poliovirus has VP1, VP2, VP3, differences in the amino-acid sequence of these three proteins determines the serotypes
  • all 3 serotypes common, so vaccine needed to be trivalent (serotype based on neutralization)
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57
Q

The pathogenesis of poliovirus infection, including the route of invasion and the mechanism by which poliovirus damages the host (paralysis)

A
  • replicates in mucosa of pharynx & intestine
  • travels to LN via lymphatics
  • viremia (prodrome)
  • crosses BBB into CNS: encephalitis & paralysis (new theory that through gut via vagal nerve); targets motor neurons in anterior horn cells of spinal cord
  • crosses blood-CSF barrier: meningitis
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58
Q

The pattern of poliovirus shedding and the immune response to the virus

A
  • shed in feces
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59
Q

The source and means of spread of poliovirus

A
  • fecal-oral
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60
Q

The two types of poliovirus vaccine and the advantages and disadvantages of each

A
  • inactivated (salk): virus grown in monkey cells & then inactivated w/formalin
  • pro: no live virus that can regain virulence or cause disease, strong humoral immunity, can be incorporated w/other vaccines
  • con: requires injection, fails to induce mucosal immunity, quality cont needed for potency & inactivation, expensive
  • oral (sabin): virus attenuated by passage in cultured cells
  • pros: mucosal & humoral immunity, may be life-long, easy to administer, inexpensive
  • con: can mutate to virulent form, cold chain needed for txp
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61
Q

measles virus morphology & surface proteins

A
  • enveloped virus
  • negative stranded ssRNA
  • two surface antigens, the hemagglutinin and fusion proteins
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62
Q

The manifestations of measles (including neurological complications)

A
  • prodromal: cough, coryza, conjunctivitis
  • red maculopapular rash
  • Koplik’s spots (ulcerating lesions in oral mucosa)
  • immunosuppresion
  • postinfectious encephalomyelitis
  • inclusion encephalities
  • subacute sclerosing panencephalitis
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63
Q

The source of measles virus

A
  • no animal or environmental reservoir
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64
Q

The pathogenesis of measles, including the spread within the host

A
  • enters via respiratory route & replicates in epithelium
  • enters lymphatics to LN
  • blood to spleen & other lypmathic tissues
  • viremia
  • dermal endothelial via blood
  • incubation pd of 10-14 days
  • prodromal
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65
Q

How the measles virus exerts a general suppressesion of the immune response

A
  • inhibition of cell-mediated immunity
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66
Q

• The efficacy of the immune response to the measles virus

A
  • virus monotypic so infection usually leads to life-long immunity
  • cell-mediated immunity impt for recovery
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67
Q

• The pathogenesis of smallpox

A
  • entry by inhalation of aerosols
  • infection of cells in resp tract & spread to macrophages –> regional lymph nodes
  • exanthema when infected cells localize to small dermal blood vessels
  • infected monocytes migrate from dermal vessels into epidermis –> basal layer cells become infected
  • necrosis & edema lead to splitting of dermis
  • inflammatory response leads to PMN arriving –> vesicule pustular
  • transmission occurs during rash stage by oral spread
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68
Q

The usual source and means of transmission of human immunodeficiency virus (HIV)

A
  • blood
  • sex
  • mother to child
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69
Q

HIV structure

A

enveloped, RNA virus

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70
Q

Key steps in HIV replication

A

attachment, penetration, reverse transcription, txp to nucleus, integration, transcription, splicing, packaging of genomic RNA/translation, packaging, budding, maturation

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71
Q

o HIV Entry into cells

A
  • gp120 interact w/CD4 on host –> conformation of gp120 that allows it to bind to chemokine receptors (ie. CCR5)
  • gp41 in viral membrane & attach to gp120
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72
Q

HIV Early Phase of cell infection:

A
  • HIV RNA is reverse transcribed to DNA which is integrated into the host genome as a provirus
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73
Q

Why a lack of CCR5 makes people resistant to HIV infection

A

homozygous mutation prevents CCR5 from making it to surface –> no way for virus to enter; heterozygous –> less opportunity for entry

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74
Q

How entry inhibitors for HIV block HIV from entering host cells

A
  • bind CCR5 to prevent gp120 binding
  • mimic of HR2 peptide binds to HR1, block natural HR2 from binding –> so no fusion peptide that brings together virus & host membrane to fuse membranes
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75
Q

The role of chemokine receptors in transmission (early) and host cell tropism of HIV

A
  • CD4 found on immune cells
  • CCR5 on activated or memory CD4 cells, early tranmission
  • CXCR4 on late HIV-1 isolates, CXCR4+ on naive, resting cells
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76
Q

How the two types of reverse transcriptase inhibitors work

A
  • nucleoside analogs bind to nucleosides & get incorporated into forming DNA, inhibits proper reverse transcription
  • non-nucleoside inhibitors bind to “thumb” part of reverse transcriptase to prevent mvt of RNA template through for reading
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77
Q

What HIV integrase does

A
  • cleaves ends of viral DNA
  • cleavage of host DNA with staggered ends
  • repair of staggered ends give repeats
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78
Q

How integrase inhibitors work

A

prevent binding of integrase complex w/host cell DNA

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79
Q

HIV Late Phase of cell infection:

A
  • HIV DNA is transcribed into RNA, which serves as the genome for new virus, and serves as mRNA to encode proteins for progeny virus
  • That transcription factors involved in activation of CD4 lymphocytes also regulate expression of the HIV provirus, so activation of an infected cell leads to activation of the virus
  • Can happen soon after HIV infects a cell, or virus may be latent and reactivate up to years later
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80
Q

What the HIV protease does

A
  • cleaves itself & other proteins w/in packaged virus

- components have to be cleaved in order for virus to be infectious

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81
Q

How protease inhibitors work

A
  • bind to active site of protease so that can’t cleave proteins for maturation
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82
Q

Mechanisms by which HIV escapes the immune system

A

o Glycosylation of surface proteins hides antibody targets
o Antigenic variation due to high rate of mutations, escape from antibody and T cell responses
o Latent virus can’t be “seen” by the immune system

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83
Q

Reasons HIV infection can’t currently be eliminated from the infected individual

A

o High rate of mutations generates drug-resistant virus

o No drugs target the latent stage of the virus

84
Q

reverse transcriptase advantage for HIV

A

makes mistakes (point mutations) when copying viral RNA to DNA because it lacks proof reading function. The high rate of mutation allows the virus to evolve and escape drugs and the immune system.

85
Q

General qualities of viral causes of hepatitis

A

That the viral causes of hepatitis are a genetically and structually diverse group of viruses which share tropism for the liver

86
Q

The source, route of transmission, potential for chronic infection and method(s) of prevention for hepatitis A, B, C, D and E viruses

A

A & E - feces, fecal oral, no chronicity (E post-Tx)

BCD - blood, percutaneous/permucosal, yes chronic

87
Q

The appropriate diagnostic tests for hepatitis virus infection(s)

A

A - HAV in blood/stool, ALT, IgM, IgG

B -

88
Q

• How viral infection damages the liver

A

o induces chronic inflammation which activates cytokines and hepatic stellate cells to secrete collagen -> fibrosis

89
Q

• The symptoms of hepatitis A virus infection in children and adults

A

o asymptomatic in children, severe cases in previously unexposed adults

90
Q

• The genetic composition of HBV and copying mechanism

A

o That HBV is a DNA virus with a genome that is part double stranded and part single stranded
o the hepatitis B polymerase has reverse transcriptase activity

91
Q

• The possible outcomes of HBV

A

o acute with resolution, or chronic infection

92
Q

• How HBV is usually transmitted in parts of the world where it is common versus those where it is uncommon

A

o Common regions – perinatal

o Uncommon regions – percutaneous or sexual

93
Q

• The pathogenesis and manifestations of HBV (in particular, the differences between neonatally acquired infection and infection acquired later in life)

A

o Late acquired - Cirrhosis, liver failure, liver cancer

o Early acquired – usually asymptomatic

94
Q

• Why HDV depends on HBV to replicate

A

o Depends on B for assembly, expression, and infection
o Wears B’s envelope
o Relies on host polymerase to replicate RNA

95
Q

• The likely outcome of HDV infection when it occurs simultaneous with versus after HBV infection

A

o Simultaneous – can become fulminant or chronic hepatitis or lead to full recovery
o After – loses option for recovery

96
Q

• That HCV is an RNA virus with a polymerase that lacks proof-reading function, leading to a high rate of mutation and antigenic variation

A

o 6 maj genotypes – often can have multiple strands circulating

97
Q

• That infection with HCV often becomes chronic

A

o Use of LDL allows for “stealth”

98
Q

• The sequelae of chronic HCV infection

A

o Short symptom presentation but only 15% recover and smolders for many years
o Continues to same fibrosis, cirrhosis, failure, and hepatocellular carcinoma

99
Q

• The general patterns of herpes viral infection (acute, latent, etc.)

A

o Latent – cannot find any virus
o Chronic – virus can be found and is not cleared
o Acute – virus active and found in blood

100
Q

• Common morphology/traits for all herpes viruses

A

o herpes viruses are all enveloped, DNA viruses

o all herpes viruses become latent

101
Q

• The common means of transmission of HSV-1 and -2 viruses from person to person

A

o Through direct contact with vesicular fluid of lesion - oral, genital mucosa, or eyes
o Self-inoculation of eyes
o Inactivated by dying

102
Q

• The manifestations of HSV-1 and HSV-2 infections

A 
o	Oral (mainly HSV-1) 
o	Encephalitis (HSV-1) 
o	Keratitis (HSV-1)
o	Genital (mainly HSV-2)
o	Neonatal disease (HSV-2)
103
Q

• The pathogenesis of HSV, including site of initial replication, mechanism and route of spread, latency and reactivation

A

o Infects mucosa and then travels up axons of sensory nerves to soma/nucleus then becomes latent
o Damage to neuron leads to activation and virus travels back down axon and infects epithelium again

104
Q

• Must you have symptoms in order to spread HSV?

A

o That genital HSV reactivation can be asymptomatic, and so can be transmitted in absence of symptoms

105
Q

• The mechanism of acyclovir action

A

o Nucleoside analog. Phosphorylated by viral Tyr kinase then viral DNA polymerase tries to incorporate into Viral DNA . Leads to chain termination and stops viral DNA replication

106
Q

• HSV and HIV

A

o That HSV-2 infection is a risk factor for infection with HIV

107
Q

• How VZV spreads from person-to-person

A

o primary infection – respiratory inhalation

o reactivation – released from a specific nerve within self

108
Q

• The pathogenesis and manifestations of acute and reactivated VZV infection

A

o primary infection – respiratory inhalation, replication in NP and reg lymph, viremia  2o sites incl sensory ganglia
o reactivation – released from a specific nerve so only a specific dermatome presents with vesicles, can cause pain/neuralgia even after cleared

109
Q

• That uses of the attenuated VZV vaccine

A

o Reduces chickenpox cases
o Larger dose of same vaccine given to >60 yr olds reduced shingles and post-herpetic neuralgia (i.e, prevented or controlled VZV reactivation).

110
Q

• How EBV enters the host

A

o Acute infection of oral mucosa leads to productive infection of epithelial cells and immortalization of B cells as latent carrier of virus

111
Q

• How EBV spreads within the host, and the usual extent of the spread

A

o B cells are latent carriers and virus persists in dividing cells

112
Q

• The manifestations of primary Epstein-Barr virus (EBV) infection and the role of CTL in the immune response to EBV

A
  • infects pharyngeal epithelial cells, replication
  • shed into throat and saliva
  • spread to B cells, immortalize
113
Q

• That primary infection with EBV elicits _______ and how they are tested for

A

heterophile antibodies, Agglutinates horse/sheep RBCs

114
Q

How EBV is spread

A

Spread in saliva

115
Q

• The role of EBV in malignancy

A

o Causes some Burkitts and other B-cell lymphomas because of immortalized B-cells
- nasopharyngeal carcinoma

116
Q

• How the genome of latent EBV genome is maintained in host cells

A

o EBNA-1 tethers viral DNA to chromosomes for segregation into daughter cells

117
Q

• Cytomegalovirus symptoms

A

o That primary CMV infection is often asymptomatic, but can cause a mononucleosis-like syndrome

118
Q

• Congenital infection of CMV sequelae

A

o can lead to severe disease in the newborn

119
Q

• CMV in immunocompromised individuals - common manifestations

A

o Can reactivate and cause disease

o Primary productive infection in mucosal epithelial cells and latent infection in hematopoietic progenitor cells

120
Q

• The usual manifestation of HHV-6

A

o Fever, rash (exanthum subitum or roseola)

o Acute infection is a childhood disease

121
Q

• That viral gastroenteritis is a common cause of death, particularly in the developing world

A

know this

122
Q

• The common means of transmission of GI viruses from person to person

A

o Fecal-oral (contaminated food/water)

123
Q

• How GI viruses enter the host

A

o Contaminated food/water, colonizes gut mucosa

124
Q

• How GI viruses spread within the host, and the usual extent of the spread

A

o Usually self-limiting to the gut

125
Q

• The most common viral causes of epidemic and endemic gastroenteritis in the world and U.S.

A

o Norovirus – 50%

o Rotavirus – most common in infants and young children

126
Q

• How viral gastroenteritis is treated

A

o Supportive measures – fluids, Rx for headache and myalgias

127
Q

• The structure of noroviruses,

A

o Icosahedral, non-enveloped

o *lack of an envelope which makes them very stable in the environment and resistant to disinfection.

128
Q

• The manifestations and timing of norovirus gastroenteritis

A

o Incubation period 18-72hrs, symptoms last 2-3 days, virus can be shed for up to 72 or even
o Nausea vomiting abdominal cramps

129
Q

• The pathogenesis of norovirus infection, including the site of replication

A

o Uncooked handled foods, waterborne, closed settings

o Replicates in jejunum (likely, stomach and rectum spared)

130
Q

• The role of blood group antigens in susceptibility to norovirus infection

A

o Blood group H carbohydrates associated with susceptibility

o Found also in gut epithel cells

131
Q

• That efficacy of the immune response to norovirus

A

o Ig- A, M, G all produced and strain specific

132
Q

• The structure of rotavirus,

A

o Icosahedral non-enveloped
o particularly their lack of an envelope which makes them stable in the environment
o 3 concentric protein layers
o dsRNA in 11 segments

133
Q

• The role of the segmented genome of rotavirus in genetic reassortment and antigenic variation of rotavirus

A

allows for mixing when multiple viruses infect the same cell.

134
Q

• The timing, manifestations of primary and recurrent rotavirus infection, and what this suggests about the efficacy of the immune response to the virus

A

o Incubation: 1-3 days, vomiting and fever: 2-3 days, watery diarrhea: 4-5days
o Mucosal injury to small intestine  net secretion of fluids, salt from gut
o Reinfection is common but asymptomatic

135
Q

• The three mechanisms of emergence of rotavirus subtypes (compare to influenza virus)

A

o Reassortment, antigenic drifting, introduction of animal rotaviruses

136
Q

• Main mechanism of immune protection against infection

A

o IgA (serum & GI)

137
Q

• That there are rotavirus vaccines available

A

o Rotateq - Live attenuated pentavalent vaccine (Jannerian) – highly protective, given orally early
o Rotarix – live attenuated monovalent, not quite as highly protective but still >80%

138
Q

• How the two rotavirus vaccines were developed

A

a

139
Q

• What is known about the efficacy of vaccines for rotavirus

A

o Very effective 80-95%

140
Q

• The symptoms of acute HIV infection

A

mononucleosis-like, +/- rash

Massive CD4 depletion in Gut

141
Q

o Association between risk of transmission and viral load

A

Increased load = increased risk transmission

142
Q

o The approximate risk of transmission of HIV from an infected mother to her child during pregnancy and delivery (with and without anti-viral therapy)

A

 1/3 without treatment, <1% if treated

143
Q

o Cells initially infected, steps to viremia and establishment of latency

A

 Dendritic cells carry to lymph nodes -> 2wks later viremia

144
Q

o The levels of HIV, CD4 cells, anti-HIV antibody and anti-HIV CTL during the initial months of HIV infection

A

 Virus peaks to highest viremia around week 2-8, CD4 #’s drop and then return

145
Q

o How the “viral load set point” predicts the rate at which manifestations of HIV will progress without treatment

A

 Equilibrium between viral levels and immune response

 Higher viral levels = worse prognosis

146
Q

• The tests used to diagnose HIV (early vs. later in infection)

A 
o	HIV p24 Ag/Ab – day 18ish
o	HIV RNA – day 14ish
o	HIV ELISA – acute: negative
o	HIV western blot - acute: negative, once positive then past acute phase 
o	HIV viral load - acute: very high
147
Q

• The tests used to guide therapy for HIV

A

o HIV load measures the level of viral RNA (speed of train approaching cliff)
o CD4 count measures the level of CD4+ cells in the blood (distance from cliff)
o Drug resistance testing is performed by sequencing parts of the HIV genome to look for mutations associated with drug resistance

148
Q

• The things that may affect the viral load set point (and so the rate of progression in the absence of treatment)

A

o The virulence of the HIV – some may replicate faster than others
o Host genetic factors (CCR5, HLA type)
o Host immune response - (CTL response fails over time b/c rely on input from CD4 cells and activated CD4 cells are killed off early on.)

149
Q

• That specific CD4 cell counts are associated with increased risk for specific opportunistic infections and cancers (you do not need to know the specific CD4 cell counts associated with various infections)

A

know

150
Q

• That opportunistic infections may be newly acquired organisms, or they may be reactivation of clinically latent infection

A

know

151
Q

significant opportunistic infections in HIV (9)

A

o Bacterial pathogens (at any CD4 cell count)
o Herpes-zoster or shingles (reactivation of VZV)
o Tuberculosis (reactivation or primary)
o Thrush or esophagitis due to overgrowth of oral Candida albicans
o Pneumocystic jirovecii/carinii pneumonia (prophylaxis is given)
o Toxoplasma gondii (reactivation of CNS infection)
o Crytptococus neoformans (yeast inhaled, disseminates and causes sub-acute meningitis. Capsule is virulence factor)
o Cytomegalovirus (reactivation causes retinitis, can cause blindness)
o Neoplastic diseases – immune also is responsible for cleaning up cancers
 Kaposi’s sarcoma
 Non-Hodgkins lymphoma (often EBV associated)

152
Q

• The goals of anti-HIV therapy

A

o Decrease viral load, increase CD4 count, decrease transmission

153
Q

• The reasons for combination therapy against HIV

A

o Fast mutating → quickly develops resistance to monotherapy
o Increase # of targets
o Synergistic interactions

154
Q

• Significant side-effects of anti-HIV therapy

A

o Fat redistribution syndrome with combination of nucleoside reverse transcriptase inhibitors (NRTI) and protease inhibitors (PI)
o A possible increase in cardiovascular disease

155
Q

• The groups of HIV infected people who should receive anti-HIV therapy

A

o All HIV-infected patients

o Must commit to lifelong treatment

156
Q

• The arguments for and against starting anti-HIV therapy in people with acute HIV

A

o FOR: establish lower viral set-point, decrease transmission, limit evolution and resistance, immune preservation and reconstitution, symptomatic relief
o AGAINST: no data, adherence → resistance issues, toxicities, longer time on therapy
o END: if you start, don’t stop, treating acute has no data

157
Q

• That interruptions in treatment for HIV should be avoided

A

o Allow evolution of resistance

158
Q

• What a “boosted” PI is

A

o Ritonavir inhibits cytochrome P450 allowing for Prolonged half-life of PIs → reduced dosing, pill burden, food restriction → improved adherence

159
Q

• The current recommended combinations for initial HIV therapy (know by drug categories, not individual drugs)

A

o 2x NRTI + (NNRTI, PI/r, INSTI)

• NRTI should include either lamivudine (3TC) or emtricitabine (FTC)

160
Q

• That drug resistant HIV can be transmitted, so drug-naïve patients may have drug-resistant virus

A

o Testing for resistance is recommended

161
Q

• How acyclovir (and related drugs) inhibit replication of HSV and VZV

A

o Inhibits viral DNA production by inserting dead end nucleotides. Restricted to cells with viral thymidine kinase

162
Q

• The role of acyclovir (and related drugs) in preventing sexual transmission of HSV-2

A

o Used as prophylaxis to prevent spread of infection and acquiring of infection in asymmetric couples

163
Q

• How ganciclovir (and related drugs) inhibit replication of CMV

A

o Acyclovir derivative, ganciclovir-3p is included in viral DNA and is a dead end

164
Q

• Foscarnet:

A

o Active vs. CMV, HSV, VZV, HIV

o Acts via a similar mechanism but does not require phosphorylation

165
Q

• Cidofavir

A

o Active against CMV (+other herpes)

o *v. long intracell. half-life = infrequent dosing (weekly)

166
Q

• The mechanisms of the anti-viral drugs that inhibit influenza virus replication

A

o Neuraminidase – act to inhibit the cleavage of sialic acid, virus cannot leave the infected cell (oseltamivir, zanamivir)
o M2 inhibiitors – interferes with ion channel properties to inhibit pH-dependent uncoating (amantadine, rimantadine)

167
Q

• The uses of the anti-viral drugs that inhibit influenza virus replication

A

o In combination with NIs because of high degree of resistance
o Prophylaxis of individuals with high exposure

168
Q

• The definition of “nosocomial” and “health-care associated” infections

A

o Nosocomial - Infection acquired in a hospital

o HAI - Infection associated with the delivery of healthcare in any setting

169
Q

• How the common modes of transmission are grouped for infection control purposes

A

o Contact, Droplet (3’), common vehicle, vector borne

170
Q

• The precautions you must take to prevent the following routes of transmission

A

o contact – hand hygiene, gloves, gown
o droplet – hand hygiene, ~single room, surgical mask, sometimes goggles
o airborne – isolation room w/ neg airflow, N95 resp, visitation restriction

171
Q

• The common-vehicle and vector borne routes of transmission of infectious disease

A

o Food, water, medication, equipment (stethoscope etc)

172
Q

• The advantages of alcohol based hand hygiene vs. soap and water

A

o Alcohol better at killing bacteria than soap/water

o Soap needed to get rid of dirt, organisms like C. diff (spores), some viruses (noroviruses)

173
Q

• When soap and water should be used instead of alcohol based hand hygiene

A

o C. difficile, norovirus

o Dirty/soiled hands

174
Q

• The steps to reduce infections to healthcare workers

A

o Vaccination (also prevents transmission)
o Use of devices with reduced risk of injury (“sticks”)
o Post-exposure prophylaxis (e.g. HIV)

175
Q

• The characteristics and general transmission of the “leftover viruses”

A

o Nonenveloped icosahedral viruses ssRNA+
o No immunoassays, poor culture, PCR
o Direct/indirect contact, f/o, respiratory (not polio)

176
Q

• Enterovirus infection general path

A

o Infect GI/Resp mucosa -> lymph -> viremia -> reticuloendothelial syst of spleen, liver, bone marrow -> major viremia -> specific organs

177
Q

• Aseptic Meningitis

virus, season, ages, prognosis

A

o Enterovirus causes 90% cases
o Late spring – fall
o Peak ages: <1 y.o. and 5-10 y.o.
o Complete recovery in 3-7 days is usual

178
Q

• Enterovirus subgroups

A

o Poliovirus
o Grp A coxackieviruses
o Grp B coxackieviruses
o Echoviruses

179
Q

• Enteroviral Exanthems and Enanthems (+2 ex)

A

o Group A coxsackieviruses
o Age 3-10
o Recover 7-10d
o Hand-foot-mouth disease (exan-) - Fever and lesions on buccal mucosa, tongue, hands, feet, buttocks
o Herpangina (enan-) - Fever, vesicles on fauces, soft palate

180
Q

• Myocarditis and Pericarditis

A

o Group B coxsackieviruses
o Myocarditis: Fever, chest pain, dyspnea, arrhythmia, rarely heart failure
o Pericarditis: Sharp, stabbing chest pain exacerbated by lying down and deep breathing, fever. Rarely leads to constrictive pericarditis or cardiac tamponade

181
Q

• The characteristics and transmission of mumps virus

A 
o	Paramyxovirus (like measles)
o	Direct/indirect contact, droplet, saliva
182
Q

• The pathogenesis of mumps virus infection

A

o Replicates in resp epithel -> viremia -> parotid glands and other sites (CNS, testes, ovaries)

183
Q

• The manifestations of mumps virus infection

A

o Incubation of ~16-18 days usual
o Nonspecific prodrome w/ fever, malaise
o Patient complains of earache and pain w/ palpation of parotid gland, followed by swelling of gland and constant pain
o Second parotid gland involved in ~75% of cases; submaxillary salivary glands involved in ~10% of cases
o Resolves in ~ 7-10 days
o Aseptic meningitis in 10%

184
Q

• The primary method for preventing mumps virus infection

A

o Vaccine – attenuated virus given @ 12-15mo & 4-12y

185
Q

• How adenoviruses are transmitted

A

o Respiratory, f/o, ocular fluid (fomites)

186
Q

• The pathogenesis of adenovirus infection

A

o Initial infection at site of entry often symptomatic
o Viremia can occur, with manifestations in other body sites
o Clinically latent infection can last for years, mechanism unknown
• Periodic, asymptomatic shedding
• Symptomatic reactivation can occur in immunocompromised

187
Q

• The mechanisms by which adenoviruses evade the immune system

A 
o	Blocks fas-fasL mediated apoptosis of infected cell by multiple mechanisms
o	Reduces class I MHC expression
188
Q

• The manifestations of adenoviral infections

A

o Respiratory, Ocular, Gastrointestinal, In immunocompromised people
o Usually self-limited, 3-5 days, with no differentiating symptoms from other respiratory viral infections
o Outbreaks in closed populations (e.g. military)

189
Q

• Ocular Adenovirus Infections

A

o Pharyngoconjunctival fever - Follicular conjunctivitis & pharyngitis, acquired from pools/lakes
o Epidemic keratoconjunctivitis - Follicular conjunctivitis → to corneal subepithelial lymphoid infiltrates, can be severe w/ corneal opacities, acquired from instruments/eyedrops

190
Q

• The epidemiology and transmission of parvovirus B19

A

o small, nonenveloped icosahedral viruses with a single strand of + or – DNA
o respiratory, vertical (less)
o outbreaks common in school-age children

191
Q

• The pathogenesis of parvovirus B19 infection

A

o Infects erythroid precursor cells by binding P-Ag-> erythroblast enlarges then dies releasing virus -> temp. stop in formation of RBCs in otherwise healthy people

192
Q

• The manifestations of parvovirus B19 infections

A

o “5th disease” or erythema infectiosum,
o Nonspecific prodrome, slapped-cheek rash -> trunk & limbs -> lacey as fades
o symmetrical swelling and pain of the small joints of the hands and feet – primarily in adults, women > men

193
Q

goal of vaccination

A
  • to prevent infection: neutralizing Ab at site of entry
  • to prevent disease: Ab limit spread of pathogen
  • to eradicate pathogen: susceptible host no longer available
194
Q

• Definition and importance of herd immunity

A
  • vaccination of a large enough part of the pop that it protects those that aren’t vaccinated
  • impt for those who aren’t able to receive vaccinations (ie. immunocompromised that can’t receive live attenuated vaccines or those w/allergies
195
Q

• Definition of adjuvant

A
  • materials that enhance/sustain immune responses to antigens
  • convert protein into particulate material that is more readily ingested by immune cells OR enhance immunogenicity (ie. microbial components)
  • ex. alum, oil in water emulsions, LPS derivatives
196
Q

toxoid vaccine, and the types of immune responses elicited

A
  • modified bacterial toxin that has been rendered nontoxic but stimulates anti-toxin formation
  • humoral response, chemical or physical inactivation of toxin
  • ex. tetanus, diphtheria
197
Q

live attenuated, and the types of immune responses elicited

A
  • Reduce pathogenicity of microbe so that it does not cause disease but still can replicate to induce good immune response
  • develop empirically by passage in cell culture
  • humoral & cellular immunity induced, generally longer lasting
    ex. polio, MMR, varicella, rotavirus
198
Q

killed microbes, and the types of immune responses elicited

A
  • inactivation of whole microorganism, need to retain antigenicity of major antigenic determinants
  • need multiple doses since non-replicating antigen
  • unlikely to elicit cellular immunity
    ex. polio, influenza, hepA
199
Q

subcellular, and the types of immune responses elicited

A
  • protein subunits of microbe

- only Ab response

200
Q

conjugate vaccines, and the types of immune responses elicited

A
  • uses principle of linked recognition: protein antigens attached to polysaccharide antigens allow T cells to help polysaccharide-specific B cells
  • ex. H influenza, pneumococcus, meningococus
201
Q

synthetic vaccines, and the types of immune responses elicited

A
  • humoral

- ex. hepB, HPV

202
Q

• How conjugate vaccines have been developed as a result of understanding how T and B cells collaborate during an immune response

A
  • B cells recognize polysaccharide & make low affinity Ab
  • B cells internalize conjugate vaccine & displays toxin-derived peptide on MHC class II
  • helper T cells generated from recogniztion of peptide will recognize peptide on B cells surface & will activate it to make high affinity anti-polysaccharide Ab
203
Q

• How route of vaccination contributes to success of vaccine

A

a

204
Q

• Advantageous and disadvantages of non-living vs. attenuated vaccine

A
  • non living pro: safe, stable, overcome problems of nonprotective Ag inducing hypersensitivity
  • non living con: unlikely to elicit CTl response, Ab may have little neutralizing activity, may differ antigenically from pathogen that infects human, expensive
  • attenuated pro: humoral & cellular immunity, immunity longer lasting, low cost
  • attenuated con: possible contamination w/other liver virus, if too attenuated won’t be immunogenic, not suitable for immunocompromised, requires cold chain
205
Q

• The definition of passive immunization and when it is used

A
  • pregnant woman immunized to protect baby

- artificial: pooling of blood that have IgG for prophylaxis or for anti-toxin

206
Q

• The definitions of preventative and therapeutic vaccines

A
  • therapeutic: designed for infected ppl; form of immune-based therapy, using a person’s immune system to control virus

Microbiology (8 decks)

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