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Invaders and Defenders > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Is a virus living or non living?

  • an obligate:
  • completely dependent on a living host cell for:
A

non living

  • parasite

reproduction

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2
Q

capsid

A

protein coat, protects viral genome

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3
Q

membrane glycoprotein

A

allows attachment to host cells

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4
Q

lipid envelope

A

extra protective layer

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5
Q

why are RNA viruses more prone to replication errors?

A
  • because it uses virus enzymes, whereas DNA viruses use host enzymes
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6
Q

the viral life cycle is ____ cell dependent

A

host

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7
Q

What are the 6 viral life cycle steps?

A
  • 1) attach to specific receptors
  • 2) enter cell through endocytosis
  • 3) Uncoat and release genome
  • 4) Use the host cell machinery to replicate
  • 5) Self assemble new virions
  • 6) Release from host cell by budding or lysis
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8
Q

viral pathogenesis is determined by?

A
  • Interaction with specific host cells
  • Interaction with immune system
    • Immune escape
    • Immune modulation or immune evasion
    • Avoid immune surveillance
  • Host immune response causing pathology
  • Cellular transformation – persistent strategy for virus, can lead to uncontrolled cell replication
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9
Q

what are the antiviral innate immune responses? (5)

A
  • Type 1 interferon (Type 1 IFNSs) is the most direct action your body takes –> limits viral spread between cells
  • Slows spread of viral infection between cells
  • Viral infection turns NK activating signals and NK cells lyse infected cells
  • Memory T cells prevent reactivation of latent virus
  • Antibodies neutralize virus on re-exposure
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10
Q

What is the importance of the 3 structural genes of HIV?

A
  • Encode internal (structural) proteins
  • Encodes reverse transcriptase, protease, and integrase
  • Encodes gp120 (binds to CD4 receptor) and gp41 (mediates fusion between viral and cellular membranes)
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11
Q

what is the importance of the 6 regulatory genes of HIV?

A
  • Regulate uncoating of HIV genome and production of virus particles
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12
Q

What is the replication cycle of HIV? (6)

A
  • 1) HIV attaches itself to the host using glycoprotein 120 via CD4 receptor and CCR5
  • 2) GP41 is used to fuse the HIV envelope within cell wall, allowing HIV capsid to enter the cell
  • 3) Once HIV attaches to cell, it uses reverse transcriptase to synthesize RNA into DNA
  • 4) Integrase helps viral DNA to integrate its DNA into host genome
  • 5) Once transcription and translation is complete, protease will cleave viral poly-protein from host genome
  • 6) buds and mature variant can exit host cell
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13
Q

Antibody test:

detects antibodies to the:

___-___ weeks for the body to make enough abs to detect

A
  • Detects Abs to the envelope glycoproteins
  • 3-12 wks. for the body to make enough abs to detect
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14
Q

Antigen test (HIV)

used?

uses abs specific for:

__-___ weeks to make enough Ags to detect

_____ tests are rapid and becoming more common

A
  • Used the most
  • Using abs specific for HIV proteins Ags
  • 2-6 weeks to make enough Ags to detect
  • Combo Ag and Ab tests are rapid and becoming more common
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15
Q

Nucleic acid tests: HIV

detects ____ using _____

detects HIV ___-____ weeks post infection

cost?

when is it used?

A
  • HIV RNA using reverse transcription PCR
  • Detects HIV 1-4 weeks post infection
  • Expensive
  • Not routinely used unless person recently had high risk exposure with early symptoms of HIV
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16
Q

Primary HIV infection characteristics

A

can’t detect antibodies

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17
Q

Acute HIV infection characteristics

A
  • Flu like symptoms
  • CD4 decreases rapidly
  • HIV viral load increases rapidly
  • Extremely infectious
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18
Q

Clinical latency HIV infection characteristics

A
  • No symptoms, or mild
  • Able to transmit HIV
  • can last years
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19
Q

AIDS characteristics

A
  • CD4 drops below a point
  • Viral load starts to increase rapidly again
  • Opportunistic infections start to develop
    • Fungal infections
  • Cancers more prevalent
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20
Q

common HIV co-infections

A
  • Hep B (10%)
  • Hep C (25%)
  • TB
  • Fungal infections (candida, Coccidioides, Cryptococcus, Pneumocystis)
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21
Q

what is PrEP?

A

given for 7-21 days for people who are at high risk exposure to HIV

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22
Q

What is PEP?

A

lasts for 28 days, given within 72 hours within exposure, only in emergency situations

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23
Q

1

Herpes:

abbrev.

Name

Disease

A

HSV-1

herpes simplex virus -1

Mucocutaneous lesions (oral>genital), encephalitis, keratitis

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24
Q

2

Herpes:

abbrev.

Name

Disease

A

HSV-2

Herpes simplex virus 2

mucocutaneous lesions (genital>oral), encephalitis, meningitis

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25
Q

3

Herpes:

abbrev.

Name

Disease

A

VZV

varicella zoster virus

chicken pox, shingles

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26
Q

4

Herpes:

abbrev.

Name

Disease

A

EBV

Epstein Barr Virus

infectious mononucleosis, Burkitt’s lymphoma, co factor in many malignancies

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27
Q

5

Herpes:

abbrev.

Name

Disease

A

CMV

cytomegalovirus

congenital CMV infection, mononucleosis, transplant and AIDS related infections

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28
Q

6

Herpes:

abbrev.

Name

Disease

A

HHV-6

Human Herpesvirus 6

Roseola

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29
Q

7

Herpes:

abbrev.

Name

Disease

A

HHV-7

Human herpesvirus 7

Roseola

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30
Q

8

Herpes:

abbrev.

Name

Disease

A

KSHV

Kaposi’s sarcoma associated Herpesvirus

Kaposi’s sarcoma, castlemans disease, primary effusion lymphoma

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31
Q

Gingivostomatitis (HSV-1)

primary disease of:

clinical manifestations:

A
  • Primarily disease of children and young adults
  • Painful lesions occur on buccal mucosa, tongue, gingiva, pharynx
  • Lesions ulcerate and resolve 5-12 days
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32
Q

Herpes Labialis (cold sore) HSV-1

clnical manifestations:

can be brought on by:

use ______ to prevent transmission

A
  • Periodic, localized recurrences of lesions, usually on vermillion border of the lip
  • Recurrence produces itching, tingling followed by lesions
  • Can be brought on by stress, illness, fatigue, menstruation
  • Use antivirals to prevent transmission
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33
Q

Herpes eye infections: Herpetic Keratoconjunctivitis

ulceration of the:

follows:

develops from:

A
  • Ulceration of the cornea
  • Follows nerve ending in cornea, called dendritic ulcer
  • Develops from latent virus living in nerve cells of the skin or eye, or direct inoculation from lesions
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34
Q

Herpes cutaneous infection: whitlow (HSV-1=60%, HSV-2=40%)

what is it?

lesions on finger become?

can be inoculated to?

misdiagnosed as?

recurrence?

A
  • Recurrent HSV infection of finger and hand, resulting from passage of virus into break in skin
  • Lesions on finger become pustular, cause severe pain, loss of feeling, and prolonged morbidity
  • Can be Inoculated to any cutaneous location aside from hand
  • Misdiagnosed as staph infection
  • recurrence is possible
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35
Q

what are the predominantly HSV-1 infections?

A

gingivostomatitis; herpes labialis (cold sores)

eye infections

cutaneous infections; whitlow

encephalitis

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36
Q

what are the HSV-2 infections?

A

genital herpes

neonatal infections

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37
Q

what are the infections you can get from herpes?

A
  • Gingivostomatitis
  • Herpes Labialis (cold sore)
  • Eye infections (Herpetic Keratoconjunctivitis)
  • Cutaneous infections; whitlow (HSV-1=60%, HSV-2=40%)
  • Encephalitis, Meningitis, Meningoencephalitis
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38
Q

What is the pathogenesis of varicella?

A
  • Infection respiratory tract and conjunctiva (day 1)
  • local replication in upper airway and regional lymph nodes
  • primary viremia and infection of lymphocytes and nerve cells
  • replication and secondary viremia
  • infection of skin (day 10-21)
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39
Q

What is a varicella infection that we see?

who are the high risk groups?

what is/clinical manifestations

A

Shingles

  • High risk groups – HIV infection, T cell dysfunction or abscens in older patients
  • disseminated VZV infection may appear as widespread blisters with or without an associated dermatomal eruption
40
Q

What is CMV?

symptomatic?

where does the virus shed?

can be transmitted in _____ settings due to?

causitive agent of?

A

Herpes virus

  • People with healthy immune systems usually keep the virus from causing illness, may be carriers for life
  • Most people asymptomatic
  • Still sheds in saliva –> can be transmitted, especially in daycare settings due to bad hygiene
  • Causative agent of Mono
41
Q

EBV:

found in?

can infect ____ cells

can shed in:

causitive agent of:

EBV-associated _______

A
  • Found in saliva
  • Can infect B cells
  • Can shed in saliva
  • Causes Mono
  • EBV-Associated Malignancy
42
Q

KSHV (Kaposi’s Sarcoma Associated Herpesvirus)

classic _____ related infection

infect ____ cells

causal agent in:

A
  • Classic AIDS related infection
  • Infects B cells, macrophages, epithelial cells, endothelial cells, and keratinocytes
  • Causal agent in Kaposi’s sarcoma
    • Primary effusion lymphoma
    • Castleman’s disease
43
Q

Hemagglutinin (HA) (influenza)

binds to ______ –> help

______ RBCs

neutralizing?

A
  • Binds to sialic acid receptor on body –> helps gain entry into body
  • Agglutinates RBCs
  • Antigenic –> (neutralizing)
44
Q

Neuraminidase (NA) (influenza)

what does it do?

cleaves _____ to ______

degrades ____

neutralizing?

A
  • Once virus gains entry and replicates, it has to detach itself from host cell and exit –> detaching viral genome and freeing it to travel to other parts of the body is what NA does
  • Cleaves sialic acid to release virus
  • Degrades mucin (by degrading mucin, it makes epithelial cells in resp tract more vulnerable to other infections)
  • Antigenic (non-neutralizing); Abs against NA do not neutralize infectivity but decrease the spread of the virus
45
Q

M2 ion channel (influenza)

what is it?

target of?

A
  • Transmembrane channel (only in influenza A)
  • Target of antiviral medicines (amantadine, rimantadine)
46
Q

Influenza subgroups and their hosts:

A

B

C

A
  • 1) influenza A – humans and animals
    • Having both animal and human hosts helps virus change their coding so that it will evade immune system
  • 2) influenza B – humans
  • 3) influenza C – humans
47
Q

what determines each year’s flu virus vaccine types?

A

different subtypes and numbers with flu

48
Q

antigenic drift

causes

what influenzas can experience this

what kind of changes in HA/NA?

____ changes

A

epidemic

  • Minor mutations in HA or NA
  • Influenza A, B. C
  • Seasonal changes
49
Q

Antigenic shift

causes:

changes in HA/NA?

only in influenza ____

A
  • Complete change of HA, NA, or both
  • Reassortment of genomic segments in a cell that is coinfected by two or more strains of influenza virus
  • Only in influenza A
50
Q

clinical manifestations of influenza

challenges in diagnosis

A
  • Fever, myalgia and malaise, headache, pharyngitis, rhinorrhea, cough
  • Challenges in diagnosis: easily spread, difficult to diagnose
51
Q

diagnostic strategies influenza

how fast?

sensitive/specific?

A

Rapid PCR test

20-60min

highly sensitive/specific (>95%)

52
Q

influenza prevention

A

hygiene

vaccine (70-90% efficacy)

53
Q

influenza treatment

A
  • neuraminidase inhibitors –> zanamivir, oseltamivir
    • influenza A and B
    • prophylaxis
    • early treatment
  • M2 blockers –> amantadine, rimantadine
    • Influenza A only
    • Problems with resistance
    • Not recommended in US
54
Q

Rhinovirus:

who gets it?

emerging cause of:

vaccine?

treatment?

is virus stable to disinfectants?

A
  • Children get 5-12 cases/yr
  • Diverse strains circulate simultaneously (>150 antigenic types)
  • Emerging cause of lower respiratory tract disease
  • No vaccine
  • no treatment
  • Virus is relatively stable to disinfectant
55
Q

Adenovirus:

transmission:

specific associations between:

clinical manifestations:

treatment?

A
  • Transmission via droplet, fecal-oral
  • Specific associations between subtypes & clinical syndromes (Type 4 - Military recruits; Type 3 &7 - Swimming pools)
  • Pharyngitis, Pneumonia, Conjunctivitis, Gastroenteritis, Acute respiratory diseases
  • No specific treatment
56
Q

RSV

Severe in:

vaccine?

A
  • Particularly severe in infants & the elderly
  • No vaccine
57
Q

Coronavirus

causes 5-30% of:

______ number of serotypes

syndromes associated with it:

A
  • Causes 5-30% of common colds
  • Unknown number of serotypes
  • Severe Acute Respiratory Syndrome (2003)
  • Middle East Respiratory Syndrome (2013 - Zoonotic)
  • SARS-CoV-2 (2019-2021)
58
Q

what are 3 complications of influenza infection?

A

primary influenza pneumonia

secondary bacterial pneumonia

reye’s syndrome

59
Q

influenza: primary influenza pneumonia

______ failure in 10-20%

_____ infection

A

respiratory failure in 10-20%

direct infection

60
Q

influenza: secondary bacterial pneumonia

more ______

what does it prime the body for?

can patient improve or worsen?

bacterial, viral, or mixed?

more common or less common than primary infl. pneumonia?

immune-impaired influenza pts may benefit from:

A

significant

primes body for secondary bacterial infection

pt may improve, the worsen

bacterial or mixed viral + bacterial

more common than primary influenza pneumonia

immune-impaired influenza pts may benefit from prophylactic use of antibacterial drugs

61
Q

Reye’s Syndrome

what is it?

clinical manifestations

is pathogenesis clear or unclear? ____ may be implicated

treatment:

____ and _____ deficiences associated with Reye’s syndrome

also related to ______

A

Rare, life threatening syndrome in children following some viral infections

Fever, rash, encephalopathy, liver failure

Pathogenesis unclear, aspirin may be implicated

Supportive care only

OTC and CPS I deficiencies associated with Reye’s syndrome

Related to chickenpox and influenza

62
Q

Enteroviruses:

host:

where do they infect?

how does it infect?

virus is ____ stable, shed from ____ or ____, becomes immediatley _____

_____ most important PRR

immune response via:

A

Humans only natural host

Infect both GI and resp. tract

Enters through RT and travels down to GI tract

Virus is acid stable, shed from the GI or RT, becomes immediately infectious

TLR 3 most important PRR

Immune responses via Type 1 interferons, IgA

63
Q

What are common infections/syndromes caused by Coxsackievirus?

What is another enterovirus?

A
  • Upper resp tract infections
  • herpangina
  • rash syndrome
  • hand, foot, mouth disease
  • muscle infections
  • meningitis
  • encephalitis

Polio

64
Q

Coxsackievirus: Upper resp tract infections

clinical manifestations

A
  • Patients may develop erythematous papules on the outside of their mouth or shallow ulcers in the oropharynx associated with erythema
65
Q

Coxsackievirus: Herpangina

___ limited to______

clinical manifestations

A

small vesicles/rash limted to the mouth/oral mucosa

  • Small vesicles with erythematous base
  • Posterior palate
  • Pharynx
  • Tonsils
  • High fever
  • Self-limiting
66
Q

Coxsackievirus: Rash syndrome

A
  • Skin manifestations as a result of secondary viremia and infection of other tissues
67
Q

Coxsackievirus: Hand, foot and mouth disease

___, ___ strains cause this

if sores in mouth accompanied by:

A
  • A-16, A-71 strains cause this
  • If sores in mouth accompanied by rash on hands and feet
68
Q

Coxsackievirus: Muscle infections

what are the 3 muscle infections?

A

Myositis –> infected muscle cells, muscles sore to the touch, difficulty walking because of pain

Myocarditis and pericarditis –> dysfunction of heart muscle and ultimate cardiac failure

69
Q

Other name for Measles

A

Rubeola

70
Q

other names for Rubella

A

German measles

3 day measles

71
Q

Measles:

clinical manifestations/presentations

vaccine?

therapy?

complications

how infectious is it?

do people know they have it right away?

A

cough, runny nose, conjunctivitis

Koplik’s spots (typical of disease), Rash (sandpaper, maculopapular, starts at head and moves down)

Vaccine – 95% efficacy, 99% with 2 doses

No specific antiviral therapy

Complications

  • Transient immunosuppression
  • Bacterial superinfection
  • Encephalitis
  • Subacute sclerosing panencephalitis (SSPE; Dawson Disease)

Extremely infectious

Contagious 4-5 days before onset of rash  pts might not know they have disease and will spread it

72
Q

Mumps:

clinical presentations

vaccine

therapy

A

Parotitis 50-70% (inflammation of salivary gland)

Vaccine – highly effective

No specific antiviral therapy

73
Q

Rubella:

clinical presentations

vaccine

therapy

A

Clinical presentations

  • Blueberry muffin rash
  • Eye inflammation

Vaccine – 97% efficacy

No specific antiviral therapy

74
Q

HAV

Viral shedding begins _______ before symptoms onset and continues _______ after symptoms resolve

Transmission:

Immunity:

Chronic state:

Treatment:

Prevention:

Outcome:

A
  • Viral shedding begins 2 weeks before symptoms onset and continues 1 week after symptoms resolve
  • Transmission: fecal, oral
  • Immunity: life long
  • Chronic state: no
  • Treatment: supportive care
  • Prevention: improved sanitation, vaccination
  • Outcome: self limited; 10-15% relapse
75
Q

HEV

Transmission:

Chronic state:

Prevention:

Vaccine?

Outcome:

A
  • Transmission: fecal, oral
  • Chronic state: no
  • Prevention: sanitation
  • NO VACCINE
  • Outcome: self limited, severe in pregnancy
76
Q

Hep D

can it replicate itself?

Transmission:

Chronic state:

Prevention:

Outcome:

A
  • Cannot replicate itself –> needs help of Hep B
  • Transmission: blood, perinatal, sexual
  • Chronic state: yes
  • Prevention: vaccination against HBV
  • Outcome: self limited, can be severe in superinfection
77
Q

Hep C

Transmission:

Chronic state:

Prevention:

Outcome:

vaccine

Do abs give immunity?

A
  • Transmission: blood > sexual > perinatal
  • Chronic state: yes
  • Prevention: screen blood products, risk reduction
  • Outcome: self limited; ~80% chronic, 25% cirrhosis, 5% risk HCC/year
  • No vaccine
  • Abs do not give immunity
78
Q

Hep B (HBV)

  • Transmission:
  • Chronic state:
  • Prevention:
  • Outcome:
  • Non ______, thus longer syndrome free incubation period (1-6 months)

Surface antibody (HBsAb)

  • What does it mean if test detects surface antigen?
  • When body makes anti-surface antibody –> this is when:
  • _______ protection’

Core antibody (HBcAb)

  • is this antibody protective?
  • does it persist for life?

E antibody (HBeAb)

  • is it protective?
  • what does the presence of this antibody tell you?
A
  • Transmission: blood, perinatal, sexual
  • Chronic state: yes
  • Prevention: vaccination
  • Outcome: self limited, chronic carriers, cirrhosis
  • Non cytolytic, thus longer syndrome free incubation period (1-6 months)

Surface antibody (HBsAb)

  • If test detects surface antigen, that is the first sign/indication of infection
  • When body makes anti-surface antibody –> this is when the body becomes protective against Hep B infection in future
  • Lifelong protection

Core Antibody (HBcAb)

  • Body also makes antibodies against core capsid
  • Antibody does not protect you even though its made
  • Antibody against core protein persists for life

E Antibody (HBeAb)

  • Body makes antibody against E antigen
  • E antibody does not protect your body
  • Presence of E antibody in serology test tells Dr. replication of virus has slowed down
  • Indicates lower infectivity (viral load going down)
79
Q

Resolution of HBV

  • HBV DNA =
  • HBsAg =
  • HBsAb =
  • HBcAb =
A
  • HBV DNA = negative
  • HBsAg = negative
  • HBsAb = positive
  • HBcAb = positive
80
Q

what happens in chronic HBV infection in terms of antibodies?

A

HBsAb never forms –> this is why you are in a chronic state vs resolved

81
Q

SARS-CoV-2 Biology

____ virus with a genomic ____ mechanism

_______ with other _______

  • infects new cell types, moves from ____ to ____

viral ________ bind to host ____ resceptor

_______ activates S proteins

  • blocks:

Use _____ to cleave ______

A

RNA, proofreading

recombination, coronaviruses

  • species, species

spike protein, ACE2

TMPRSS2

  • viral entry

furin, S proteins

82
Q

SARS-CoV-2 Biology Cont.

can infect and reproduce in:

carried in the ______

excessive _______ —> leads to

A

the upper respiratory tract

blood

excessive immune response –> multiple organ failure, death (cytokine storm)

83
Q

SARS-CoV-2 variant

how does it come about?

what varient is classified as a varient of concern?

  • is it more contagious? severity?
A

AA substitution –> conformational change –> increases binding to ACE2 –> higher viral loads

Delta

  • more contagious, more severe illness
  • vaccines still effective
84
Q

Extrapulmonary complications of Covid

A
  • heart disease
  • reproductive system
  • neurological system
  • psychology
  • immune and hematology systems
  • urinary system
  • digestive system
85
Q

SARS-CoV-2 transmission

close contact with infected people via:

modes of transmission

is fomite transmission demonstrated?

A

via saliva, respiratory secretions/droplets

  • 1) inhalation
  • 2) deposition of virus on exposed mucous membranes
  • 3) touching mucous membranes iwth soiled hands contaminated with virus

no fomite transmission

86
Q

SARS-CoV-2 transmission Cont

where is it detected?

_______ transmission of the virus during:

spread through _____ in the absence of ____

A

detected in serum, urine, stool, breastmilk

airborne transmision during aerosol generating procedures

spread through aerosols in the absence of AGPs

87
Q

Guidance for dental setting for covid

A

establish a process identifying - positive test, symptoms, criteria for quarantine

source control and physical distancing

  • 6 feet of space and physical barriers between chairs
  • orient operatories parallel to the direction of airflow and place pts head near the return air vents

correct use of PPE

postpone non urgent treatment for pts with suspected infection

AGPs on patients who are not suspected or confirmed to have infection

  • four handed dentistry
  • high vac suction
  • dental dams
88
Q

Covid Infection Time line

Covid detected ___-___ days prior to the onset of symptoms

asymptomatic persons ___-____ weeks

pts with mild/moderate symptoms up to _____ weeks

does detection of viral RNA mean that a person is infectious or able to transmit the virus?

A

1-3 days

1-2 weeks

3 weeks

viral RNA does not necessarily mean a person is infectious

89
Q

How to prevent covid transmission

A

get vaccinated

limit close contact between infected people and others

identifying, testing, and isolating infectious cases as quickly as possible

contact tracing and quarentine

use masks, physical distancing, avoid indoor crowded gatherings, resp. etiquette, hand hygeine

90
Q

why is the treshold for covid herd immunity difficult to determine?

A

breakthrough infections

reinfection

duration of protection from future infections unknown

variants

acheiving high levels of vaccination could lead to manageablle Covid

91
Q

Covid treatment: supportive care

A

acetaminophen or ibuprofen to reduce fever

stay hydrated or IV fluids

get plenty of rest

92
Q

covid treatment: hospitalization

A

antiviral (remdesivir) to slow the virus from multiplying and spreading

steroid to reduce an overreactive immune response for patients on supplemental oxygen

blood thinners to prevent or treat blood clots

93
Q

covid treatment: not enough evidence to recommend

A

convalescent plasma

  • no significant benefit

monoclonal antibodies

  • potential benefits do not outweigh risks
94
Q

how do mRNA vaccines work?

A

strip of mRNA for S protein in lipid bubble

S protein generated

APCs present S proteins to T helper cells

Cytotoxic T cells generated –> virus infected cells killed

B cells generate antibodies –> new infection prevented

95
Q

How do viral vector vaccines work?

A

spike protein genetic material extracted

inserted into inactive adenovirus

–> same steps as regular mRNA vaccine

96
Q
A

Invaders and Defenders (5 decks)

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