Week 3 Flashcards
(96 cards)
1
Q
Is a virus living or non living?
- an obligate:
- completely dependent on a living host cell for:
A
non living
- parasite
reproduction
2
Q
capsid
A
protein coat, protects viral genome
3
Q
membrane glycoprotein
A
allows attachment to host cells
4
Q
lipid envelope
A
extra protective layer
5
Q
why are RNA viruses more prone to replication errors?
A
- because it uses virus enzymes, whereas DNA viruses use host enzymes
6
Q
the viral life cycle is ____ cell dependent
A
host
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
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
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
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)
11
Q
what is the importance of the 6 regulatory genes of HIV?
A
- Regulate uncoating of HIV genome and production of virus particles
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
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
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
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
16
Q
Primary HIV infection characteristics
A
can’t detect antibodies
17
Q
Acute HIV infection characteristics
A
- Flu like symptoms
- CD4 decreases rapidly
- HIV viral load increases rapidly
- Extremely infectious
18
Q
Clinical latency HIV infection characteristics
A
- No symptoms, or mild
- Able to transmit HIV
- can last years
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
20
Q
common HIV co-infections
A
- Hep B (10%)
- Hep C (25%)
- TB
- Fungal infections (candida, Coccidioides, Cryptococcus, Pneumocystis)
21
Q
what is PrEP?
A
given for 7-21 days for people who are at high risk exposure to HIV
22
Q
What is PEP?
A
lasts for 28 days, given within 72 hours within exposure, only in emergency situations
23
Q
1
Herpes:
abbrev.
Name
Disease
A
HSV-1
herpes simplex virus -1
Mucocutaneous lesions (oral>genital), encephalitis, keratitis
24
Q
2
Herpes:
abbrev.
Name
Disease
A
HSV-2
Herpes simplex virus 2
mucocutaneous lesions (genital>oral), encephalitis, meningitis
25
Herpes:
#3
abbrev.
Name
Disease
VZV
varicella zoster virus
chicken pox, shingles
26
Herpes:
#4
abbrev.
Name
Disease
EBV
Epstein Barr Virus
infectious mononucleosis, Burkitt's lymphoma, co factor in many malignancies
27
Herpes:
#5
abbrev.
Name
Disease
CMV
cytomegalovirus
congenital CMV infection, mononucleosis, transplant and AIDS related infections
28
Herpes:
#6
abbrev.
Name
Disease
HHV-6
Human Herpesvirus 6
Roseola
29
Herpes:
#7
abbrev.
Name
Disease
HHV-7
Human herpesvirus 7
Roseola
30
Herpes:
#8
abbrev.
Name
Disease
KSHV
Kaposi's sarcoma associated Herpesvirus
Kaposi's sarcoma, castlemans disease, primary effusion lymphoma
31
**Gingivostomatitis (HSV-1)**
**primary disease of:**
**clinical manifestations:**
* Primarily disease of children and young adults
* Painful lesions occur on buccal mucosa, tongue, gingiva, pharynx
* Lesions ulcerate and resolve 5-12 days
32
Herpes Labialis (cold sore) HSV-1
clnical manifestations:
can be brought on by:
use ______ to prevent transmission
* 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
33
Herpes eye infections: Herpetic Keratoconjunctivitis
ulceration of the:
follows:
develops from:
* 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
34
Herpes cutaneous infection: whitlow (HSV-1=60%, HSV-2=40%)
what is it?
lesions on finger become?
can be inoculated to?
misdiagnosed as?
recurrence?
* 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
35
what are the predominantly HSV-1 infections?
gingivostomatitis; herpes labialis (cold sores)
eye infections
cutaneous infections; whitlow
encephalitis
36
what are the HSV-2 infections?
genital herpes
neonatal infections
37
what are the infections you can get from herpes?
* **Gingivostomatitis**
* **Herpes Labialis (cold sore)**
* **Eye infections (Herpetic Keratoconjunctivitis)**
* **Cutaneous infections; whitlow (HSV-1=60%, HSV-2=40%)**
* **Encephalitis, Meningitis, Meningoencephalitis**
38
What is the pathogenesis of varicella?
* 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)
39
What is a varicella infection that we see?
who are the high risk groups?
what is/clinical manifestations
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
What is CMV?
symptomatic?
where does the virus shed?
can be transmitted in _____ settings due to?
causitive agent of?
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
EBV:
found in?
can infect ____ cells
can shed in:
causitive agent of:
EBV-associated \_\_\_\_\_\_\_
* Found in saliva
* Can infect B cells
* Can shed in saliva
* **Causes Mono**
* **EBV-Associated Malignancy**
42
**KSHV (Kaposi’s Sarcoma Associated Herpesvirus)**
**classic _____ related infection**
**infect ____ cells**
**causal agent in:**
* 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
**Hemagglutinin (HA)** (influenza)
binds to ______ --\> help
\_\_\_\_\_\_ RBCs
neutralizing?
* Binds to sialic acid receptor on body --\> helps gain entry into body
* Agglutinates RBCs
* Antigenic --\> (neutralizing)
44
**Neuraminidase (NA)** (influenza)
what does it do?
cleaves _____ to \_\_\_\_\_\_
degrades \_\_\_\_
neutralizing?
* 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
M2 ion channel (influenza)
what is it?
target of?
* Transmembrane channel (only in influenza A)
* Target of antiviral medicines (amantadine, rimantadine)
46
Influenza subgroups and their hosts:
A
B
C
* 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
what determines each year's flu virus vaccine types?
different subtypes and numbers with flu
48
antigenic drift
causes
what influenzas can experience this
what kind of changes in HA/NA?
\_\_\_\_ changes
epidemic
* Minor mutations in HA or NA
* Influenza A, B. C
* Seasonal changes
49
Antigenic shift
causes:
changes in HA/NA?
only in influenza \_\_\_\_
* 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
clinical manifestations of influenza
challenges in diagnosis
* Fever, myalgia and malaise, headache, pharyngitis, rhinorrhea, cough
* Challenges in diagnosis: easily spread, difficult to diagnose
51
diagnostic strategies influenza
how fast?
sensitive/specific?
Rapid PCR test
20-60min
highly sensitive/specific (\>95%)
52
influenza prevention
hygiene
vaccine (70-90% efficacy)
53
influenza treatment
* 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
Rhinovirus:
who gets it?
emerging cause of:
vaccine?
treatment?
is virus stable to disinfectants?
* 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
**Adenovirus**:
transmission:
specific associations between:
clinical manifestations:
treatment?
* 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
RSV
Severe in:
vaccine?
* Particularly severe in infants & the elderly
* No vaccine
57
Coronavirus
causes 5-30% of:
\_\_\_\_\_\_ number of serotypes
syndromes associated with it:
* 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
what are 3 complications of influenza infection?
primary influenza pneumonia
secondary bacterial pneumonia
reye's syndrome
59
influenza: primary influenza pneumonia
\_\_\_\_\_\_ failure in 10-20%
\_\_\_\_\_ infection
respiratory failure in 10-20%
direct infection
60
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:
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
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 \_\_\_\_\_\_
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
**Enteroviruses**:
host:
where do they infect?
how does it infect?
virus is ____ stable, shed from ____ or \_\_\_\_, becomes immediatley \_\_\_\_\_
\_\_\_\_\_ most important PRR
immune response via:
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
What are common infections/syndromes caused by Coxsackievirus?
What is another enterovirus?
* Upper resp tract infections
* herpangina
* rash syndrome
* hand, foot, mouth disease
* muscle infections
* meningitis
* encephalitis
Polio
64
Coxsackievirus: Upper resp tract infections
clinical manifestations
* Patients may develop erythematous papules on the outside of their mouth or shallow ulcers in the oropharynx associated with erythema
65
Coxsackievirus: Herpangina
\_\_\_ limited to\_\_\_\_\_\_
clinical manifestations
small vesicles/rash limted to the mouth/oral mucosa
* Small vesicles with erythematous base
* Posterior palate
* Pharynx
* Tonsils
* High fever
* Self-limiting
66
Coxsackievirus: Rash syndrome
* Skin manifestations as a result of secondary viremia and infection of other tissues
67
Coxsackievirus: Hand, foot and mouth disease
\_\_\_, ___ strains cause this
if sores in mouth accompanied by:
* A-16, A-71 strains cause this
* If sores in mouth accompanied by rash on hands and feet
68
Coxsackievirus: Muscle infections
what are the 3 muscle infections?
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
Other name for Measles
Rubeola
70
other names for Rubella
German measles
3 day measles
71
Measles:
clinical manifestations/presentations
vaccine?
therapy?
complications
how infectious is it?
do people know they have it right away?
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
Mumps:
clinical presentations
vaccine
therapy
Parotitis 50-70% (inflammation of salivary gland)
Vaccine – highly effective
No specific antiviral therapy
73
Rubella:
clinical presentations
vaccine
therapy
Clinical presentations
* Blueberry muffin rash
* Eye inflammation
Vaccine – 97% efficacy
No specific antiviral therapy
74
**HAV**
Viral shedding begins _______ before symptoms onset and continues _______ after symptoms resolve
Transmission:
Immunity:
Chronic state:
Treatment:
Prevention:
Outcome:
* 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
**HEV**
Transmission:
Chronic state:
Prevention:
Vaccine?
Outcome:
* Transmission: fecal, oral
* Chronic state: no
* Prevention: sanitation
* NO VACCINE
* Outcome: self limited, severe in pregnancy
76
Hep D
can it replicate itself?
Transmission:
Chronic state:
Prevention:
Outcome:
* 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
**Hep C**
Transmission:
Chronic state:
Prevention:
Outcome:
vaccine
Do abs give immunity?
* 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
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?
* 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
Resolution of HBV
* HBV DNA =
* HBsAg =
* HBsAb =
* HBcAb =
* HBV DNA = negative
* HBsAg = negative
* HBsAb = positive
* HBcAb = positive
80
what happens in chronic HBV infection in terms of antibodies?
HBsAb never forms --\> this is why you are in a chronic state vs resolved
81
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 \_\_\_\_\_\_
RNA, proofreading
recombination, coronaviruses
* species, species
spike protein, ACE2
TMPRSS2
* viral entry
furin, S proteins
82
SARS-CoV-2 Biology Cont.
can infect and reproduce in:
carried in the \_\_\_\_\_\_
excessive _______ ---\> leads to
the upper respiratory tract
blood
excessive immune response --\> multiple organ failure, death (cytokine storm)
83
SARS-CoV-2 variant
how does it come about?
what varient is classified as a varient of concern?
* is it more contagious? severity?
AA substitution --\> conformational change --\> increases binding to ACE2 --\> higher viral loads
Delta
* more contagious, more severe illness
* vaccines still effective
84
Extrapulmonary complications of Covid
* heart disease
* reproductive system
* neurological system
* psychology
* immune and hematology systems
* urinary system
* digestive system
85
SARS-CoV-2 transmission
close contact with infected people via:
modes of transmission
is fomite transmission demonstrated?
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
SARS-CoV-2 transmission Cont
where is it detected?
\_\_\_\_\_\_\_ transmission of the virus during:
spread through _____ in the absence of \_\_\_\_
detected in serum, urine, stool, breastmilk
airborne transmision during aerosol generating procedures
spread through aerosols in the absence of AGPs
87
Guidance for dental setting for covid
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
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?
1-3 days
1-2 weeks
3 weeks
viral RNA does not necessarily mean a person is infectious
89
How to prevent covid transmission
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
why is the treshold for covid herd immunity difficult to determine?
breakthrough infections
reinfection
duration of protection from future infections unknown
variants
acheiving high levels of vaccination could lead to manageablle Covid
91
Covid treatment: supportive care
acetaminophen or ibuprofen to reduce fever
stay hydrated or IV fluids
get plenty of rest
92
covid treatment: hospitalization
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
covid treatment: not enough evidence to recommend
convalescent plasma
* no significant benefit
monoclonal antibodies
* potential benefits do not outweigh risks
94
how do mRNA vaccines work?
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
How do viral vector vaccines work?
spike protein genetic material extracted
inserted into inactive adenovirus
--\> same steps as regular mRNA vaccine
96
