Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease and Defense Unit III Derm & Virology > Virology > Flashcards

Virology Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

Frank Pathogen vs. Opportunistic

A

Frank pathogens can cause disease in healthy people, opportunistic need compromised host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Koch’s Postulates

A
  1. Specific Microbe found in disease lesions
  2. Microbes can be isolated and grown in vitro
  3. injection of Microbes into animals reproduces disease
  4. same Microbes can be re-isolated from second host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

6 Stages of Pathogenesis

A

Encounter, Entry, Spread, Multiplication, Damage, Outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Encounter

A

how the agent meets the host, exogenously or endogenously. Mechanism of spread, route of infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Entry

A

how the agent enters the host (invasion or passive)

Colonization and adherence to body tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Spread

A

Spreading factors from infection site, includes hyaluronidase elastase or coagulase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Multiplication

A

how agent multiplies in host, must exceed elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Damage

A

how agent damages tissue or how host responds. Can be direct damage or interference w/ normal physiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outcome:

A

who wins? host dies? microbe dies? mutualism?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Variance in microbiome

A

location on body, diet, ABX, genetics, barriers,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cholera

A

Toxin-mediated pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pneumonia

A

acute inflammation pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tuberculosis

A

facultative intracellular bacteria infection pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rheumatic Fever

A

autoimmune cross-reaction pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Properties of Viruses (4)

A

Submicroscopic
Obligate Parasites
No growth or division
synthesized w/in host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Viral survival strategies

A

Capsulation
Genome has complete infectious cycle information
Host relationships- benign to pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2 methods of viral classification

A 
Physical properties (genetic material, capsid structure) 
Baltimore mRNA production scheme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 types of capsid structures

A

Helical or Icosahedral
Maximal contact and non-covalent interaction
Envelopes: lipid bilayers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

DNA viruses

A

Must transcribe RNA from - strand of genome so replication is required. Most use host RNA polymerase II.
Circular genomes have reverse transcriptase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Poxviruses

A

Have their own RNA polyermase encoded so they use cytoplasmic replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

+RNA Virus

A

genomes translated by host ribosomes w/ amplification by RdRp. Anti-genome must be made by RdRp before replication occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

-RNA Virus

A

packaged RdRp to transcribe genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

+RNA w/ DNA intermediates

A

copy ssRNA to dsDNA via packaged reverse transcriptase, dsDNA added to host genome for transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Tissue Tropism Characteristics (4)

A

Access to tissue, receptor expression, gene expression for production, failure of host defenses
Affected by route of entry, initial replication site, spread mechanism, transmission, and pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute Local Disease

A

Affects epithelial cells at body surface, short incubation times, many serotypes reduce IgA immunity so reinfections are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Acute Systematic Disease

A

primary epithelial infection but viremia allows spread to secondary replication sites, longer incubation, lifetime immunity through IgG and IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Healthy Host Infections

A

shorter disease course, faster immune response, more pronounced immune-related symptoms, reduced shedding and transmission

28
Q

Compromised Host Infections

A

longer infections, increased virus-related symptoms, more shedding and transmission

29
Q

Persistent Infections

A

viruses produce new progeny over long period of time

30
Q

Latent Infections

A

viruses w/ silent genomes that do not produce progeny unless reactivated

31
Q

Slow infections

A

very long incubation period so symptoms take long time to develop and immunity may never develop

32
Q

Viral Effects on Cells (7)

A

Nuclear shrinking, membrane proliferation, cytoplasmic vaculolization, syncytia, chromosomal margination, detachments of cells, inclusion body formation

33
Q

Interferon Anti-Viral State

A

Type I IFN from all cells, Type II from T and NK cells
JAK/STAT signalling of IFN I and II controls ISRE and GAS-controlled genes respectively. In this state, dsRNA reduces cell proliferation and protein synthesis through OAS and PKR

34
Q

Primary Response ABs

A

Low affinity IgM

35
Q

Secondary Response ABs

A

Faster, Higher Affinity, More Diverse Functions due to memory cells

36
Q

Viral Immune Evasion Mechanisms (8)

A

Rapid Mutation to avoid detection by memory cells
Adaption to mimic immune cells
Reduced expression of viral genes in latent phase
Producing inhibitor or decoy molecules
Down regulation of host proteins (MHC, adhesions)
Infection of immunoprivileged sites
Direct infection of immune system
Inhibition of apoptosis

37
Q

Herpes Simplex Type 1 vs Type 2

A

Type 1 is usually orofacial

Type 2 is usually genital

38
Q

Herpes Simplex Pathology

A

dsDNA Primary mucosal infection w/ latency in ganglion, 2-12 day incubation w/ painful lesions, transmitted w/ close contact

39
Q

Herpes Simplex Treatment

A

Acyclovir or derivative, No vaccine

40
Q

Varicella Zoster Pathology

A

dsDNA, primary mucosal, latency in ganglion 10-21 day incubation, itchy vesicular rash in crops, transmission through contact or droplets

41
Q

Varicella Treatment

A

Early acyclovir or IGs. Prophylactic live attenuated vaccine available.

42
Q

Cytomegalovirus pathology

A

dsDNA, primary epithelia of salivary glands or respiratory tract, latency in monocytes/lymphocytes, 2 week to 2 month incubation, F/LA/hepatitis if compromised, transmission through bodily fluids

43
Q

CMV Treatment

A

Treated w/ gancyclovir or IGs, Prophlyactic w/ IVIG in compromised

44
Q

Herpes Virus Structure

A

dsDNA in icosahedral capsid surrounded by glycoprotein rich envelope.

45
Q

Causes of reactivation (5)

A

Illness, Sunlight, Stress, Menstruation, Immune Suppression

46
Q

HSV Primary Infection Symptoms

A

gingivostomatosis, herpetic whitlow (finger), genital herpes, herpes keratitis (cornea), encephalitis

47
Q

HSV reactivation symptoms

A

asymptomatic, cold sore, genital herpes, keratitis, encephalitis

48
Q

Varicella primary symptoms

A

chickenpox (crops of lesions in stages)

49
Q

Varicella reactivation symptoms

A

asymptomatic or shingles

50
Q

CMV primary symptoms

A

asymptomatic unless immune compromised, then F, LA, hepatitis

51
Q

CMV reactivation symptoms

A

asymptomatic unless compromised, then lots of itis’

52
Q

Which herpes viruses have asymptomatic shedding?

A

HSV and CMV

53
Q

Complications of Varicella

A

secondary cellulitis, pneumonia, necrotizing fasciitis, encephalitis, hepatitis, congenital varicella

54
Q

Varicella Vaccines

A

Children: live attenuated 12-15 months w/ booster at 4-6

Shingles vaccine is 14x more concentrated for 50+

55
Q

3 types of vertical transmission of HSV

A

Skin-eye-mucous membrane
CNS
Disseminated

56
Q

Congenital Varicella

A

Birth defects if contracted 8-20 weeks of pregnancy

57
Q

Congenital CMV

A

3-5% transplacental and asymptomatic, 50% from breast feeding and birth canal contact.
Low weight, hearing loss, jaundice, microcephaly

58
Q

CMV Histology

A

Owl eye cells: dark nucleus w/ pale halo of intranuclear inclusions of viral proteins/virions

59
Q

Influenza Structure

A

segmented ssRNA, lipid envelope w/ M1, M2, Hemagglutinin, and Neuraminidase surface glycoproteins

HG binds sialic acid on host cells in respiratory tract
NA helps w/ budding of enveloped virus

60
Q

RSV Structure

A

non-segmented ssRNA w/ Fusion and G surface protein.
F allows fusion to host membrane and syncytia.
G allows binding to host membrane.

61
Q

Influenza Pathology

A

Droplets or fomites contact mucosal surface, 1-3 day incubation in respiratory tract, desquamation occurs

62
Q

RSV Pathology

A

invades conjuntiva or oropharynx w/ 3-5 day incubation followed by syncytia, smooth muscle constriction, bronchoconstriction, and expansion from mucous plugging

63
Q

influenza transmission and prevention

A

Transmitted through droplets or fomites
Live attenuated quadravalent or inactivated trivalent vaccines (70-90% effective, 30-40% in elderly)
Vaccinate at 6 months + w/ priority for vulnerable

64
Q

RSV transmission and prevention

A

recurrent infections common due to incomplete AB coverage, previous vaccine studies showed increased hospitalizations and higher virulence w/ injections. Very expensive IV ABs available for prophylaxis.

65
Q

Antigenic Drift

A

minor point mutations in viral genome that changes the HG binding w/ sialic acid but does not change subtype

66
Q

Antigenic Shift

A

only in type A influenza (it can affect multiple species) where the subtype is changed by 2 strains infecting one host and viral segments are rearranged.

67
Q

Pandemic Criteria

A

new subtype that infects human w/ serious illness and has sustained human-human transmission and spreads easily

Disease and Defense Unit III Derm & Virology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions