Brainscape's Knowledge GenomeTM

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


See full index

Virology > Q4 > Flashcards

Q4 Flashcards

1
Q

Difference between orthomyxo- and paramyxo- ?

A

orthomyxo- and paramyxo- are both Enveloped & ss-RNA virus with a Helical nucleoside
*orthomyxo- is SEGMENTED RNA thus can result in genetic shift/drift but paramyxo- is an one segment RNA thus lack antigenic shifts.

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

Does M & M cause viremia?

A

Yes, it is through viremia that they cause systemic infections.
Obligated viremia also allows neutralization IgG.

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

How many serotypes does mumps have?

A

One

- Human is the only reservoir

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

Transmission of mumps?

A
  • Respiratory droplet
  • Incubation time 18-21 days
    (Prodromal period of fever and anorexia followed by swelling of parotid glands)
  • Most infections are symptomatic
    -Orchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Immunization for mumps?

A
  • Live, attenuated vaccine (given TWICE)
  • Life long immunity
  • NO antiviral therapy for mumps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Most contagious virus known?

A

Measles! - almost NEVER cause subclinical infections.

- Epidemic is caused by antigenically the same measles virus (NO antigentic variation)

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

Transmission of Measles?

A
  • Respiratory droplets
  • Prodromal symptoms (before reaching the 14 day incubation period - rash): fever, cold like symptoms, KOPLIC’s SPOTS (= measles), photophobia
  • NO treatment , immune response ultimately result in life-long immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does measles virus induce cell fusion?

A
  • Multi-nucleated GIANT cells in respiratory and lymphoid nodes
  • Through insertion of measles fusion proteins into the infected cell plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does measles virus cause previously positive tuberculin test to become negative?

A
  • Profound suppression of CELL-MEDIATED immunity

- Transit loss of cell mediated immunity is called “Anergy” (measles caused death incidences)

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

Does measles virus need human to survive?

A

YES

- ONE serotype and humans are the ONLY reservoir

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

Is cell-mediated immunity critical in self defense against measles in human?

A

YES

  • One rare complication: lethal GIANT-CELL Pneumonia without any measles rash when cell-mediated immunity is defective (*Proof that cell-mediated immunity plays a role in the genesis of the rash)
  • People with congenital agammaglobulinemia - can recover from viral infections though are susceptible to recurrent bacteria infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Immunization for measles?

A
  • Live attenuated vaccine (MMR, given TWICE)
  • Vit A supplement has also greatly reduced childhood mortality rate
  • HIGH mortality rate in developing countries.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Does HIGHER dose vaccine improve the effectiveness of the vaccination?

A

NO
- maternal passive immunity can effectively neutralize the virus… (also remains as a challenge for eradication of measles in developing countries)

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

Slow viruses?

A
  • LONG incubation time (can be up to years…)
  • follow a SLOW but RELENTLESS course to death
  • tend to have a GENETIC predisposition
  • often re-emerge from latency during immune suppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Examples of slow viruses?

A
  • HIV
  • JC virus (papovavirus family) _ causes a Progressive Multifocal Leukoencephalopathy (PML) _ only seen in immunocompromised individuals
  • BK nephropathy (papovavirus) _ renal transplants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SSPE?

A
  • Subacute Sclerosing Panencephalitis
  • insidious onset of intellectual deterioration, generally fatal with terminal paralysis and blindness (inclusion bodies in the brain)
  • very HIGH Ab titers to measles and their CNS contains measles viral antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Unconventional agent that causes slow viruses?

A

PRIONS!

- Protein containing particles that lack of any detectable nucleic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Human diseases that are caused by prions?

A
  • Transmittable spongiform encephalopathies:
    1. KURU
    2. Creutzfeld-Jacob Disease (CDJ)
    3. Variant CDJ (mad cow disease)
    4. Gerstmann-Straussler-Scheinker syndrome (GSS)
    5. Fatal familiar insomnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Who are oncogenic viruses?

A

RNA: retrovirus/flavivirus
DNA: Adenovirus/Hepadnavirus/Herpesvirus/Papilliomavirus/Polyomavirus/Poxvirus

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

What are papovavirus?

A
  • small, naked, icosahedral, double stranded circular DNA virus
  • relies heavily on host cell proteins (DNA/RNA polymerase) for replication and gene expression
  • Family member includes (papovavirus - human; polyomavirus - rodents; SV40 - monkeys)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is temporal regulation of viral gene expression and DNA replication?

A

Papovavirus has two classes of genes: early and late genes.
SV40: large T-antigen gene (CRITICAL) is expressed early and is a multifunctional proteins and binds to and inactivates tumor suppressor genes Rb and P53. This overcomes cell growth inhibition leading to tumor development.

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

How do DNA viruses cause transformation of cells?

A
  • Interfere/Inactivate tumor suppressors

- Especially p53

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

HPV!

A

Infect keratinizing or squamous epithelium

  • HPV16 and 18 are highest risk
  • E6/7 interfere with p53/Rb tumor suppressors
  • Recombinant vaccine: based on viral capsid proteins expressed in yeast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of HPV?

A
  • Imiquimod (Aldara) topical cream
  • Potent agonist of TLR7 and IFNalpha
  • Resolution of lesions from 0-5 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Adenovirus cause tumor in human?

A
  • NO, cause tumors in hamsters and transform rat cells in vitro
  • E1A can partially transform cells on its own and E1B increased levels of E1A (does NOT transform)
  • E1 binds to tumor suppressor proteins Rb, p300, and CBP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Herpesvirus?

A
  • LARGE, linear dsDNA, icosahedral, surrounded by a protein tegument enclosed in a glycoprotein bearing envelope.
  • Oncogenic: EBV (integration of viral genes is NOT required for cell transformation) and HHV8 (G-protein coupled receptor induced VEGF expression and angiogenesis + virally-encoded cyclin homolog and the LANA antigen has been shown to activate cellular genes promoting cell growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is retrovirus?

A
  • Retrovirus is an Enveloped virus containing two IDENTICAL copies of +sense single strand RNA
  • All encodes gag (nucleocapsid and capsid proteins), pol (reverse transcriptase), and env (envelop glycoprotein)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Classification of retrovirus?

A
  • Oncoviruses: associated with tumor formation = Rous Sarcoma Virus (RSV), FeLV, ALV, MuLV, HTLV1,2
  • Lentiviruses: NOT directly associated with tumor formation: HIV1,2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the two phases of retrovirus life cycle?

A
  1. Extracellular phase: viral particle, retroviral virion has a single stranded RNA genome
  2. Intracellular phase as a provirus: a DOUBLE stranded DNA, integrate into host cell genome, viral replication starts.
    * ** LTR (long terminal repeats_powerful enhancer) at 5’ and 3 ends, which contains regulatory elements for viral transcription. Genome replication and mRNA transcription occurs from the DNA provirus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the three kinds of transforming retroviruses?

A
  • Transducing (defective virus)
  • Non-transducing
  • Non-transducing, long latency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Example of acute transforming retrovirus?

A

Rous sarcoma virus (contains an oncogene Src)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Oncogenesis cause of HTLV1?

A

NO oncogene.
In addition to gag/pol/env/LTRs, HTLV has tax
Tax - NFketaB - IL-2 - proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are Herpesvirus?

A
  • large, ENVELOPED, icosahedral virus with linear dsDNA assembled in nucleus (***inclusion bodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Classification of Herpesvirus?

A
  • Alphaherpesviruses (HSV-1): latency in neurons
  • Betaherpesviruses (CMV): latency in monocytes
  • Gammaherpesviruses (EBV): latency in lymphocytes, associated with cell transformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is latency?

A
  • Single MOST important biological characteristic of herpes virus
  • patients whose infection is clinically latent may sporadically produce infectious virions while remaining asymptomatic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How to distinguish Herpes Simplex 1 and 2?

A

Monoclonal antibody or PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where do HSV1/2 and Varicella-zoster virus stay latent in?

A

sensory ganglion cells

NO viremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Most common cause of Herpes Simplex Encephalitis?

A

HSV1 is the most common cause (route to the CNS is probably neural), temporal lobe is most commonly infected.
but HSV2 also causes it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is CMV?

A

MOST frequent viral congenital infection (MMR reduced incidence of rubella)
Infected cells are much larger (with a nuclear inclusion - Owl’s eye!)
Latency in leukocytes
anti-CMV IgM is first made in infected fetus/after birth anti-CMV IgG is also made. URINE is the best source for CMV detection in neonates.
BIG problem in organ transplants (when donor is seropositive and recipient is seronegative - transplanted organ contains latently infected cells)
Mononucleosis - presence of large amount of mononuclear cells in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the most common cause of infectious mononucleosis?

A

EBV!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Treatment of cytomegalovirus infection?

A

Ganciclovir
Foscarnet (analogue of pyrophosphate): inhibitor of the DNA polymerase of herpes viruses has much less effect on the DNA polymerase of human cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Treatment of Herpes Simplex Encephalitis?

A

Adenine arabinosides

Acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the drugs that target thymidine kinase?

A

Acyclovir
Iododeoxyuridine (NO LONGER USED)
Triflurodine CANNOT be used systemically due to effects on tissues with rapid DNA synthesis, bone marrows etc (recurrent keratitis _ or can be treated using systemic acyclovir)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What’s the difference between phenotypic mixing and genetic shifting?

A

Phenotypic mixing is when two viruses infect the same cells. But it only last for one cycle (when the virus go on to infect another cell only ONE type will be made).
Genetic shifting occurs when viruses affect different species got mixed and shifted. In the case of influenza, genetic shifting leads to pandemic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Arbovirus?

A

small, ENVELOPED picornavirus:
enveloped, icosahedral, +ssRNA

transmitted by (blood suckling arthropod vectors) mosquitos!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Major taxonomic groups of Arbovirus?

A

Togavirus & Flavivirus (though transmission does NOT apply to rubella virus _ togavirus & Hepatitis C _ flavivirus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How long is INTRINSIC incubation period?

A

in humans - about one week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How long is EXTRINSIC incubation period?

A

in mosquitos (or other arthropods) - about 14 days, during which time, virus is replicating in the arthropods but can NOT be transmitted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the possible causes of encephalitis?

A

In US: Eastern Equine Encephalitis/Western Equine Encephalitis, St. Louise Encephalitis, West Nile Encephalitis (both are flavivirus), California Group of Encephalitis (group of bunyavirus), Venezuelan Encephalitis (occasionally seen in Texas)

50
Q

Is there direct human-to-human transmission for arbovirus?

A

NO, exception being blood transfusions.

51
Q

What is the cause of the MOST deadly encephalitis in the US?

A

EEE! It infects mostly children!

52
Q

Why are humans dead-end hosts for EEE?

A

Because human (and horse) viremia rarely reaches the level required to infect mosquitos. Virus is maintained in the wild mostly by birds/mosquitos.

53
Q

What are the standard control methods for EEE/WEE?

A

1) reduction of mosquito population

2) avoidance of mosquitos during epidemic outbreak

54
Q

What is the most common arbovirus infection in the US? World wide?

A

West Nile Encephalitis in the US.

Japanese Encephalitis in the world (there’s a vaccine suggested for travelers).

55
Q

Outside of US, what other patterns of disease have been shown for arbovirus?

A

1) Severe systemic disease with degeneration of liver (yellow fever)
2) Non-fatal systemic disease with muscle pain and rash (dengue fever)

56
Q

How many antigenic types of cross reacting dengue virus are there?

A

Four, and sufficient viremia occurs in human for infecting mosquitos (same for yellow fever)

57
Q

Why is sequential infection of two antigenic cross-reacting dengue fever viruses lethal?

A

In the second infection, the NON-neutralizing but cross-reacting antibodies from the first infection binds the virion to the macrophage through a Fc receptor and promote macrophage infection. The massive macrophage infection results in overproduction of lymphokins and cytokines.

58
Q

How long is the incubation time for yellow fever?

A

About 7 days.

59
Q

Characteristics of yellow fever?

A

fever, nausea, jaundice (from viral damage to liver cells), and hemorrhage (black vomit), viral multiplication is extensive in spleen, liver, and kidney

60
Q

Is there a vaccine for yellow fever?

A

YES

Live-attenuated vaccine (life long immunity)

61
Q

What is neonatal infections acquired from mothers called? What are the pathways?

A

vertical infections:

1) perinatal (infected at birth) _ HBV, HIV, HSV-2
2) transplacental (infected by virus that cross the placenta) _ results in congenital abnormalities_parvovirus B19, rubella virus, cytomegalovirus, lymphocytic choriomeningitis virus

62
Q

Why are most maternal virus NOT a threat to developing fetus?

A

1) Placental barrier is IMPERMEABLE to particles the size of the smallest viruses.
2) Fetus have maternal IgG/fetal antibody IgM/interferon/cell-mediated immunity??

63
Q

What is parvovirus? Route of infection?

A
  • small, UNENVELOPED, icosahedral virions that contains linear ssDNA
  • inhalation of a respiratory aerosol from respiratory tract of an infected person.
64
Q

What causes ERYTHEMA INFECTIOSUM?

A

Parvovirus - normally asymptomatic (can cause transient arthritis), after a 14-day incubation time presents a rash (probably caused by immune complexes deposits on capillaries)

65
Q

What virus has a tropism for erythroid precursors?

A

Parvovirus B19!
It inhibits RBC production for about a week. Normal individuals can tolerant except patients with pre-existing deficit in red cell production (i.e. sickle cell anemia) will have a TRANSIENT APLASIC CRISS.

66
Q

What can cause hydrops fetalis?

A

transplacental route of infection of parvovirus B19 during the first and second trimester though it’s the relatively uncommon cause.

67
Q

Why is rubella NOT an arbovirus?

A

It’s a togavirus but NOT transmitted by arthropod, but rather by respiratory aerosols from the respiratory tract of an infected person.

68
Q

How long is the incubation time for rubella?

A

18 days, rash lasts about 3 days with a fever and lymphadonopathy. Virus is excreted from the respiratory tract ONE week before and after the rash.

69
Q

What might cause transit arthritis?

A

Parvovirus B19 & Rubella

70
Q

Is there a vaccine for rubella?

A

YES, live-attenuated vaccine (MMR)

71
Q

Rubella virus from viremia PRIMARY infection during pregnancy (FIRST trimester) crosses placenta. True or false?

A

YES!

The earlier the infection takes place, the more severe deformation of the fetus there will be.

72
Q

What is the major purpose for the live-attenuated vaccine?

A

Prevent congenital rubella!

  • EVERYONE needs to be vaccinated.
  • Individual immunity must be maintained through the child-bearing years to reduce the susceptible pregnant women.
73
Q

What causes congenital defect?

A

CMV (#1 now)
Rubella
Varicella (skin scarring/limb atrophy)

74
Q

What causes retinitis and pneumonia in patients deficient in helper T cells?

A

CMV

75
Q

What causes encephalitis, especially in the temporal lobe?

A

HSV type 1

76
Q

What is human papillomavirus?

A

DNA non-enveloped virus

77
Q

What virus has part of its genome DNA being synthesized by the virion polymerase?

A

Hepatitis B virus

78
Q

Mumps orchitis in children prior to puberty often causes sterility. True or false?

A

False!

After puberty, it’s when orchitis causes sterility.

79
Q

Immunosuppression is a frequent predisposing factor for SSPE. True or false?

A

False!
Age (young, measles infection, higher chance)
Antibody titer to measles (stronger, higher chance)

80
Q

Varicella-zoster virus do NOT shed.

A

TURE!

Only when you are stressed or immune deficiency (with past chicken pox infection).

81
Q

About EBV, the earlier in life primary infection is acquired, the more likely the typical picture of infectious mononucleosis will be manifested. Correct?

A

WRONG!

young kids or babies would present with subclinical symptoms.

82
Q

What is the structure of HIV?

A

human T cell lymphotrophic retrovirus (HIV-1) is:
enveloped
ss+RNA
TWO identical strands (diploid)
virion carries 3 enzymes: reverse transcriptase/integrase/protease

83
Q

What’s special about HIV virus compare to other retrovirus?

A

It’s a complex retrovirus and it has regulatory genes that are not present in most other retroviruses.

84
Q

What are the life cycle steps of HIV?

A 
attachment 
co-receptor binding (*) 
fusion (*)
reverse transcription (*site of drug targeting) 
integration (*)
transcription (*)  
translation 
cleavage of precursor proteins (*)
nucleocapsid assembly 
budding 
virion maturation (*)
85
Q

What determines HIV tropism?

A

gp120 protein in the virion envelope
(binding of gp120 to the CD4 molecule is a required step for HIV attachment and entry)
- CD4+ host cells
- primarily: CD4+ helper T lymphocytes, others include monocytes: macrophages, microglial cells, dendritic cells, and occasionally other cell types.

86
Q

Is binding to CD4 antigen alone sufficient for HIV entry into the host cell?

A

NO!
- interaction with a host cell coreceptor (primary CCR5) is essential
CCR5 - member of the chemokine receptor superfamily

87
Q

What’s the first step when HIV gets into the cell?

A

Reverse transcriptase engages a host tRNA as a primer and and the HIV RNA genome as the template to make a single stranded RNA (+RNA to -RNA), then to reverse transcribe into ssDNA, then dsDNA, then integrate into host genome..

88
Q

What does HIV protease do?

A

Activated infected CD4+ cells will activate the expression of HIV mRNA from the proviral integrated HIV genome. Then HIV RNA enters the cytoplasma and is translated into HIV precursor proteins. HIV protease then cleaves HIV precursor proteins into MATURE HIV protein product.

89
Q

Through what method does HIV virion leave the host cell to infect other cells?

A

BUDDING!
Though the virion at this point is not yet fully mature and HIV protease also functions within the virion to mature the infectivity of HIV virions (gp120 & gp41 are cleavage products that are critical for penatration/adhesion).

90
Q

KEY: the reverse transcriptase that makes the DNA copy of HIV and the host cell RNA polymerase that make the viral mRNA have NO proofreading functions. - ERROR-PRONE

A

(see front)

91
Q

A few CD4+ T lymphocytes with integrated proviral HIV can remain latent for many years. True or false?

A

True!

Probably within the resting, memory CD4+ T lymphocyte population.

92
Q

What are the paths of transmission for HIV?

A

Sexual contact (could be through transfer of HIV virus or HIV-infected cells)
Blood
Transplacental/Perinatal
Breast feeding
***HIGHER concentration of HIV (e.g. higher HIV levels in the blood = higher viral load) = HIGHER risk of transmission.

93
Q

Is there a vaccine for HIV?

A

NO…

94
Q

How to diagnose acute infection?

A

It is diagnosed by HIV viral load.

antibody production is delayed _ within a few months

95
Q

What happens to the number of circulating CD4+ T lymphocytes during acute HIV infection?

A

Dramatic decline…
Activated CD4+ helper T cells are at risk of being infected by HIV or actively making HIV virus if infected… Acute HIV infection kills CD4+ T cells faster than these cells can be made (1. infection. 2. due to overwhelming immune activation: activation-induced cell death)
Then a robust immune response is triggered and immune system regains control. Viral load decreases to a set point. BUT the immune response fails to clear HIV infection…
***Despite the initial decrease in viral load when the set point is established, HIV replication is EXTENSIVE in lymphoid tissue during chronic infection.

96
Q

How to diagnose chronic HIV infection?

A

HIV serology
ELISA followed by confirmatory Western blot to HIV antigen.
*MOST individuals with chronic HIV infection are asymptomatic thus epidemiology risks and screening are necessary to make the diagnosis.
SLOW and RELENTLESS decline in the CD4+ T cell count occurs during chronic infection.

97
Q

“Viral escape”?

A

HIV mutates to evade the immune response(s)
*Chronic activation of immune system is thought to be a key mechanism underlying disease pathogenesis. - It leads to decreased ability to control HIV infection, promotes HIV replication in activated CD4+ T cells, and causes activation-induced cell death. Bone marrow exhaustion…

98
Q

What predicts the rate of progression to AIDS (prognosis)?

A

HIV viral load set point that’s established following acute infection.
HIV viral load (determined by PCR to measure HIV RNA) _ predicts the rate of progression to HIV) and the CD4+ T cell count _ determines vulnerability to infection and then antiretroviral therapy should be initiated_ are the clinical measurements.

99
Q

What is AIDS?

A

It’s defined as the presence of one of ~27 conditions (AIDS-defining infections or cancers) indicative of severe immunodeficiency, or HIV infection in a person with CD4+ T cell counts less than 200 cells per mm3 (or a CD4+ T cell percentage less than 15% of total lymphocytes).

100
Q

Clinical course of AIDS?

A

Accelerated immune deficiency due to extreme loss of CD4+ cells (CD8+ T cells are also lost late in AIDS).
Patients are more susceptible to malignancy; variety of viral infections including Hep B/C, Herpes, CMV, EBV, PML caused by JC virus; psychiatric disease in chronic HIV infection; risks of cardiovascular disease.

101
Q

What are two situations where treatment is always prescribed to AIDS/HIV patients?

A
  1. Pregnant women

2. Hep B & HIV patients

102
Q

Goals for HIV/AIDS treatment?

A
  1. Reduced HIV viral load

2. Restore CD4+ counts and immune function

103
Q

What is HAART therapy?

A

“Highly active antiretroviral therapy”
At least three drugs from at least two different drug classes (mechanism of action).
*immune reconstitution syndrome (if another infection is present at the time of treatment) - can NOT eliminate the virus
- Current standard of HAART therapy primarily uses some combination of nRTI, nnRTI, and PI

104
Q

Example of Nucleoside Reverse Transcriptase Inhibitors (NRTI) drugs?

A

(look like nucleosides, biochemically called chain terminators)
AZT!

105
Q

Example of Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI)?

A

do NOT look like nucleosides- inhibit RT by binding outside but near the active site of the enzyme and reduce its activity, block synthesis of HIV DNA.

106
Q

Other drugs used in antiretroviral treatment?

A
  • Protease Inhibitor (PI): block the protease activity of the HIV protease, which is required to cleave HIV precursor proteins - NO infectious form virus.
  • CCR5 Antagonists: blocking HIV virion binding to the co-receptor CCR5 - failed infection attempts…
  • Fusion Inhibitor: interfere with the formation of the gp41 fusion complex and block fusion of the viral envelope with the host cell plasma membrane - failed infection attempts…
  • Integrase Inhibitor: block integrase and prevent integration of HIV proviral DNA - HIV virus production canNOT occur.
107
Q

What are poxviruses?

A
  • dsDNA, LARGEST nucleic acid content of all animal virus (contains a RNA polymerase)
  • LARGE/brick shaped
  • No obvious symmetry
  • can be either enveloped (budding) or NON-enveloped (host cell lysis), DIFFERENT antibodies neutralize these two forms of viruses. ***UNenveloped form of the virion is stable to adverse conditions such as drying
108
Q

What is the only DNA virus that have a gene for their own RNA polymerase?

A

Poxvirus!

109
Q

Where does poxviruses form inclusion bodies?

A

Cytoplasma!

110
Q

How is molluscum contagiosum transmitted? How long is the incubation time?

A
  • cutaneous contact (young children, wrestlers, lovers)
  • 2-8 weeks but is self-limiting (can take months or years)
  • Difficult to diagnose: grows very poorly in culture
111
Q

How is smallpox transmitted?

A

Respiratory route
initial mild upper respiratory infection with growth in mucosa and lymph nodes
* FIRST viremia infects: lungs, liver, spleen
2nd viremia: skin

112
Q

Is there a vaccine for smallpox?

A

YES!
Cowpox - live vaccine
Smallpox has been eradicated by immunization with the live vaccine
*single serotype/NO non-human reservoirs

113
Q

What are the complications of smallpox vaccination?

A
  1. Post-vaccinial encephalitis: most common and more frequent in adults
  2. Vaccinia necrosum: spreading necrosis at the vaccination site
  3. Eczema vaccinatum: spread of lesion in pre-existing eczema (inflammation of the skin)
  4. Generalized vaccinia: spread of lesion in the absence of eczama
  5. Myo/pericarditis
  6. Passive immunization with human vaccinia-immune globulia is used for severe complications
114
Q

What is rhabdoviruses? Example?

A
  • virion is bullet shaped, medium sized
  • envelop is modified cell membrane that contains viral glycoproteins, virions released by BUDDING
  • helical nucleocapsid contains a single molecule of -RNA (*Virion contains an RNA-dependent RNA polymerase)
    RABIES!
115
Q

How is Rabies transmitted?

A
  • bite of an infected animal that has virus in its saliva
  • pathogenesis does NOT require viremia
  • tropism: NERVE cells
  • incubation time (weeks to months) but infection in human and dog is nearly always FATAL.
116
Q

Symptoms of rabies?

A

Early: fever anorexia
Later: hydrophobia/CNS defect from virus destruction/death

117
Q

How to diagnose rabies?

A

Histological demonstration of Negri bodies (cytoplasmic inclusions) in nerve cells.
Fluorescent Ab to rabies is used to confirm that these inclusion bodies are from rabies virus.

118
Q

Is there a vaccine for rabies?

A 
YES! 
Killed vaccine (made in diploid cells and then inactivated). Long incubation period allows highly successful immunization after infection. (Though once clinical symptoms begin in the CNS, the vaccine or any other treatment will NOT prevent death...)
119
Q

Treatment for rabies?

A

passive immunization (hyperimmune human serum given to delay symptoms) and killed vaccine is recommended in ALL cases of possible contact with rabies virus.

120
Q

How is rabies virus maintained?

A

Nucleotide sequencing of the rabies genome allows ID of the animal host species in which the virus was maintained. (In the US, mostly it’s from wild animals.)

Virology (5 decks)

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