Patterns of Infections Flashcards

(74 cards)

1
Q

Natural infections can be ____ and self-limiting (____ infection) or ____ (____ infection)

A

rapid; acute; long-term; persistent

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2
Q

Most latent infections begin as an ___ infection of one cell type, but when they encounter a different cell type, no ___ ____ are produced

A

acute; infectious particles

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3
Q

A smoldering infection can occur in which ___ ___ ___ ___ occurs in face of a strong immune response

A

low-level viral replication

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4
Q

slow infections and ____ infections are more complicated variants of persistent infections

A

transforming

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5
Q

Patterns of infection can be very ____ and _____ for the virus family

A

stable; characteristic

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6
Q

an acute virus runs a ___ but ___ course; hallmarks are rapid production of virion followed by _____ of infection and ____. What are some viruses that cause acute infections?

A

short; severe; elimination; clearance; rhinovirus, influenza

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7
Q

Effector cells and antibodies begin to clear infected tissues after - days

A

4-5

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8
Q

Incubation periods can vary from ______ to ____

A

1-2 days; years

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9
Q

What is the initial period before symptoms of disease are seen? What occurs during this time? What causes the classic symptoms of an acute infection? What are these symptoms?

A

incubation period; viral replication and host response in the form of release of IFN-gamma and other cytokines; IFN-gamma and other cytokines; (Fever, malaise, aches, pains, and nausea)

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10
Q

Short incubation periods generally indicate that symptoms of disease are from where?

A

The primary infection site

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11
Q

Long incubation periods generally indicate that symptoms of disease are from where?

A

A secondary infection site

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12
Q

For acute infections, ___ and ___ defenses limit and contain most of them. If someone is immunocompromised they can be serious and can result in? What does the healthy host depend on for immune clearance?

A

innate and intrinsic; systemic infections and damage of multiple organs; the adaptive response

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13
Q

For Varicella-zoster virus (chicken pox): primary replication is in the primary lymph nodes. It takes X days before what happens?
What is the period of non-specific symptoms? How does chicken pox reach the skin?

When can they reappear and how does it happen?

A

4-6; infected t cells enter bloodstream (primary viremia);

The prodromal period

It infects skin-homing T-cells, which brings the infection to the epidermis.

Later in life, when the immune system’s function is reduced the virions travel back down from the peripheral neurons to the skin again.

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14
Q

Antigenic variation: Why we get acute infections repetitively. After infection survival, the individual is immune to infections by the -__ ____. Some acute infections with ______ occur repeatedly despite robust immune response. Why?

A

same virus; rhinovirus and influenza; selection pressures lead to shedding of virions resistant to immune clearance. This is due to structural properties of virions and the capacity of neutralizing antibodies to block infectivity.

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15
Q

Virus that tolerate many amino acid substitutions while remaining infectious are said to have:

A

structural plasticity

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16
Q

There are over ___ different serotypes of rhinovirus maintained in humans all the time, so you may contract more than one each year. What does this mean for the possibility of a cold vaccine?

A

100; it is difficult to produce.

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17
Q

Antigenic drift is what?

A

Small changes due to slight alterations of surface proteins

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18
Q

Antigentic shift is what?

A

major changes in surface proteins that encodes a completely new surface protein.

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19
Q

When can antigenic shift occur? What is exchanged?

A

When an organism is coinfected with two viral serotypes; virus with segmented genomes exchange blocks of genetic information; also when recombination occurs between co-replicating genomes

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20
Q

Viruses with segmented genomes can exchange ____ genomes. Resulting hybrid virions may be temporarily better at what?

A

segments; evading immune defenses

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21
Q

Persistent infections occur when? What is it called when a persistent infection is eventually cleared? What’s it called when it lasts the life of the host?

A

Primary infection is not cleared efficiently; chronic; latent

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22
Q

Virions may be produced even in the presence of an ____ ____ ____

A

active immune response

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23
Q

Sometimes ___ _____ ____ after viral proteins are no longer detected

A

viral genomes remain

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24
Q

The persistent pattern is surprisingly common, especially for ___ _____ ____

A

non-cytopathic virus

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25
Herpesvirus have a ___ and ___ viral transcription pattern
latent and lytic
26
When viral ____ effects and host defenses are ___ a persistent infection is likely
cytopathic; reduced
27
A virus can reduce production of ____, reduce ___ protein expression, or inhibit ____ in order to cause a persistent infection.
IFN; MHC; apoptosis
28
What is one of the most powerful antiviral responses?Th and cyt. T populations found after some infections are limited, the T cells respond to ____ viral peptides. These peptides are said to be ________.
CTL response; few; immunodominant
29
properties of latent infections
viral gene products that promote virion production aren't made cells harboring the latent genome are poorly recognized by the immune system The viral genome persists intact and may reactivate a a later time
30
How could a latent genome be maintained?
A non-replicating chromosome in a non-dividing cell IE neuron; may be a self-replicating chromosme in a dividing cell Could be integrated into the host chromosome
31
What could replication in a mucosal epithelium form? What cell defenses limits its spread?
A lesion; IFN and cytokines
32
sometimes all infected cells fuse together. what is this called?
syncytia (SP?)
33
Virions released in herpes infections leave the ___ ____ of the epithelium. There it may find a ____ and switch to a ____ state
basal membrane; neuron; latent
34
In Herpes SImplex virus (HSV), the viral genome is silenced and coated with nucleosomes (t/f) Does it need to divide?
T; no, because the neuron doesn't divide
35
What is syncytia?
fusing of multiple infected cells. This causes instability
36
HIV ____ CD4 T-Cell numbers and helper cell maintenance of CD8 T-cell, macrophage, and other cell functions
reduces
37
The provirus is?
DNA version of retrovirus???
38
HIV infects _____ _____ during sexual activity
mucosal surfaces
39
Those with a mutation in ____ co-receptor are resistant to HIV infection
CCR5
40
A persistent HIV infection is seen in ____, ____, _____ and hematopoietic stem cells. These serve as the ___- ____
macrophages, DCs, memory T cells; major reservoirs
41
AIDS development correlates with increased ___ of virus and decreased ____ cells
release; Th
42
Nef protein does what to the HIV infection
promotes progression of HIV infection to aids
43
What is the first phase of HIV infection? What is viral concentration?
acute phase, 10E7 particles/mL
44
During clinical latency period, HIV replication continues where?
lymph nodes
45
What other type of immune cell decreases with an HIV infection? What does this cause?
CD8 cells due to lymph node distruction; immunosuppression
46
what cd4 cell concentration is an indicator for onset of AIDS? What concentration is full blown AIDS?
350 cells/microliter; <200cells/microliter
47
Activated CD4 T cells intitiate immune response by ____ ____ used for activation of other leukocytes
releasing cytokines
48
HIV can also cause neurologic abnormalities. The ____ cell and _____ are the predominant infected cells in the brain. Why are they dangerous?
microglial, macrophage. They cause cellular release of neurotoxic substances or chemotactic factors that promote inflammatory response and neuronal death in the brain
49
What HIV viral load involves onset of more significant diseases?
>75k copies/mL
50
What is HIV wasting syndrome?
weight loss and diarrhea for >1 month
51
AIDS-related dementia can result from ____ infection or HIV infection of ____ and microglial brain cells
opportunistic; macrophages
52
HIV epidemiology: Since it's enveloped it is ____ ____ and must be transmitted via ____ ____. There is a long ______ period. Virus can be shed before development of identifiable ______.
easily inactivated, bodily fluids. prodromal: generalized flu-like symptoms; symptoms
53
Transmission of HIV: Virus is present in ___ ___ and ____ secretions. at risk are: ____ ____ ___ ____ ; blood and organ transplant recipients, and hemophiliacs treated before ____.
blood, semen, vaginal secretions; IV drug abusers, sexually active people with many partners, prostitutes, newborns of HIV+ mothers; 1985
54
Modes of HIV control: ____ ___ limit progression of disease, lack of ___ needles, safe sex, large scale _____ ____
antiviral drugs; sterile; screening programs
55
in 2009, how many people have HIV, how many infections per day? how many deaths per year?
33.5 million; 7k, 1.8 million
56
Tests for HIV infection performed for four reasons:
identification of those infected so antiviral drug therapy can be initiated; to identify carriers who can transmit infection; to follow course of disease and confirm diagnosis of AIDS, evaluate efficacy of treatment.
57
Chronic nature of the HIV disease allows the use of ____ tests; however these cannot identify ____ ___ people
serologic; recently infected
58
Recent HIV infection or late stage disease are identified by lots of ___ ____ in blood, ____ ___ ____ ____, or detection of ___ enzyme
viral RNA; p24 viral capsid antigen; RT
59
What is the first step for HIV lab diagnosis? what's after that?
Detection of antibodiy and p24 capsid antigen; determining HIV-1 or HIV-2
60
AIDS treatment: What is the Anti-HIV therapy called? What is the advantage of this?
Highly active antiretroviral treatment (HAART); multiple mechanisms of action reduces potential to select for resistance.
61
Multidrug therapy can reduce blood levels of virus to ___ and reduce ___ and ____ in advanced AIDS patients
0; morbidity; mortality
62
Initiation of HAART is done at Th cell levels of; alternatively it is recommended for ___ events
300-500; post-exposure prophylaxis (e.g. needle stick)
63
What is the function of a nucleoside analog? RT inhibitor? Protease inhibitor? fusion inhibitor?
It inhibits viral polymerases by incorporating a terminal nucleoside; sterically disrupts RT catalytic site; prohibits protein cleavage at late stage of HIV replication cycle; blocks viral and cellular membrane fusion step involved in virus entry into cells
64
Potential subunit vaccines have been unsuccessful. What were the subunits used? Why are they unsuccessful?
GP120, gp 160; They elicit only an antibody to a single strain of HIV and aren't successful.
65
Most recent HIV vaccines do what?
prime T-cell responses via a different virus such as canarypox, herpesvirus, vaccinia, or defective adenovirus vector
66
____ vaccine consisting of eukaryotic expression vectors (plasmid) was tried for GP160
DNA
67
A vaccine gneerating an antibody against the CD4 binding site is under investigation and may elicit ____ ____ to most HIV strains
neutralizing antibody
68
In a healthy host, in an acute infection _____and ____-_____ ____ are destroyed (______) by the immune system in days
virions and virus infected-cells; cleared
69
What are the defenses available to fight off a recurring infection?
antibodies; residual effector cells; and memory cells
70
If viral replication occurs in the presence of antibody that neutralizes virions, antibody-resistant ____ are selected for and _____. These shed virions can then reinfect whom?
mutants; shed; individuals who have already been exposed and have adaptive immunity towards the pre-mutated virus.
71
Which viruses have little structural plasticity? What does this mean for antibody-resistant mutants?
Measles, poliovirus, yellow fever; they have a low probability of being selected
72
How many serotypes of poliovirus are circulating? What does this mean for the vaccine?
3; vaccines that were effective in the 1950s are still effective today.
73
What is antigenic variation?
It's mutation of the virus in response to antibody selection.
74
How are primary infections cleared?
The adaptive immune response clears them through close integration with the intrinsic and innate response