Patterns of Infections Flashcards

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
Q

Herpesvirus have a ___ and ___ viral transcription pattern

A

latent and lytic

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26
Q

When viral ____ effects and host defenses are ___ a persistent infection is likely

A

cytopathic; reduced

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27
Q

A virus can reduce production of ____, reduce ___ protein expression, or inhibit ____ in order to cause a persistent infection.

A

IFN; MHC; apoptosis

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28
Q

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 ________.

A

CTL response; few; immunodominant

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29
Q

properties of latent infections

A

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

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30
Q

How could a latent genome be maintained?

A

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
Q

What could replication in a mucosal epithelium form? What cell defenses limits its spread?

A

A lesion; IFN and cytokines

32
Q

sometimes all infected cells fuse together. what is this called?

A

syncytia (SP?)

33
Q

Virions released in herpes infections leave the ___ ____ of the epithelium. There it may find a ____ and switch to a ____ state

A

basal membrane; neuron; latent

34
Q

In Herpes SImplex virus (HSV), the viral genome is silenced and coated with nucleosomes (t/f) Does it need to divide?

A

T; no, because the neuron doesn’t divide

35
Q

What is syncytia?

A

fusing of multiple infected cells. This causes instability

36
Q

HIV ____ CD4 T-Cell numbers and helper cell maintenance of CD8 T-cell, macrophage, and other cell functions

A

reduces

37
Q

The provirus is?

A

DNA version of retrovirus???

38
Q

HIV infects _____ _____ during sexual activity

A

mucosal surfaces

39
Q

Those with a mutation in ____ co-receptor are resistant to HIV infection

A

CCR5

40
Q

A persistent HIV infection is seen in ____, ____, _____ and hematopoietic stem cells. These serve as the ___- ____

A

macrophages, DCs, memory T cells; major reservoirs

41
Q

AIDS development correlates with increased ___ of virus and decreased ____ cells

A

release; Th

42
Q

Nef protein does what to the HIV infection

A

promotes progression of HIV infection to aids

43
Q

What is the first phase of HIV infection? What is viral concentration?

A

acute phase, 10E7 particles/mL

44
Q

During clinical latency period, HIV replication continues where?

A

lymph nodes

45
Q

What other type of immune cell decreases with an HIV infection? What does this cause?

A

CD8 cells due to lymph node distruction; immunosuppression

46
Q

what cd4 cell concentration is an indicator for onset of AIDS? What concentration is full blown AIDS?

A

350 cells/microliter; <200cells/microliter

47
Q

Activated CD4 T cells intitiate immune response by ____ ____ used for activation of other leukocytes

A

releasing cytokines

48
Q

HIV can also cause neurologic abnormalities. The ____ cell and _____ are the predominant infected cells in the brain. Why are they dangerous?

A

microglial, macrophage. They cause cellular release of neurotoxic substances or chemotactic factors that promote inflammatory response and neuronal death in the brain

49
Q

What HIV viral load involves onset of more significant diseases?

A

> 75k copies/mL

50
Q

What is HIV wasting syndrome?

A

weight loss and diarrhea for >1 month

51
Q

AIDS-related dementia can result from ____ infection or HIV infection of ____ and microglial brain cells

A

opportunistic; macrophages

52
Q

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 ______.

A

easily inactivated, bodily fluids. prodromal: generalized flu-like symptoms; symptoms

53
Q

Transmission of HIV: Virus is present in ___ ___ and ____ secretions. at risk are: ____ ____ ___ ____ ; blood and organ transplant recipients, and hemophiliacs treated before ____.

A

blood, semen, vaginal secretions; IV drug abusers, sexually active people with many partners, prostitutes, newborns of HIV+ mothers; 1985

54
Q

Modes of HIV control: ____ ___ limit progression of disease, lack of ___ needles, safe sex, large scale _____ ____

A

antiviral drugs; sterile; screening programs

55
Q

in 2009, how many people have HIV, how many infections per day? how many deaths per year?

A

33.5 million; 7k, 1.8 million

56
Q

Tests for HIV infection performed for four reasons:

A

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
Q

Chronic nature of the HIV disease allows the use of ____ tests; however these cannot identify ____ ___ people

A

serologic; recently infected

58
Q

Recent HIV infection or late stage disease are identified by lots of ___ ____ in blood, ____ ___ ____ ____, or detection of ___ enzyme

A

viral RNA; p24 viral capsid antigen; RT

59
Q

What is the first step for HIV lab diagnosis? what’s after that?

A

Detection of antibodiy and p24 capsid antigen; determining HIV-1 or HIV-2

60
Q

AIDS treatment: What is the Anti-HIV therapy called? What is the advantage of this?

A

Highly active antiretroviral treatment (HAART); multiple mechanisms of action reduces potential to select for resistance.

61
Q

Multidrug therapy can reduce blood levels of virus to ___ and reduce ___ and ____ in advanced AIDS patients

A

0; morbidity; mortality

62
Q

Initiation of HAART is done at Th cell levels of; alternatively it is recommended for ___ events

A

300-500; post-exposure prophylaxis (e.g. needle stick)

63
Q

What is the function of a nucleoside analog? RT inhibitor? Protease inhibitor? fusion inhibitor?

A

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
Q

Potential subunit vaccines have been unsuccessful. What were the subunits used? Why are they unsuccessful?

A

GP120, gp 160; They elicit only an antibody to a single strain of HIV and aren’t successful.

65
Q

Most recent HIV vaccines do what?

A

prime T-cell responses via a different virus such as canarypox, herpesvirus, vaccinia, or defective adenovirus vector

66
Q

____ vaccine consisting of eukaryotic expression vectors (plasmid) was tried for GP160

A

DNA

67
Q

A vaccine gneerating an antibody against the CD4 binding site is under investigation and may elicit ____ ____ to most HIV strains

A

neutralizing antibody

68
Q

In a healthy host, in an acute infection _____and ____-_____ ____ are destroyed (______) by the immune system in days

A

virions and virus infected-cells; cleared

69
Q

What are the defenses available to fight off a recurring infection?

A

antibodies; residual effector cells; and memory cells

70
Q

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?

A

mutants; shed; individuals who have already been exposed and have adaptive immunity towards the pre-mutated virus.

71
Q

Which viruses have little structural plasticity? What does this mean for antibody-resistant mutants?

A

Measles, poliovirus, yellow fever; they have a low probability of being selected

72
Q

How many serotypes of poliovirus are circulating? What does this mean for the vaccine?

A

3; vaccines that were effective in the 1950s are still effective today.

73
Q

What is antigenic variation?

A

It’s mutation of the virus in response to antibody selection.

74
Q

How are primary infections cleared?

A

The adaptive immune response clears them through close integration with the intrinsic and innate response