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MICRObio@123 > Pathogenesis And Control- Virology > Flashcards

Pathogenesis And Control- Virology Flashcards

1
Q

What is syndrome

A

Specific group of signs and symptoms

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2
Q

What is the fundamental process of viral infection?

A

viral replicative cycle.

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3
Q

Viral infections that fail to produce any symptoms in the host are said to be?

A

inapparent (subclinical).

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4
Q

What are the Important principles that pertain to viral disease?

A

(1) many viral infections are subclinical;
2) the same disease syndrome may be produced by a variety of viruses;
(3) the same virus may produce a variety of diseases; and
(4) the outcome in any particular case is determined by both viral and host factors and is influenced by the environmental context and genetics of each.

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5
Q

Majority of Virus entry into the host is through which body surface?

A

through the mucosa of the respiratory or gastrointestinal tract

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6
Q

What happens after viral entry?

A

After entry, the viral nucleic acid and virion-associated proteins interact with cellular macromolecules to ultimately produce new virions that are released from the host cell by shedding or cell lysis.

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7
Q

What is the common route for viral spread in the human host?

A

The blood stream or lymphatics.

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8
Q

What is viremia?

A

The presence of virus in the blood

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9
Q

viral tropism

A

Tropism determines the pattern of systemic illness produced during a viral infection

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10
Q

What are receptors?

A

Receptors are components of the cell surface which a region of the viral surface (capsid or envelope) can specifically interact and initiate infection

Receptors are cell constituents that function in normal cellular metabolism but also happen to have an affinity for a particular virus

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11
Q

What is the most prominent innate immune response?

A

the induction of cytokines such as IFNs

IFNs also modulate humoral and cellular immunity and have broad cell growth regulatory activities.

There are multiple species of IFNs that fall into three general groups: designated IFN-α , IFN-β, and IFN-γ.
Both IFN-α and IFN-β are considered type I or viral IFNs; IFN-γ is type II or immune IFN.

Infection with viruses is a potent inducer of IFN-α and IFN-β production; RNA viruses are stronger inducers of IFN than DNA viruses.

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12
Q

What s the mechanism for IFN action?

A

IFN is secreted and binds to cell receptors, where it induces an antiviral state by prompting the synthesis of other proteins that inhibit viral replication.

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13
Q

What is the inflammatory reaction of uncomplicated viral lesions.

A

infiltration with nuclear cells and lymphocytes

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14
Q

What serves as targets for the immune response.?

A

Virus-encoded proteins

Virus-infected cells may be lysed by cytotoxic T lymphocytes as a result of recognition of viral polypeptides on the cell surface.

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15
Q

What protects the host against reinfection by the same virus?

A

Humoral immunity

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16
Q

What blocks the initiation of viral infection, presumably at the stage of attachment, entry, or uncoating?

A

Neutralizing antibody directed against capsid proteins

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17
Q

What is the function of Secretory IgA antibody?

A

important in protecting against infection by viruses through the respiratory or gastrointestinal tracts.

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18
Q

What is acute infection?

A

Infections are acute when a virus first infects a susceptible host.

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19
Q

What is chronic or persistent infection?

A

those in which replicating virus can be continuously detected, often at low levels; mild or no clinical symptoms may be evident.

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20
Q

What is latent infection?

A

those in which the virus persists in an occult (hidden or cryptic) form most of the time when no new virus is produced.

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21
Q

What are the most common cause of mortality for children younger than 5 years?

A

Respiratory infections

with diarrheal disease the second leading cause.

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22
Q

major causes of gastroenteritis

A

Rotaviruses,

noroviruses,

Asymptomatic ones include:
Enteroviruses,
coronaviruses, and
adenoviruses

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23
Q

Why does viruses infecting the epidermal remain localized?

A

The epidermal layer is devoid of blood vessels and nerve fibers.

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24
Q

What happens to viruses that are introduced into the dermis?

A

Viruses that are introduced deeper into the dermis have access to blood vessels, lymphatics, dendritic cells, and macrophages and usually spread and cause systemic infections.

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25
Q

What causes macules?

A

Macules, which are caused by local dilation of dermal blood vessels, progress to papules if edema and cellular infiltration are present in the area.

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26
Q

How does vesicles and pustules occur?

A

Vesicles occur if the epidermis becomes focally detached, and they become pustules if an inflammatory reaction delivers polymorphonuclear leukocytes to the lesion.

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27
Q

How does Hemorrhagic and petechial rashes occur?

A

Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

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28
Q

What are the 2 routes by which viruses gain access to the brain?

A

y the bloodstream (hematogenous spread) and by peripheral nerve fibers (neuronal spread).

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29
Q

Pathologic reactions to cytocidal viral infections of the CNS include:

A

necrosis, inflammation, and phagocytosis by glial cells.

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30
Q

Features of neuro degenerative disorders

A

Features of these infections include
a long incubation period (months to years)
followed by the onset of clinical illness and
progressive deterioration, resulting in death in weeks to months; usually only the CNS is involved.

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31
Q

The postinfectious encephalitis that occurs after measles infections (about one per 1000 cases) and more rarely after rubella infections is characterized by?

A

Autoimmune demyelination without neuronal degeneration.

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32
Q

What are spongiform encephalopathies?

A

group of chronic, p gressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions.

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33
Q

What are prions?

A

Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents.

Some examples of prion” infections are scrapie in sheep, bovine spongiform encephalopathy in cattle and kuru and Creutzfeldt-Jakob disease in humans.

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34
Q

What are the features of the subacute spongiform encephalopathies, typified by scrapie?

A

They are prion diseases. In those i tions, characteristic neuropathologic changes occur, but no inflammatory or immune response is elicited.

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35
Q

Three principles are involved in the production of congenital defects:

A

(1) the ability of the virus to infect the p nant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly (by infection of the fetus) or indirectly (by infection of the mother), resulting in an altered fetal environment (eg, fever).

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36
Q

What causes macules?

A

Macules, which are caused by local dilation of dermal blood vessels, progress to papules if edema and cellular infiltration are present in the area.

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37
Q

How does vesicles and pustules occur?

A

Vesicles occur if the epidermis becomes focally detached, and they become pustules if an inflammatory reaction delivers polymorphonuclear leukocytes to the lesion.

How well did you know this?
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38
Q

How does Hemorrhagic and petechial rashes occur?

A

Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

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39
Q

What are the 2 routes by which viruses gain access to the brain?

A

y the bloodstream (hematogenous spread) and by peripheral nerve fibers (neuronal spread).

How well did you know this?
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40
Q

Pathologic reactions to cytocidal viral infections of the CNS include:

A

necrosis, inflammation, and phagocytosis by glial cells.

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41
Q

Features of neuro degenerative disorders

A

Features of these infections include
a long incubation period (months to years)
followed by the onset of clinical illness and
progressive deterioration, resulting in death in weeks to months; usually only the CNS is involved.

How well did you know this?
1
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2
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42
Q

The postinfectious encephalitis that occurs after measles infections (about one per 1000 cases) and more rarely after rubella infections is characterized by?

A

Autoimmune demyelination without neuronal degeneration.

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

What are spongiform encephalopathies?

A

group of chronic, p gressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions.

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

What are prions?

A

Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents.

Some examples of prion” infections are scrapie in sheep, bovine spongiform encephalopathy in cattle and kuru and Creutzfeldt-Jakob disease in humans.

45
Q

What are the features of the subacute spongiform encephalopathies, typified by scrapie?

A

They are prion diseases. In those i tions, characteristic neuropathologic changes occur, but no inflammatory or immune response is elicited.

46
Q

Three principles are involved in the production of congenital defects:

A

(1) the ability of the virus to infect the p nant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly (by infection of the fetus) or indirectly (by infection of the mother), resulting in an altered fetal environment (eg, fever).

47
Q

What causes macules?

A

Macules, which are caused by local dilation of dermal blood vessels, progress to papules if edema and cellular infiltration are present in the area.

48
Q

How does vesicles and pustules occur?

A

Vesicles occur if the epidermis becomes focally detached, and they become pustules if an inflammatory reaction delivers polymorphonuclear leukocytes to the lesion.

49
Q

How does Hemorrhagic and petechial rashes occur?

A

Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

50
Q

What are the 2 routes by which viruses gain access to the brain?

A

y the bloodstream (hematogenous spread) and by peripheral nerve fibers (neuronal spread).

51
Q

Pathologic reactions to cytocidal viral infections of the CNS include:

A

necrosis, inflammation, and phagocytosis by glial cells.

52
Q

Features of neuro degenerative disorders

A

Features of these infections include
a long incubation period (months to years)
followed by the onset of clinical illness and
progressive deterioration, resulting in death in weeks to months; usually only the CNS is involved.

53
Q

The postinfectious encephalitis that occurs after measles infections (about one per 1000 cases) and more rarely after rubella infections is characterized by?

A

Autoimmune demyelination without neuronal degeneration.

54
Q

What are spongiform encephalopathies?

A

group of chronic, p gressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions.

55
Q

What are prions?

A

Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents.

Some examples of prion” infections are scrapie in sheep, bovine spongiform encephalopathy in cattle and kuru and Creutzfeldt-Jakob disease in humans.

56
Q

What are the features of the subacute spongiform encephalopathies, typified by scrapie?

A

They are prion diseases. In those i tions, characteristic neuropathologic changes occur, but no inflammatory or immune response is elicited.

57
Q

Three principles are involved in the production of congenital defects:

A

(1) the ability of the virus to infect the p nant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly (by infection of the fetus) or indirectly (by infection of the mother), resulting in an altered fetal environment (eg, fever).

58
Q

What causes macules?

A

Macules, which are caused by local dilation of dermal blood vessels, progress to papules if edema and cellular infiltration are present in the area.

59
Q

How does vesicles and pustules occur?

A

Vesicles occur if the epidermis becomes focally detached, and they become pustules if an inflammatory reaction delivers polymorphonuclear leukocytes to the lesion.

60
Q

How does Hemorrhagic and petechial rashes occur?

A

Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

61
Q

What are the 2 routes by which viruses gain access to the brain?

A

y the bloodstream (hematogenous spread) and by peripheral nerve fibers (neuronal spread).

62
Q

Pathologic reactions to cytocidal viral infections of the CNS include:

A

necrosis, inflammation, and phagocytosis by glial cells.

63
Q

Features of neuro degenerative disorders

A

Features of these infections include
a long incubation period (months to years)
followed by the onset of clinical illness and
progressive deterioration, resulting in death in weeks to months; usually only the CNS is involved.

64
Q

The postinfectious encephalitis that occurs after measles infections (about one per 1000 cases) and more rarely after rubella infections is characterized by?

A

Autoimmune demyelination without neuronal degeneration.

65
Q

What are spongiform encephalopathies?

A

group of chronic, p gressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions.

66
Q

What are prions?

A

Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents.

Some examples of prion” infections are scrapie in sheep, bovine spongiform encephalopathy in cattle and kuru and Creutzfeldt-Jakob disease in humans.

67
Q

What are the features of the subacute spongiform encephalopathies, typified by scrapie?

A

They are prion diseases. In those i tions, characteristic neuropathologic changes occur, but no inflammatory or immune response is elicited.

68
Q

Three principles are involved in the production of congenital defects:

A

(1) the ability of the virus to infect the p nant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly (by infection of the fetus) or indirectly (by infection of the mother), resulting in an altered fetal environment (eg, fever).

69
Q

What causes macules?

A

Macules, which are caused by local dilation of dermal blood vessels, progress to papules if edema and cellular infiltration are present in the area.

70
Q

How does vesicles and pustules occur?

A

Vesicles occur if the epidermis becomes focally detached, and they become pustules if an inflammatory reaction delivers polymorphonuclear leukocytes to the lesion.

71
Q

How does Hemorrhagic and petechial rashes occur?

A

Hemorrhagic and petechial rashes occur when there is more severe involvement of the dermal vessels.

72
Q

What are the 2 routes by which viruses gain access to the brain?

A

y the bloodstream (hematogenous spread) and by peripheral nerve fibers (neuronal spread).

73
Q

Pathologic reactions to cytocidal viral infections of the CNS include:

A

necrosis, inflammation, and phagocytosis by glial cells.

74
Q

Features of neuro degenerative disorders

A

Features of these infections include
a long incubation period (months to years)
followed by the onset of clinical illness and
progressive deterioration, resulting in death in weeks to months; usually only the CNS is involved.

75
Q

The postinfectious encephalitis that occurs after measles infections (about one per 1000 cases) and more rarely after rubella infections is characterized by?

A

Autoimmune demyelination without neuronal degeneration.

76
Q

What are spongiform encephalopathies?

A

group of chronic, p gressive, fatal infections of the CNS caused by unconventional, transmissible agents called prions.

77
Q

What are prions?

A

Prions are not viruses, but are proteins whose structural alterations can cause conformational changes in host proteins leading to aggregation and dysfunction, and are transmissible similar to other infectious agents.

Some examples of prion” infections are scrapie in sheep, bovine spongiform encephalopathy in cattle and kuru and Creutzfeldt-Jakob disease in humans.

78
Q

What are the features of the subacute spongiform encephalopathies, typified by scrapie?

A

They are prion diseases. In those i tions, characteristic neuropathologic changes occur, but no inflammatory or immune response is elicited.

79
Q

Three principles are involved in the production of congenital defects:

A

(1) the ability of the virus to infect the p nant woman and be transmitted to the fetus;
(2) the stage of gestation at which infection occurs;
(3) the ability of the virus to cause damage to the fetus directly (by infection of the fetus) or indirectly (by infection of the mother), resulting in an altered fetal environment (eg, fever).

80
Q

What are the primary viruses responsible for congenital defects in humans?

A

Rubella virus and CMV

Congenital infections can also occur with herpes simplex, varicella-zoster, hepatitis B, measles, and mumps virus, as well as with HIV, parvovirus, and some enteroviruses

81
Q

Effects of utero infections include?

A

fetal death
premature birth
intrauterine growth retardation
persistent postnatal infection.

82
Q

Developmental malformations in utero infections include?

A 
Congenital heart defects
cataracts
deafness
microcephaly
limb hypoplasia
83
Q

What are Viral infection and multiplication effects on fetal cells ?

A

It may destroy rapidly replicating fetal cells or alter cell function.

Lytic viruses, such as herpes simplex, may result in fetal death. Less cytolytic viruses, such as rubella, may slow the rate of cell division.

84
Q

What are the specific age groups for major impact of the following viruses?
Rubella virus
Rotavirus
St. Louis encephalitis

A

rubella is most serious during gestation;

rotavirus is most serious for infants

St. Louis encephalitis is most serious in elderly adults.

85
Q

Mode of action of Rapid antigen detection methods

A

Rapid antigen detection methods use virus-specific monoclonal antibodies for detection.

86
Q

Mode of action for Nucleic acid or polymerase chain reaction (PCR) tests

A

They make use of specific primers and probes to detect viral nucleic acid.

The PCR tests can be multiplexed, allowing detection of multiple viruses concurrently.

87
Q

Use of Virus culture and serological test

A

Virus culture and serological testing for specific antibody responses are slow to provide results but are useful for epidemiologic and research studies

88
Q

virus-specific functions that can serve as targets for antiviral therapy includes;

A

Stages during viral infections that could be targeted include:

1) attachment of virus to host cells
2) uncoating of the viral genome
3) viral nucleic acid synthesis
4) translation of viral proteins, and
5) assembly and release of progeny virus particles

89
Q

Mode of action for Nucleoside and Nucleotide Analogs

A

They inhibit nucleic acid replication by inhibition of viral polymerases essential for nucleic acid replication.

In addition, some analogs are incorporated into the nucleic acid as chain terminators and block further synthesis.

90
Q

Mechanism of action for Nonnucleoside reverse transcriptase inhibitors

A

It acts by binding directly to virally encoded reverse transcriptase and inhibiting its activity.

However, resistant mutants emerge rapidly, making it useful only in the context of multidrug therapy.

91
Q

Mechanism is of action for Protease inhibitors

A

Such drugs inhibit the viral protease that is required at the late stage of the replicative cycle to cleave the viral gag and gag-pol polypeptide precursors to form the mature virion core and activate the reverse transcriptase that will be used in the next round of infection.

Protease inhibitors have been used successfully for treatment of HIV and HCV infections.

92
Q

Mechanism of integrase inhibitors

A

blocks the activity of viral integrase, a key enzyme in HIV replication.

Without integration of virally encoded DNA into the host chromosome, the life cycle cannot continue

93
Q

Mechanism of action for Fusion Inhibitors

A

HIV fusion inhibitors act by disrupting the fusion of viral envelope with the cell membrane, preventing cellular infection.

The prototype agent, enfuvirtide, is a peptide that binds to gp41 and blocks the required conformational change that initiates membrane fusion.

94
Q

The purpose of viral vaccine

A

The purpose of viral vaccines is to use the adaptive immune response of the host to prevent viral disease

95
Q

Immunity to viral infection is based on what?

A

based on the development of an immune response to specific antigens located on the surface of virus particles or virus-infected cells.

96
Q

Mucosal i nity (local IgA) is important in resistance to what type of infection?

A

It is important in resistance to infection by viruses that replicate in mucosal membranes (rhinoviruses, influenza viruses, rotaviruses) or invade through the mucosa (papillomavirus).

97
Q

serum IgG antibodies is important for what type of infection?

A

Viruses that have a viremic mode of spread (polio, hepatitis A and B, yellow fever, varicella, mumps, measles)

98
Q

Cell-mediated immunity also is involved in what type of infection?

A

involved in protection against systemic infections (measles, herpes).

99
Q

What characteristics of a virus or of a viral disease may complicate the generation of an effective vaccine.?

A

The existence of many serotypes, as with rhinoviruses

large numbers of antigenic variants in animal reservoirs, as with influenza virus

integration of viral DNA into host chromosomal DNA (retroviruses)

infection of cells of the host’s immune system (HIV).

100
Q

How are Inactivated or killed-virus vaccines made?

A

made by purifying viral preparations to a certain extent and then inactivating viral infectivity in a way that does minimal damage to the viral structural proteins; mild formalin treatment is frequently used.

101
Q

What does Killed-virus vaccines stimulate in the body?

A

stimulate the development of circulating antibody against the coat proteins of the virus, conferring some degree of resistance to that virus strain.

102
Q

Advantages of inactivated vaccines include?

A

there is no reversion to virulence by the vaccine virus

vaccines can be made when no acceptable attenuated virus is available.

103
Q

Disadvantages of killed-virus vaccines include?

A

relatively brief immunity requiring boosting shots to maintain effectiveness

poor cell-mediated response

occasional hypersensitivity to subsequent infection.

104
Q

Attenuated Live-Virus Vaccines makes use of what?

A

It uses virus mutants that antigenically overlap with wild-type virus but are restricted in some step in the pathogenesis of disease

105
Q

Advantages of Attenuated live-virus vaccines

A

Acts more like the natural infection with regard to their effect on immunity.

They multiply in the host and tend to stimulate longer-lasting antibody production

induce a good cell-mediated response

and induce antibody production and resistance at the portal of entry

106
Q

Disadvantages of attenuated live-virus vaccines include

A

risk of reversion to greater virulence

severe infection in immunocompromised hosts

limited storage and shelf life in some cases

Additionally, unrecognized adventitious agents have been found in vaccine stocks (eg, simian polyomavirus SV40, porcine circovirus).

107
Q

Immunoglobulins produced in killed vaccine is ?

A

IgG

108
Q

Immunoglobulins produced in live virus vaccine

A

IgA and IgG

MICRObio@123 (3 decks)

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