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(4) VMCB > Lesson 2: Pathogenesis of viral infections > Flashcards

Lesson 2: Pathogenesis of viral infections Flashcards

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1
Q

the production of disease as a result of viral infection

A

Viral pathogenesis

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2
Q

concerned with the cellular events and pathological mechanisms that connect the virus to cell/tissue/organ damage and the resulting clinical signs.

A

Viral pathogenesis

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3
Q

It refers to the relative ability of viruses to produce disease in a host

A

Virulence

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4
Q

It is dependent on the attributes of both the virus and its host

A

Virulence

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5
Q

The following factors influence virulence

A

> dose and route of entry of the virus and the species
age
immune status of the host

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6
Q

Routes of infection

A

> Skin: Breaks in skin epithelia
Respiratory tract: Mucous membranes
Alimentary tract: through ingestion, some resp. viruses enter the oral cavity by ciliated epithelium
Genital tract: abrasion in the urethral, anal, or vaginal mucosa (venereal tumors)
In utero (congenital diseases)

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7
Q

some respiratory viruses enter the oral cavity by _________.

A

ciliated epithelium

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8
Q

abrasion in urethral, anal, or vaginal mucosa causes what?

A

venereal tumors

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9
Q

In utero causes

A

congenital diseases

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10
Q

Stages of viral infection

A
  1. Initiation of Infection at Primary Site (Infection of the Target Tissue)
  2. Replication of Virus and Spread to Secondary Site
  3. Manifestations of the viral diseases
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11
Q

many viruses cause infection in these sites

A

oral mucosa or upper respiratory tract

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12
Q

Replication of viruses at these sites may be accompanied by clinical symptoms

A

primary sites

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13
Q

some viruses may disseminate to other tissues through these secondary sites and cause a systemic infection

A

bloodstream, lymphatic system, and
neurons

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14
Q

Transport of virus in the blood

A

viremia

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15
Q

It is when the virus enters the bloodstream after multiplication in the lymph nodes.

A

Primary viremia

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16
Q

Primary viremia is when the virus enters the
bloodstream after multiplication in this organ

A

lymph nodes

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17
Q

When the virus replicate in the macrophages and in these organs, it will result in massive production of viruses causing secondary viremia signaling the onset of clinical signs

A

> endothelial lining of blood vessels
spleen
liver

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18
Q

Manifestations of the viral diseases are dependent on the virulence of the virus and host factors: ENUMERATE

A

a) Age, general health and immune status of the host
b) Dose of infective virus
c) Genetics of host and the virus.

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19
Q

It is the time taken by the virus to spread from the site of entry to the organs of viral replication and then to the target organs for production of lesions.

A

Incubation period

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20
Q

incubation period may be short (1-3 days) because site of entry of the virus and lesions are the same

A

local infections

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21
Q

may have longer incubation periods (usually 10-20 days) because lesions are produced far from the site of entry

A

systemic infection

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22
Q

Severity of viral infections

A

a) inapparent infection
b) acute infection
c) chronic or persistent infection

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23
Q

(a) the infection is controlled before the virus reaches the target tissues,
(b) the infected tissue is not damaged,
(c) the tissue is damaged but it is rapidly repaired, or
(d) the severity of damage is below a functional threshold for the particular disorder.

A

inapparent infection

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24
Q

occurs when the immune system acts rapidly to
control the infection

A

acute infection

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25
when the immune system fails to act effectively or slowly, it may result in chronic viral disease or persistent viral infection in the case of slow viruses that takes years before progressing to manifestation of the disease
chronic or persistent infection
26
Types of host cell in terms of virus-host interaction:
1. Permissive cell 3. Semipermissive cell 2. Nonpermissive cell
27
a cell that allows replication of a particular type of strain of virus by providing biosynthesis compounds, such as transcriptional factors and posttranslational enzymes
Permissive cell
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a cell which does not provide any biosynthesis compound, hence does not support replication of the viruses.
Nonpermissive cell
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a cell that may support some but not all the stages in viral infection
Semipermissive cell
30
Ion channel blockers
Uncoating
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is the interval from invasion of the host to the development of clinical signs
incubation period
32
Cellular changes resulting from replication of virus:
1. Cell death (cytocidal effect) 2. Cell lysis (cytolysis) 3. Transformation of cells (to malignant cells) 4. Alteration in cell’s morphology, functions or antigenicity 5. Steady state of infection without causing injury to the host cell 6. Cytopathic effects (cell culture)
33
Cytopathic effects (cell culture) examples
negri bodies in the cytoplasm of rabies virus infected cell
34
Types of virus infection at cellular level:
1. Abortive infection 2. Lytic infection 3. Persistent viral infection
35
Types of virus infection at cellular level: failed infection
Abortive infection
36
Types of virus infection at cellular level: results to cell death
Lytic infection
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Types of virus infection at cellular level: infection without cell death
Persistent viral infection
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(a) nonlytic and productive (chronic), (b) latent, limited production of viral macromolecules in the absence of synthesis of virus (c) recurrent (d) transforming
Persistent viral infection
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no progeny viruses are produced
Abortive viral infection
40
where the host cell is not killed, although progeny virus is released
Productive viral infection
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Mechanisms used by virus to cause cell death
1. Inhibition of cellular protein synthesis 2. Cell fusion 3. Transformation 4. Cytopathic effect
42
Inhibition of cellular protein synthesis GIVE EXAMPLES OF VIRUSES THAT HAVE THIS MECHANISM
(HPPT) HSV poliovirus poxviruses togaviruses
43
A mechanism during replication produce proteins that inhibit synthesis of cellular DNA and/or RNA.
Inhibition of cellular protein synthesis
44
A mechanism wherein infections of cells with certain viruses results in the expression of glycoproteins on the cell surface causing the cells to fuse, in the production of giant multinucleated cells called syncytia (ex: paramyxoviruses, herpes viruses, and retroviruses)
Cell fusion
45
Cell fusion GIVE EXAMPLES OF VIRUSES THAT HAVE THIS MECHANISM
(RPH) retroviruses paramyxoviruses herpes viruses
46
giant multinucleated cells
syncytia
47
A mechanism wherein an irreversible genetic process caused by the integration of viral DNA with the DNA of the host cell transforming normal cells to malignant cells. The viruses that stimulate uncontrolled cell growth causing the transformation of immortalization of the cell are known as oncogenic viruses.
Transformation
47
Transformation of immortalization of the cell are known as
oncogenic viruses
48
is a term that denotes any visible change in the appearance of target cells infected by viruses
Cytopathic effect (CPE)
49
are the intracytoplasmic eosinophilic inclusion bodies in the neural cells and are pathognomonic of rabies
Negri bodies
50
are small, multiple inclusions found in vaccinia-infected cells.
Guarnieri bodies
51
are large inclusions seen in fowl
Bollinger bodies
52
are very large inclusion bodies seen in the molluscum contagiosum infected cell
Molluscum bodies
53
Release of viral progeny from the apical surface of mucosal cells favours what type of infection
localized infection
54
release of virus from the basal surface into subepithelial tissues facilitates what type of infection
systemic infection
55
virus is either free in the plasma (ex: parvovirus or picornavirus) or associated with circulating cells (ex: Marek’s disease virus, canine distemper virus) and is passively transported into distant sites of the body to settle and replicate
Haematogenous spread
56
viruses are either free in the plasma
(PP) parvovirus or picornavirus
57
viruses associated with circulating cells
(MC) Marek’s disease virus Canine distemper virus
58
Neurotropic viruses such as rabies virus, Aujeszky’s disease virus and Borna disease virus can invade the central nervous system (CNS) through peripheral nerves
Neural spread
59
2 types of virus spread
1. Haematogenous spread 2. Neural spread
60
also occurs when older animals are more susceptible to infections than younger animals
reverse age resistance
61
viruses that also target the cells of the immune system that can lead either to an immunodeficient state or hypersensitivity of the immune system particularly in persistent viral infections
infectious bursal disease
62
Infection early in gestation - results in?
foetal death (resorption or abortion)
63
infection occurs at a later stage - results to?
congenital defects
64
TRUE or FALSE Infection towards the end of pregnancy - induces a protective immune response
TRUE
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sheds enteric viruses
Faeces
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Arthropod vectors for these viruses
arboviruses
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highly contagious virus
influenza virus
68
viruses capable of surviving for long periods in the environment
parvoviruses, poxviruses and many enteric viruses
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present shedding of large amounts of virus over a short period.
Acute infection
70
These viruses are either highly contagious or capable of surviving for long periods in the environment
Acute infection
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present constant or intermittent shedding at low levels. Infections of this type, produced by lentiviruses, jaagsiekte sheep retrovirus and prions, have a progressive clinical course, usually resulting in death
Persistent or chronic viral infections
72
are characterized by persistence of the virus in a non-productive form, either integrated into the genome of the host (ex: retrovirus, or as an episome, in the case of herpesviruses).
Latent infections
73
viruses which produce productive infections in epithelial cells and latent infections in sensory neurons
alphaherpesviruses, such as feline herpesvirus 1
74
occurs from a common source, for example, infected food, and is seen only in clusters of people
Outbreak
75
occurs due to introduction of a new strain of virus into an immunologically susceptible population, e.g., influenza epidemic
Epidemic
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resulting from introduction of a new strains virus, e.g., HIV
Pandemic
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usual reservoir, serves as source of infection for other susceptible hosts
Human reservoir
78
infected animals transmit viral infection to humans termed as zoonotic viral diseases
Animal reservoir
79
some arthropods act as vectors for transmission of viruses (arboviruses)
Arthropod-vectors
80
are also important source of infection, virus are shed before the onset of clinical signs
Asymptomatic patients
81
transmission of picornavirus and reovirus
fecal–oral route
82
type of virus usually transmitted by respiratory droplets, saliva, mucus, blood or semen, organ transplantation, and by ingestion, instead of fecal–oral route where they can be destroyed rapidly in the gastrointestinal tract of the infected humans/animals due to presence of acid (except Hepatitis B virus and coronavirus)
enveloped viruses
83
are sturdy viruses which can resist drying, extremes of pH and temperature, and the effects of detergents
naked viruses or nonenveloped viruses
84
Prevention of Viral Diseases
a) Adoption of good hygiene b) control of the vectors c) by immunization of the population (herd immunity via vaccines)
84
Therefore, these viruses are generally transmitted by the respiratory and fecal–oral routes and also often by contaminated objects (fomites).
naked viruses or nonenveloped viruses
85
arthropod-borne viruses
Arboviruses
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are defined as viruses maintained in nature through biological transmission between vertebrate hosts by haematophagous arthropods. The viruses multiply in the tissues of the arthropod vector (ex: mosquitoes, ticks, sandflies and midges) which remains infected for life. Domestic animals and humans are generally ‘deadend’ hosts as they do not develop sufficient viraemia to contribute to the transmission of
Arboviruses
87

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