LESSON 2: PATHOGENESIS of viral infections Flashcards

1
Q

the production of disease as a result of viral infection, is
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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2
Q

refers to the relative ability of viruses to produce disease in a host,
dependent on the attributes of both the virus and its host,

A

Virulence

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2
Q

and is influenced by
factors such as the

A

-dose and route of entry of the virus
and the species,
- age and
- immune status of the host.

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3
Q

Routes of infection:
 Skin

A

Breaks in skin epithelia

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3
Q

Respiratory tract: M

A

Mucous membranes

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4
Q

Genital tract:

A

abrasion in urethral, anal or vaginal mucosa (venereal tumors)

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5
Q

Alimentary tract: through

A

ingestion, some resp. viruses enter the oral cavity by
ciliated epithelium

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6
Q

Stages of viral infection

A

1.Initiation of Infection at Primary Site (Infection of the Target Tissue):

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7
Q

In utero

A

(congenital diseases)

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8
Q

: some viruses may
disseminate to other tissues through blood stream, lymphatic system, and
neurons (secondary sites) and cause a systemic infection.

A

Replication of Virus and Spread to Secondary Site

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9
Q

(secondary sites) and cause a

A

systemic infection

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10
Q

Transport of virus in
the blood is known as v

A

viremia

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10
Q

is when the virus enters the
blood stream after multiplication in the lymph nodes.

A

Primary viremia

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11
Q

When virus replicate in the macrophages, in the endothelial lining of blood vessels, or in the spleen and liver it will result in
massive production of viruses causing

A

secondary viremia

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12
Q

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

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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13
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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14
Q

Severity of viral infections:

A

 inapparent infection
 acuteinfection
 chronic or persistent infection:

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14
Q

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

A

systemic infections

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15
Q

occurs when immune system acts rapidly to
control the infection

A

acuteinfection

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15
Q

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.

A

acuteinfection:

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16
Q

Types of host cell in terms of virus-host interaction:

A
  1. Permissive cell:
  2. Nonpermissive cell
  3. Semipermissive cell:
    :
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17
Q

a cell that allows replication of a particular type of strain of
virus by providing biosynthesis compounds, such as transcriptional factors and
posttranslational enzymes

A

Permissive cell:

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18
Q

a cell which does not provide any biosynthesis
compound, hence does not support replication of the viruses

A

Nonpermissive cell

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19
Q

Cellular changes resulting from replication of virus:
1. Cell death

A

(cytocidal effect)

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20
Q

a cell that may support some but not all the stages in
viral infection

A

Semipermissive cell

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21
Q

. Cell lysis

A

(cytolysis)

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22
Q
  1. Cytopathic effects (cell culture) ex: n
A

negri bodies in the cytoplasm of rabies virus infected cells

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22
Q
  1. Transformation of cells
A

(to malignant cells)

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23
Q

Types of virus infection at cellular level:

A
  1. Abortive infection: failed infection
  2. Lytic infection: results to cell death
  3. Persistent viral infection: infection without cell death
    a) nonlytic and productive (chronic),
    b) latent, limited production of viral macromolecules in the absence of
    synthesis of virus
    c) recurrent
    d. transforming
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24
Q

Infections of cells with certain viruses results in the expression of
glycoproteins on the cell surface causing the cells to fuse, g in the production of giant
multinucleated cells called

A

syncytia

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24
Q

Mechanisms used by virus to cause cell death:

A
  1. Inhibition of cellular protein synthesis
  2. Cell fusion:
  3. Transformation
  4. Cytopathic effect
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25
Q

examples : during replication produce proteins that inhibit synthesis of cellular DNA
and/or RNA

A

HSV, poliovirus, togaviruses, and
poxviruses)

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26
Q

Cell fusion (ex:

A

paramyxoviruses, herpes viruses, and
retroviruses).

26
Q

an irreversible genetic process caused by the integration of viral
DNA with the DNA of the host cell transforming normal cells to malignant cells.

A

Transformation

27
Q

The
viruses that stimulate uncontrolled cell growth causing the transformation of
immortalization of the cell are

A

oncogenic viruses

28
Q

is a term that denotes any visible
change in the appearance of target cells (ex:appearance of inclusion bodies)
infected by viruses.

A

Cytopathic effect:

29
Q

presence of such bodies facilitates laboratory diagnosis:

A

■ Negri bodies
- Guarnieri bodies
■ Bollinger bodies
■ Molluscum bodies

30
Q

are the intracytoplasmic eosinophilic inclusion bodies in the
neural cells and are pathognomonic of rabies

A

Negri bodies

31
Q

are small, multiple inclusions found in vaccinia-infected
cells.

A

Guarnieri bodies

32
Q

are large inclusions seen in fowl pox.

A

■ Bollinger bodies

33
Q

are very large inclusion bodies seen in the molluscum
contagiosum infected cell

A

■ Molluscum bodies a

34
Q

localized infection in tubular structures such as the air passages and the intestine
release

A

as the air passages and the intestine

35
Q

l tissues facilitates
systemic infection.

A

basal surface into subepithelial tissues

36
Q

However, the preferential use of one route of spread does not
necessarily exclude spread by other routes

A
  1. Haematogenous spread:
  2. Neural spread
37
Q

virus is either free in the plasma (ex:

A

parvovirus or
picornavirus

37
Q

associated with circulating cells ex:

A

Marek’s disease virus, canine
distemper virus)

37
Q

Neurotropic viruses such as rabies virus, Aujeszky’s
disease virus and Borna disease virus can invade the central nervous system (CNS)
through peripheral nerves.

A
  1. Neural spread;
38
Q

virus is either free in the plasma or associated with circulating cells and is passively transported into distant sites of the body to settle
and replicate

A
  1. Haematogenous spread:
39
Q

the clinical manifestations of viral diseases depend on complex
interaction of virus and host factors such as:

A

-age,
-general health, and
-immune status of the person, the
-dose of the infective virus, the
-genetics of the host and
-virus.

40
Q

also occurs when older animals are
more susceptible to infections than younger animals

A

reverse age resistance

41
Q

There are 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 (ex:

A

(ex: infectious bursal disease).

42
Q

results to congenital defects

A

 Infection occurs at a later stage

43
Q

usually indicative of substantial damage to
the tissues of the placenta or foetus

A

Abortion following viral infection

43
Q

The effect on the foetus is often influenced by
the stage of gestation and by the virulence of the virus:

A

 Infection early in gestation
 Infection occurs at a later stage
 Infection towards the end of pregnancy

44
Q

results in foetal death (resorption or abortion)

A

 Infection early in gestation

45
Q

induces a protective immune
response

A

 Infection towards the end of pregnancy

46
Q

Routes by which viruses are shed:

A
  1. Coughing and sneezing: transmit virus in aerosol
  2. Faeces: sheds enteric viruses
    . Body fluids such as saliva, semen, urine and milk may contain particular
    viruses
  3. Arthropod vectors for arboviruses
  4. Surgical procedures for some blood-borne viruses
  5. Transplacental route or via birth canal
  6. DNA of germ cells
47
Q

The shedding of infectious virions from surfaces or orifices via

A

aerosols,
droplets, scabs, body fluids, excretions and secretions (saliva, blood, semen, milk,
urine, faeces)

48
Q

present shedding of large amounts of virus over a short period.

A

Acute infection

48
Q

capable of
surviving for long periods in the environment ex:

A

parvoviruses, poxviruses and
many enteric viruses)

48
Q

These viruses are either highly contagious (

A

(influenza virus)

49
Q

present constant or intermittent shedding at low levels

A

Persistent or chronic viral infections

50
Q

are characterized by persistence of the virus in a non
productive form, either integrated into the genome of the host

A

Latent infections

51
Q

infections of this type, produced by

A

lentiviruses,
jaagsiekte sheep
retrovirus and
prions,

52
Q

Latent infections ex:

A

(ex: retrovirus, or
as an episome, in the case of herpesviruses).

53
Q

Periodic reactivation of productive infection with shedding of infectious virus may
occur (ex:

A

alphaherpesviruses, such as feline herpesvirus 1,

54
Q

which produce
productive infections in epithelial cells and latent infections in sensory neurons).

A

alphaherpesviruses, such as feline herpesvirus 1,

55
Q

occurs from a common source, for example, infected food,
and is seen only in clusters of people

A

Outbreak

56
Q

occurs due to introduction of a new strain of virus into an
immunologically susceptible population, e.g.,

A

influenza epidemic

57
Q

resulting from introduction of a new strains virus, e.g.

A

HIV

58
Q

usual reservoir, serves as source of infection for
other susceptible hosts

A

a) Human reservoir

58
Q

infected animals transmit viral infection to humans
termed as

A

zoonotic viral diseases

59
Q

some arthropods act as vectors for transmission of
viruses –

A

(arboviruses)

60
Q

. Respiratory viruses are secreted in
aerosol droplets, hence are transmitted by

A

inhalation

60
Q

enteric viruses are
excreted in the feces and are transmitted by fecal–oral route (e.g.,

A

(e.g.,picornavirus and reovirus).

61
Q

must be intact to retain
infectivity; they are 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

A

enveloped viruses expect 9 HEPARITIS B and corona virus)

62
Q

are sturdy viruses
which can resist drying, extremes of pH and temperature,
and the effects of detergents.

A

naked viruses

63
Q

Therefore, these viruses are
generally transmitted by the respiratory and fecal–oral routes
and also often by contaminated objects

A

(fomites)

64
Q

Arboviruses: (arthropod-borne viruses) are defined as viruses maintained in
nature through biological transmission between vertebrate hosts by

A

haematophagous arthropods

64
Q

 Prevention of Viral Diseases

A

a) Adoption of good hygiene
b) control of the vectors
c) byimmunization of the population (herd immunity via vaccines

65
Q

The viruses multiply in the tissues of the arthropod
vector (ex: m

A

mosquitoes, ticks, sandflies and midges) which remains infected for
life.

66
Q

Domestic animals and humans are generally —-’ hosts as they do not
develop sufficient viraemia to contribute to the transmission of the virus.

A

deadend