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IMMUNE 1 LEC > VIRAL INFECTIONS CONT. & HEPATITIS > Flashcards

VIRAL INFECTIONS CONT. & HEPATITIS Flashcards

1
Q
A

 Viral Hepatitis
 HIV
 Dengue
 Herpes Virus infections: infectious mononucleosis, Epstein Barr Virus, Cytomegalovirus

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2
Q

Submicroscopic particle (size is measured in nanometers)

A

VIRUSES

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3
Q

VIRUSES Basic Structure:

A

core of DNA or RNA

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4
Q

Intracellular pathogens

A

VIRUSES

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5
Q

First line of protection (nonspecific immunity)

A

INNATE IMMUNITY AGAINST VIRUSES

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6
Q

Interferon-a and Interferon-b

A

INNATE IMMUNITY AGAINST VIRUSES

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7
Q

Inhibits viral replication

A

Interferon-a and Interferon-b

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8
Q

Enhances activity of NK cells

A

Interferon-a and Interferon-b

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9
Q

B cells and plasma cells

A

HUMORAL DEFENSE

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10
Q

Produces virus specific antibodies

A

HUMORAL DEFENSE

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11
Q

Ab prevents spread of viral replication through neutralization

A

HUMORAL DEFENSE

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12
Q

: promotes phagocytosis thru opsonization

A

IgG

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13
Q

: Agglutinates viral particles

A

IgM

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14
Q

Upon activation of [?], CD8+ Cytotoxic T cells (CTL) become programmed to expand in number and attack the virus-infected cells.

A

CD4+ T helper cells and cytokines

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15
Q

Cytotoxic T cells (CTL) produce

A

proteins and proteases

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16
Q
  • pore forming protein, bubutasan nila ung host cell. It will create a pore in the membrane of the host cell.
A

Perforin

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17
Q
  • they will now enter the pore and will activate apoptosis
A

Granzymes

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18
Q

Increase [?] its original number

A

50,000 times out of

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19
Q

Produces new viral antigens – not recognized immediately by initial immune response

A

They undergo frequent genetic mutations

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20
Q

Ex. Covid-19

Frequently undergo genetic mutation due to presence of nucleic acids

Production of new viral antigens that are not recognized immediately by the innate immune response

A

They undergo frequent genetic mutations

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21
Q

For example, the Hepatitis C virus (HCV) can block the degradation of viral RNA that is induced by interferons.

A

Some viruses can evade actions of the component of the immune response

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22
Q

For example, cytomegalovirus and human immunodeficiency virus can reduce the expression of major histocompatibility complex molecule on the surface of virus infected cells making them less likely to be recognized by B cells

A

Viruses can evade the hosts defense by suppressing the immune system

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23
Q

STRATEGIES ON HOW VIRUSES ESCAPES IMMUNE MECHANISMS

A

They undergo frequent genetic mutations

Some viruses can evade actions of the component of the immune response

Viruses can evade the hosts defense by suppressing the immune system

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24
Q

LABORATORY TESTING FOR VIRAL INFECTION 

A

Serologic testing

Molecular assays

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25
Q

– monitors the course of infection, detects past infection, can assess immune status

A

Serologic testing

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26
Q

Indicates current or recent infection or acute infection

A

Specific IgM antibody

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27
Q

[?] in newborns indicates congenital infection with virus

A

Specific IgM antibody

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28
Q

Indicates current or past infection and in most cases immunity

A

IgG antibodies

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29
Q

[?] in newborns are mainly maternal antibodies

A

IgG antibodies

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30
Q

can cross the placenta; thus normal

A

IgG

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31
Q

Demonstrated using [?] (compound for bacteria)

A

electron microscope

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32
Q

DNA or RNA is packed in [?] and some virus’s capsid is surrounded by outer envelope such as glycolipids and proteins.

A

protein coat or capsid

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33
Q

 They are going to rely on host cells for replication and survival.

A

Intracellular pathogens

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34
Q

No host =

A

dormant

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35
Q

[?]infects the host cell by attaching to specific receptors in their target cells

A

Virion

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36
Q

It penetrates the cell membrane

A

Virion

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37
Q

directs the host cell machinery to produce more viral nucleic acid and proteins

A

Release of nucleic acid (RNA or DNA)

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38
Q

assemble inside the cell to form the intact virus, which is released thru cell lysis or budding of the cell surface

A

Release of nucleic acid (RNA or DNA)

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39
Q

Viruses destroy the cells leading to [?]

A

decreased cell count

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40
Q

Target cell:

A

CD4 T cells

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41
Q

(virus-infected cells; produced in the recognition of TLRs)

A

Interferon-a and Interferon-b

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42
Q

By inducing transcription of several genes that will code for proteins w/ antiviral activity

A

Inhibits viral replication

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43
Q

Binds virus-infected cells and release cytotoxic proteins like perforin (substance that create pores) and granzymes

A

Enhances activity of NK cells

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44
Q

– primary cells involved of humoral defense

A

B cells and plasma cells

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45
Q

antibodies specific for a component of the virus that binds to a receptor on the host cell membrane will bind to the virus and prevent it from attaching to and penetrating the cell

A

Produces virus specific antibodies

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46
Q

neutralize viruses in the mucosal surfaces

A

Secretory IgA antibodies

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47
Q

can bind to viruses in the bloodstream and inhibit dissemination of the infection.

A

IgM and IgG antibodies

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48
Q

promote phagocytosis of viruses through their opsonizing activity

A

IgG antibodies

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49
Q

can also inactivate viral particles by agglutinating them.

A

IgM antibodies

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50
Q

also activate complement

A

IgG and IgM antibodies

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51
Q

leading to elimination of intracellular viruses required for replication

A

Cytotoxic T cells (CTL)

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52
Q

General term for inflammation of the liver

A

HEPATITIS

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53
Q

([?]– liver,[?] – inflammation)

A

hepa; itis

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54
Q

T or F

Most people though that the cause of hepatitis is virus but there are also other causes

A

T

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55
Q

HEPATITIS Causes:

A

viral infection, chemicals, ionizing radiation and autoimmune process

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56
Q

HEPATITIS TWO STAGES

A

Acute stage
Progressive/Chronic stage

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57
Q

: General flu like symptoms

A

Acute stage

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58
Q

Hepatomegaly (enlargement of the liver)

A

Progressive/Chronic stage

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59
Q

jaundice (yellowish discoloration of the skin)

A

Progressive/Chronic stage

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60
Q

dark urine (due to increase of urobilinogen passing through urine)

A

Progressive/Chronic stage

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61
Q

light feces (due to increase of stercobilin)

A

Progressive/Chronic stage

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62
Q

(enlargement of the liver)

A

Hepatomegaly

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63
Q

(yellowish discoloration of the skin)

A

jaundice

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64
Q

dark urine (due to increase of [?] passing through urine)

A

urobilinogen

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65
Q

light brown feces (due to increase of [?])

A

stercobilin

66
Q

INITIAL LABORATORY TEST

A

Elevations in bilirubin and liver enzymes (ALT)

67
Q

Non-enveloped, single stranded RNA virus.

A

HEPATITIS A VIRUS

68
Q

They belong to the Hepatovirus genus of Picornaviridae family.

A

HEPATITIS A VIRUS

69
Q

It is responsible for tens of millions of hepatitis A virus infection worldwide.

A

HEPATITIS A VIRUS

70
Q

MOT: fecal-oral route, close person to person contact, and ingestion of contaminated food.

A

HEPATITIS A VIRUS

71
Q

This may be due to poor sanitation, poor hygiene, and overcrowding.

A

HEPATITIS A VIRUS

72
Q

The infection caused do not usually progress to chronic stage, only to acute stage.

A

HEPATITIS A VIRUS

73
Q

Symptoms are usually self-limiting, typically result within two months.

A

HEPATITIS A VIRUS

74
Q

DIAGNOSIS: Demonstration of [?] to HAV

A

IgM antibodies

75
Q

Detected by Solid phase antibody-capture enzyme immunoassay

A

HEPATITIS A VIRUS

76
Q

Detectable on the onset of clinical symptom (present infection)

A

HEPATITIS A VIRUS

77
Q

TEST for TOTAL HAV detects [?]

A

IgG

78
Q

Competitive inhibition EIA format

A

HEPATITIS A VIRUS

79
Q

Major cause of mortality and morbidity worldwide.

A

HEPATITIS B VIRUS

80
Q

WHO estimated about 500,000 to 1.2 million deaths each year due to liver disease.

A

HEPATITIS B VIRUS

81
Q

Highly endemic in far east, middle east, and subSaharan Africa & amazon.

A

HEPATITIS B VIRUS

82
Q

HEPATITIS B VIRUS MOT:

A

Parenteral route by contaminated blood (main) and Sexual transmission by semen, vaginal secretion, and saliva

83
Q

It also has something to do with the production of antigens and antibodies when it comes to HBV infection.
Mnemonic:

A

SEC-CES

84
Q

The first 3 letters will denote the [?] and the last 3 letters denote [?].

A

antigen

antibodies

85
Q

For the letters SEC:

A

surface antigen
envelope antigen
core antigen

86
Q

For the last 3 letters CES:

A

core antigen
envelope antigen
surface antigen

87
Q

INCUBATION PERIOD HEPATITIS B VIRUS

A

Average (8-13 weeks)

88
Q

The time between being exposed to the viral hepatitis and showing the first symptoms.

A

HBV ACUTE INFECTION

89
Q

2 weeks- 3 months

A

HBV ACUTE INFECTION

90
Q

So the 1st antigen to produce is surface

A

HBV ACUTE INFECTION

91
Q

Next antigen produced is the envelope antigen.

A

HBV ACUTE INFECTION

92
Q

Lastly, core antigen is produced.

A

HBV ACUTE INFECTION

93
Q

3-6 months

A

HBV EARLY RECOVERY

94
Q

HBV EARLY RECOVERY

First Ab produced is [?] followed shortly by [?]

Then, [?]. Maproduced na kasabay ng pagdecline ng Ag.
Lastly, [?].

A

Anti-HBC total or Core Ab; Anti-HBc IgM

Anti-HBe; Anti-HBs

95
Q

REMEMBER: SECCES

A

Antigen (Surface, Envelope, Core)
Antibody (Core, Envelope, Surface)

96
Q

appears shortly after HBsAg

A

HBEAG

97
Q

Maybe elevated during acute phase

A

HBEAG

98
Q

Present during period of active replication

A

HBEAG

99
Q

Indicated that virus has high degree of infectivity (mabilis makahawa)

A

HBEAG

100
Q

Not detected in the serum.

A

HBCAG

101
Q

Detected in liver biopsy.

A

HBCAG

102
Q

First to appear

A

IGM ANTIHBC

103
Q

Indicates current or recent infection.

A

IGM ANTIHBC

104
Q

Appears during recovery period in acute infection.

A

ANTI-HBS

105
Q

Pinakalast Ab na maproproduce.

A

ANTI-HBS

106
Q

It will appear few weeks after HBs antigen disappears and will persist for years and provide protective immunity.

A

ANTI-HBS

107
Q

– means the patient doesn’t show any signs or symptoms

A

Window Period

108
Q

– period wherein the antigen slowly drops down and slowly increases the antibodies

A

Covalascent

109
Q

Progress to chronic state

A

Covalascent

110
Q

METHODS INTRODUCE TO PREVENT HBV INFECTION

A

Screening of blood donors

Treating plasma derived products to inactivate HBV

Implementing infectious control measures

Immunization with Hepatitis B vaccine

111
Q

Screening of blood donors

A

(Hepatitis C, Hepa B, syphilis, malaria, HIV)

112
Q

known as a major public health problem, also known as Non-A or Non-B infection (NANB)

A

HEPATITIS C VIRUS

113
Q

Common worldwide

A

HEPATITIS C VIRUS

114
Q

RNA, flaviviridae

A

HEPATITIS C VIRUS

115
Q

Transmission: parenteral

A

HEPATITIS C VIRUS

116
Q

Less common to sexual transmission than hepatitis B

A

HEPATITIS C VIRUS

117
Q

Asymptomatic

A

HEPATITIS C VIRUS

118
Q

HCV Average incubation period:

A

7 weeks

119
Q

Screening test for HCV:

A

Detection of HCV IgG antibodies using third generation (ex: rapid test kits)

120
Q

Confirmatory test for HCV

A

Recombinant Immunoblot Assay (RIBA)

121
Q

Replaced with molecular methods

A

Recombinant Immunoblot Assay (RIBA)

122
Q

Incomplete or defective virus

A

HEPATITIS D VIRUS

123
Q

Needs Hepa B Virus to replicate: requires surface Ag for replication

A

“Coinfection”

124
Q

HEPATITIS D VIRUS also known as

A

Delta hepatitis

125
Q

is a nonenveloped, single-stranded ribonucleic acid (RNA) virus that belongs to the genus Hepevirus, in the family Hepeviridae

A

HEPATITIS E VIRUS

126
Q

MOT: ingestion (like Hep A), fecal-oral route

A

HEPATITIS E VIRUS

127
Q

Following an incubation period of 3 to 8 weeks

A

HEPATITIS E VIRUS

128
Q

causes an acute, self-limiting hepatitis that lasts 1 to 4 weeks in most people who become infected

A

HEPATITIS E VIRUS

129
Q

Like HAV, the infection does not progress to a chronic carrier state

A

HEPATITIS E VIRUS

130
Q

Diagnosis relies on serologic testing (Because HEV is not easily cultured)

A

HEPATITIS E VIRUS

131
Q

Acute infection demonstrate the presence of [?]

A

IgM antiHEV

132
Q
  • detectable during clinical onset
A

IgM antiHEV

133
Q

Identified by highly sensitive enzyme immunoassay

A

IgM antiHEV

134
Q

: Conjugation of bilirubin

A

LIVER

135
Q

Waste product of heme

A

BILIRUBIN

136
Q

120 days: apoptosis. - release of Hb - dissected to heme and globin - waste prod:

A

indirect/unconjugated bilirubin (toxic)

137
Q

Excretion thru [?]

A

urine and stool

138
Q

Further converted to [?] (yellow color of urine)

A

urobilin/urochrome

139
Q

: brown color of urine

A

Stercobilin

140
Q

: Yellowish discoloration of the skin

A

Jaundice

141
Q

: Yellowish discoloration of the brain

A

Kermicterus

142
Q

: Specimen req for bilirubin due to photo-sensitivity

A

Carbon paper/amber bottle

143
Q

Ingestion of street foods; Shed in stool

A

HEPATITIS A VIRUS

144
Q

Persists for life

A

HEPATITIS A VIRUS

145
Q

May be positive in the context of (-) IgM test

A

HEPATITIS A VIRUS

146
Q

Blood transfusion, Occupational needlestick injury, IV drug users - ex. Heroin, Tattooing

A

HAV

147
Q

hepatitis B surface antigen, or HBsAg, HBeAg, With signs and symptoms

A

After incubation period

148
Q

: 3 to 6 months,Anti-HBc

A

Early recovery

149
Q

: Anti-HBs

A

Decline phase

150
Q

is not seen in serum, only in liver biopsy

A

Core antigen

151
Q

Blood bank in the US

A

HBV

152
Q

: whole blood w/o plasma

A

Packed rbc

153
Q

: processed as a base in vaccine; converted to Albumin

A

Plasma

154
Q

Treated w/ chemicals such as detergents (to inactivate virus)

A
155
Q

Blood transfusion, IV drug users, Hemodialysis, Organ transplantation

A

HCV

156
Q

Only seen in chronic infection

A

HEPATITIS C VIRUS

157
Q

Most commonly progress to chronic state

A

HEPATITIS C VIRUS

158
Q

Causes LIVER CIRRHOSIS

A

HEPATITIS C VIRUS

159
Q

Only increased during chronic infection

A

HCV IgG antibodies

160
Q

Most common cause of blood transfussion hepatits

A

HCV IgG antibodies

161
Q

Tests for RNA content (same w/ PCR); Old test but expensive

A

Recombinant Immunoblot Assay (RIBA)

IMMUNE 1 LEC (28 decks)

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