VIRAL INFECTIONS CONT. & HEPATITIS Flashcards
Viral Hepatitis
HIV
Dengue
Herpes Virus infections: infectious mononucleosis, Epstein Barr Virus, Cytomegalovirus
Submicroscopic particle (size is measured in nanometers)
VIRUSES
VIRUSES Basic Structure:
core of DNA or RNA
Intracellular pathogens
VIRUSES
First line of protection (nonspecific immunity)
INNATE IMMUNITY AGAINST VIRUSES
Interferon-a and Interferon-b
INNATE IMMUNITY AGAINST VIRUSES
Inhibits viral replication
Interferon-a and Interferon-b
Enhances activity of NK cells
Interferon-a and Interferon-b
B cells and plasma cells
HUMORAL DEFENSE
Produces virus specific antibodies
HUMORAL DEFENSE
Ab prevents spread of viral replication through neutralization
HUMORAL DEFENSE
: promotes phagocytosis thru opsonization
IgG
: Agglutinates viral particles
IgM
Upon activation of [?], CD8+ Cytotoxic T cells (CTL) become programmed to expand in number and attack the virus-infected cells.
CD4+ T helper cells and cytokines
Cytotoxic T cells (CTL) produce
proteins and proteases
- pore forming protein, bubutasan nila ung host cell. It will create a pore in the membrane of the host cell.
Perforin
- they will now enter the pore and will activate apoptosis
Granzymes
Increase [?] its original number
50,000 times out of
Produces new viral antigens – not recognized immediately by initial immune response
They undergo frequent genetic mutations
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
They undergo frequent genetic mutations
For example, the Hepatitis C virus (HCV) can block the degradation of viral RNA that is induced by interferons.
Some viruses can evade actions of the component of the immune response
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
Viruses can evade the hosts defense by suppressing the immune system
STRATEGIES ON HOW VIRUSES ESCAPES IMMUNE MECHANISMS
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
LABORATORY TESTING FOR VIRAL INFECTION
Serologic testing
Molecular assays
– monitors the course of infection, detects past infection, can assess immune status
Serologic testing
Indicates current or recent infection or acute infection
Specific IgM antibody
[?] in newborns indicates congenital infection with virus
Specific IgM antibody
Indicates current or past infection and in most cases immunity
IgG antibodies
[?] in newborns are mainly maternal antibodies
IgG antibodies
can cross the placenta; thus normal
IgG
Demonstrated using [?] (compound for bacteria)
electron microscope
DNA or RNA is packed in [?] and some virus’s capsid is surrounded by outer envelope such as glycolipids and proteins.
protein coat or capsid
They are going to rely on host cells for replication and survival.
Intracellular pathogens
No host =
dormant
[?]infects the host cell by attaching to specific receptors in their target cells
Virion
It penetrates the cell membrane
Virion
directs the host cell machinery to produce more viral nucleic acid and proteins
Release of nucleic acid (RNA or DNA)
assemble inside the cell to form the intact virus, which is released thru cell lysis or budding of the cell surface
Release of nucleic acid (RNA or DNA)
Viruses destroy the cells leading to [?]
decreased cell count
Target cell:
CD4 T cells
(virus-infected cells; produced in the recognition of TLRs)
Interferon-a and Interferon-b
By inducing transcription of several genes that will code for proteins w/ antiviral activity
Inhibits viral replication
Binds virus-infected cells and release cytotoxic proteins like perforin (substance that create pores) and granzymes
Enhances activity of NK cells
– primary cells involved of humoral defense
B cells and plasma cells
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
Produces virus specific antibodies
neutralize viruses in the mucosal surfaces
Secretory IgA antibodies
can bind to viruses in the bloodstream and inhibit dissemination of the infection.
IgM and IgG antibodies
promote phagocytosis of viruses through their opsonizing activity
IgG antibodies
can also inactivate viral particles by agglutinating them.
IgM antibodies
also activate complement
IgG and IgM antibodies
leading to elimination of intracellular viruses required for replication
Cytotoxic T cells (CTL)
General term for inflammation of the liver
HEPATITIS
([?]– liver,[?] – inflammation)
hepa; itis
T or F
Most people though that the cause of hepatitis is virus but there are also other causes
T
HEPATITIS Causes:
viral infection, chemicals, ionizing radiation and autoimmune process
HEPATITIS TWO STAGES
Acute stage
Progressive/Chronic stage
: General flu like symptoms
Acute stage
Hepatomegaly (enlargement of the liver)
Progressive/Chronic stage
jaundice (yellowish discoloration of the skin)
Progressive/Chronic stage
dark urine (due to increase of urobilinogen passing through urine)
Progressive/Chronic stage
light feces (due to increase of stercobilin)
Progressive/Chronic stage
(enlargement of the liver)
Hepatomegaly
(yellowish discoloration of the skin)
jaundice
dark urine (due to increase of [?] passing through urine)
urobilinogen
light brown feces (due to increase of [?])
stercobilin
INITIAL LABORATORY TEST
Elevations in bilirubin and liver enzymes (ALT)
Non-enveloped, single stranded RNA virus.
HEPATITIS A VIRUS
They belong to the Hepatovirus genus of Picornaviridae family.
HEPATITIS A VIRUS
It is responsible for tens of millions of hepatitis A virus infection worldwide.
HEPATITIS A VIRUS
MOT: fecal-oral route, close person to person contact, and ingestion of contaminated food.
HEPATITIS A VIRUS
This may be due to poor sanitation, poor hygiene, and overcrowding.
HEPATITIS A VIRUS
The infection caused do not usually progress to chronic stage, only to acute stage.
HEPATITIS A VIRUS
Symptoms are usually self-limiting, typically result within two months.
HEPATITIS A VIRUS
DIAGNOSIS: Demonstration of [?] to HAV
IgM antibodies
Detected by Solid phase antibody-capture enzyme immunoassay
HEPATITIS A VIRUS
Detectable on the onset of clinical symptom (present infection)
HEPATITIS A VIRUS
TEST for TOTAL HAV detects [?]
IgG
Competitive inhibition EIA format
HEPATITIS A VIRUS
Major cause of mortality and morbidity worldwide.
HEPATITIS B VIRUS
WHO estimated about 500,000 to 1.2 million deaths each year due to liver disease.
HEPATITIS B VIRUS
Highly endemic in far east, middle east, and subSaharan Africa & amazon.
HEPATITIS B VIRUS
HEPATITIS B VIRUS MOT:
Parenteral route by contaminated blood (main) and Sexual transmission by semen, vaginal secretion, and saliva
It also has something to do with the production of antigens and antibodies when it comes to HBV infection.
Mnemonic:
SEC-CES
The first 3 letters will denote the [?] and the last 3 letters denote [?].
antigen
antibodies
For the letters SEC:
surface antigen
envelope antigen
core antigen
For the last 3 letters CES:
core antigen
envelope antigen
surface antigen
INCUBATION PERIOD HEPATITIS B VIRUS
Average (8-13 weeks)
The time between being exposed to the viral hepatitis and showing the first symptoms.
HBV ACUTE INFECTION
2 weeks- 3 months
HBV ACUTE INFECTION
So the 1st antigen to produce is surface
HBV ACUTE INFECTION
Next antigen produced is the envelope antigen.
HBV ACUTE INFECTION
Lastly, core antigen is produced.
HBV ACUTE INFECTION
3-6 months
HBV EARLY RECOVERY
HBV EARLY RECOVERY
First Ab produced is [?] followed shortly by [?]
Then, [?]. Maproduced na kasabay ng pagdecline ng Ag.
Lastly, [?].
Anti-HBC total or Core Ab; Anti-HBc IgM
Anti-HBe; Anti-HBs
REMEMBER: SECCES
Antigen (Surface, Envelope, Core)
Antibody (Core, Envelope, Surface)
appears shortly after HBsAg
HBEAG
Maybe elevated during acute phase
HBEAG
Present during period of active replication
HBEAG
Indicated that virus has high degree of infectivity (mabilis makahawa)
HBEAG
Not detected in the serum.
HBCAG
Detected in liver biopsy.
HBCAG
First to appear
IGM ANTIHBC
Indicates current or recent infection.
IGM ANTIHBC
Appears during recovery period in acute infection.
ANTI-HBS
Pinakalast Ab na maproproduce.
ANTI-HBS
It will appear few weeks after HBs antigen disappears and will persist for years and provide protective immunity.
ANTI-HBS
– means the patient doesn’t show any signs or symptoms
Window Period
– period wherein the antigen slowly drops down and slowly increases the antibodies
Covalascent
Progress to chronic state
Covalascent
METHODS INTRODUCE TO PREVENT HBV INFECTION
Screening of blood donors
Treating plasma derived products to inactivate HBV
Implementing infectious control measures
Immunization with Hepatitis B vaccine
Screening of blood donors
(Hepatitis C, Hepa B, syphilis, malaria, HIV)
known as a major public health problem, also known as Non-A or Non-B infection (NANB)
HEPATITIS C VIRUS
Common worldwide
HEPATITIS C VIRUS
RNA, flaviviridae
HEPATITIS C VIRUS
Transmission: parenteral
HEPATITIS C VIRUS
Less common to sexual transmission than hepatitis B
HEPATITIS C VIRUS
Asymptomatic
HEPATITIS C VIRUS
HCV Average incubation period:
7 weeks
Screening test for HCV:
Detection of HCV IgG antibodies using third generation (ex: rapid test kits)
Confirmatory test for HCV
Recombinant Immunoblot Assay (RIBA)
Replaced with molecular methods
Recombinant Immunoblot Assay (RIBA)
Incomplete or defective virus
HEPATITIS D VIRUS
Needs Hepa B Virus to replicate: requires surface Ag for replication
“Coinfection”
HEPATITIS D VIRUS also known as
Delta hepatitis
is a nonenveloped, single-stranded ribonucleic acid (RNA) virus that belongs to the genus Hepevirus, in the family Hepeviridae
HEPATITIS E VIRUS
MOT: ingestion (like Hep A), fecal-oral route
HEPATITIS E VIRUS
Following an incubation period of 3 to 8 weeks
HEPATITIS E VIRUS
causes an acute, self-limiting hepatitis that lasts 1 to 4 weeks in most people who become infected
HEPATITIS E VIRUS
Like HAV, the infection does not progress to a chronic carrier state
HEPATITIS E VIRUS
Diagnosis relies on serologic testing (Because HEV is not easily cultured)
HEPATITIS E VIRUS
Acute infection demonstrate the presence of [?]
IgM antiHEV
- detectable during clinical onset
IgM antiHEV
Identified by highly sensitive enzyme immunoassay
IgM antiHEV
: Conjugation of bilirubin
LIVER
Waste product of heme
BILIRUBIN
120 days: apoptosis. - release of Hb - dissected to heme and globin - waste prod:
indirect/unconjugated bilirubin (toxic)
Excretion thru [?]
urine and stool
Further converted to [?] (yellow color of urine)
urobilin/urochrome
: brown color of urine
Stercobilin
: Yellowish discoloration of the skin
Jaundice
: Yellowish discoloration of the brain
Kermicterus
: Specimen req for bilirubin due to photo-sensitivity
Carbon paper/amber bottle
Ingestion of street foods; Shed in stool
HEPATITIS A VIRUS
Persists for life
HEPATITIS A VIRUS
May be positive in the context of (-) IgM test
HEPATITIS A VIRUS
Blood transfusion, Occupational needlestick injury, IV drug users - ex. Heroin, Tattooing
HAV
hepatitis B surface antigen, or HBsAg, HBeAg, With signs and symptoms
After incubation period
: 3 to 6 months,Anti-HBc
Early recovery
: Anti-HBs
Decline phase
is not seen in serum, only in liver biopsy
Core antigen
Blood bank in the US
HBV
: whole blood w/o plasma
Packed rbc
: processed as a base in vaccine; converted to Albumin
Plasma
Treated w/ chemicals such as detergents (to inactivate virus)
Blood transfusion, IV drug users, Hemodialysis, Organ transplantation
HCV
Only seen in chronic infection
HEPATITIS C VIRUS
Most commonly progress to chronic state
HEPATITIS C VIRUS
Causes LIVER CIRRHOSIS
HEPATITIS C VIRUS
Only increased during chronic infection
HCV IgG antibodies
Most common cause of blood transfussion hepatits
HCV IgG antibodies
Tests for RNA content (same w/ PCR); Old test but expensive
Recombinant Immunoblot Assay (RIBA)