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MYCV Lec 1

Viral Hepatitis Virus

Review of Liver o Localized in genitalia, if it is not


- Is considered as the largest internal organ treated can be disseminate into the
- Situated in right part of the abdomen, below blood stream and reach the liver
diaphragm [Fitz-Hugh-Curtis syndrome 
- Able to regenerate [except cirrhosis and inflammation, Hepatitis]
Carcinoma] - Amoeba [Entamoeba histolytica]
- Functions o Left untreated.
o Detoxification  toxins in our body - Virus is commonly caused inflammation of
from the foods and fluids taken in. the liver
 Working in nutrient Viral Hepatitis
o Production of different protein Primary Hepatitis
necessary for metabolic process
- 95% percent, attack primarily the liver,
 Albumin
little direct effect on other organ system
 Prothrombin
o HAV
o Responsible somehow part for
o HBV
coagulation event in our body.
o HCV
- Chronic hepatitis
o Not that damage yet o HDV
o Still the liver is sick o HEV
- Cirrhosis o HGV
o Scarring, cause possible damage o TTV [Transfusion transmitted virus]
already and causing consequences in Secondary Hepatitis
the body - Involved the liver secondarily, course of
o Can regenerate as long as diagnosis systemic infection.
already. - Not attacking primarily, the liver
- Hepatocellular carcinoma [with cirrhosis] o Yellow Fever Virus [transmitted via a
o Carcinoma  cancer of the liver vector from mosquito bites]
o Terminal, it is difficult to regenerate o EBV [Epstein-Barr virus] B
Hepatitis lymphocyte  infectious
- Inflammation of the liver mononucleosis
o CMV [Cytomegalovirus]
Caused by o HSV [Herpes Simplex Virus]
Alcohol o Rubella Virus
- Hard liquor if too much [beer, gin] Forms of Viral Hepatitis
Drugs - Manifestation of sign and symptoms varies
- medicine that we take in if it is too much. - Undergo treatment
- Frequent medication may also cause possible - Restricted form various activities; stress, no
damage to kidney. And Liver drinking alcohol, toxic foods [high fat diet or
Infectious Agents cholesterol]
- Early diagnosis led to proper intervention
- Most common  Bacteria, Parasite, Viruses - Hepatitis A, E
- Neisseria gonorrhea o Only have Acute form of hepatitis
o Localized gonorrhea [Tulo] o Have sub-clinical

JOHN FERNAN LOS BAÑES


MYCV Lec 2

- Hepatitis B, C, D o Defend on the stage


o Both acute and chronic, as well as
Primary
fulminant.
Hepatitis A Virus
o Have sub-clinical
- the sign and symptoms is Generalized, cannot Hepatitis B Virus
know if you based on the sign and symptoms. Transfusion Transmitted Virus
Subclinical [Inapparent] - Primary Viral Hepatitis
- Non-Ag Hepatitis virus [does not react to
- No clinical signs and symptoms yet.
any other antigen]
- Incubation period of the disease
- Single strand Virus same with Hepatitis B
- Active in the replication in the hepatocytes.
- Isolated in 1997 from a post transfusion
- There is no manifestation, you don’t know if
you have virus, but your immune system is General Diagnosis
strong not go to another stage Epidemiological Data
Acute - HA, HE
- Already sign and symptoms, observed and o food, water, seasonal [rainy seasons
see from the patients  High rate], age
- Manifest a certain period of time, it varies, - HB, HC, HD, HG
ranges from weeks to 3 months. o blood and blood product
- May have tendency to have chronic or transfusion, contact history [sexual
fulminant acute intercourse], inoculation history
[needle stick injury, Parenteral]
Chronic
Clinical Diagnosis
- It may have manifestation of hepatitis
- Sign and symptoms of hepatitis - Acute hepatitis
- Serologically detected on the blood ** - Chronic hepatitis
- Can be cured Treatment
Fulminant Acute Chronic hepatitis
- Considered as terminal stage - Symptomatic therapy
- Liver may already reach cirrhosis or - Diet
scarring and carcinoma - Rest
- Irreversible. - Supporting therapy
Clinical Findings of Viral Hepatitis [Generalized] - Immunomodulator [antibodies present in
vaccine]
- It is not necessary all of this, can be two or
three Fulminant hepatitis
- Fever, 37.5 can be manifested - General and supporting therapy
- Anorexia o Rest: Strict bed rest
- Nausea o Diet and Liver Transplant
- Vomiting
Prevention
- Jaundice [common manifestation]
o Discoloration of the skin as well - Control of source of infection
sclera of the eyes. - Cut off the route of transmission
- Dark urine [pigment from RBC] - Protection of susceptible populations
- Pale feces [almost no color] o Active immunity [Antigen]
- Elevated transaminase [blood test, ACT, o Passive immunity [give Antibody]
ALT]

JOHN FERNAN LOS BAÑES


MYCV Lec 3

JOHN FERNAN LOS BAÑES


MYCV Lec 4

Viral Hepatitis Virus Tabulated


Hepatitis A Virus Hepatitis B Virus [only DNA]
Disease Hepatitis A Hepatitis B
Causative Hepatitis A Virus Hepatitis B Virus
agent
Family - Picornaviridae [Smallest RNA Virus] - Hepadnaviridae
Genus - Enterovirus [Large intestine] / Hepatovirus - Orthohepadnavirus
Morphology - Naked - Enveloped [less stable]
- Icosahedral - Icosahedral
- Linear - Circular
- SS RNA - DS DNA
- 28 nm - 42 nm
Other Names - Infectious hepatitis - Serum hepatitis [transmitted via blood]
- Enterovirus 72 - Dane Particle
- Short incubation hepatis - Long incubation hepatitis
- Australian hepatitis [Australian aborigine]
Transmission - Fecal-route route [Ingestion] - Parenteral [contaminated needles] [most cases] [injection]
- Excreted from defecation [stool] - Perinatal [vertically, infected mother to baby during
- Spread in different ways pregnancy  transmit to placenta. Acute  high risk]
 Vectors [Flies]  Food [temporarily]  Eat - Sexual intercourse [high viral load during acute phase,
 Not wash thoroughly  prepare of food  other people low viral during chronic stage is not possible]
 Street foods
Incubation - 15-45 days - 40-180 days [more than 1 month]
period - Neonate: possible consequences, high risk.
Treatment - Supportive care [Clinically sign and symptoms] not directed to - Supportive care [Chronic]
the disease - Acute or Acute fulminant or carcinoma
 Fever: Tylenol, Paracetamol [Antipyretic]  Interferon
 Body Pain: Analgesic  Lamivudine
- Liver transplant
- HB immunoglobin [antibody, acute, carcinoma, Fulminant]
Prevention - Inactivated vaccine [Twinrix]: 2 doses - Inactivated vaccine [3 doses] interval time of 1 month
 Inactivated vaccine, killed virus

JOHN FERNAN LOS BAÑES


MYCV Lec 5

- Treatment of water
- Good Hygiene and proper disposal
- Can have a lifetime immunity [if previously infected and
cured by the immune system]
Diagnosis - Serologically is specific - HBsAg
 IgM anti-HAV [during Acute]  1st marker to appear as incubation period
 IgG anti-HAV  Screening blood donor
o Start to develop antibodies  Indicator of both active and Chronic
o Convalescence stage  Prolonged carriers and risk of chronic
o Recovered  Some cannot be detected
- HAV Ag [Acute Form]  Window period – transition of incubation to active
- Monitoring Transaminases [does not specific, high ALT and infection]
AST] - HBeAg
 Marker of high infectivity and vertical
 Most of the time acute phase
 High viral load, high risk of transmission during
sexual intercourse
- HBcAg
 biopsies of infected liver, not part of serologically]
- IgM Anti-HBc
 1st to produce and detected
 Indication of active infection
 Window period only can be detected
- IgG Anti-HBc
 starts of convalescence or immunity
- Anti-HBe
 marker of low infectivity, negative to HBeAg
- Anti-HBs
 last antibody to produce
 Appears during recovery of acute
 Indicator or marker of past infection or
immunization]
- HBV DNA
 Nucleic acid via PCR
 good marker during incubation period
 less likely positive serological test.
 Most appropriate test if the newborn baby is infected

JOHN FERNAN LOS BAÑES


MYCV Lec 6

Pathogenesis - X axis [Weeks] - X axis period of the disease


- Y axis [Different Stages, manifestation] - Y axis, manifestation expected level of antibody or antigen
- [0] Ingested contaminated food or water - Transmission of the virus from extraction of blood and
- [2-4 weeks] incubation period accidentally prick your own finger
- 2 weeks [viremia] - Days to weeks to have manifestation of sign and symptoms
 Target Cell hepatocyte, undergo viral replication [Incubation 8-13 weeks]
 Spread in the circulation [no signs and symptoms] - End of incubation period [viremia] [Acute infection – 2-
 Can detect Antigen [HAV Ag] weeks – 3 months]
- Deposit to the large intestine, excrete the virus in the stool  [1] HBsAg
 No sign and symptoms [yellow decolorization]  [2] HBeAg
- At the end of 3rd week  Antigen drops, antibody will release
 Elevated AST and ALT enzymes of the liver  Anti HBc [constant]
- 4th weeks  Anti HBc [Constant]
 Manifestation of sign and symptoms [Jaundice]  Anti HBe [low]
 Will last until 7th week  Anti HBs
 Produce antibody IgM [peek 6th week] and IgG [several
weeks, serves as immunity] [Anti-HAV IgG 
recovered or vaccinated]
- Resistance to Ether, High temperature 60 for 1 hour
Structure - Spherical
 Does not contain nucleic acid, only protein part [non-
infectious  Capsid
 Small and numerous, circulating in the blood stream
 Contains membrane and capsid.
- Tubular / Filamentous
 Same with spherical, Enveloped and Capsid is present.
- Dane Particle
 Have nucleic acid, infectious
 Largest form or structure
 Nucleic acid, Capsid and Enveloped
- Different Parts
 Enveloped
o Different antigenic sites [binding site of
antibody]
o Surface antigen
o Core antigen [matrix protein]
o Enveloped antigen [enveloped part]

JOHN FERNAN LOS BAÑES


MYCV Lec 7

 DNA polymerase
o DS nucleic acid

Hepatitis B Disease State Healthy


Early Acute early Acute Chronic Late Resolved Vaccinated
acute
HBsAg + + + + + - -
HBeAg - + + + - - -
Anti-HBc - - - + +/- + -
Anti-HBs - - - - - + +
Anti-HBe - - - - +/- +/- -
DNA Virus + + + + + - -

Hepatitis C Virus [post blood transfusion Hepatitis D Virus Hepatitis E Virus Hepatitis G Virus
 Major cause]
Disease - Hepatitis C - Hepatitis D - Only Acute, high
- 70-90 % Chronic mortality  20%
- 10% chronic active to cirrhosis, may lead among pregnant
to hepatocellular carcinoma women
Causative agent - Hepatitis C Virus - Hepatitis D Virus - Hepatitis E Virus - Hepatitis E Virus
Family - Flaviviridae [yellow] - Deltaviridae - Hepeviridae - Flaviviridae
Genus - Hepacivirus - Deltavirus - Hepevirus - Flavivirus
Morphology - Enveloped - Enveloped - Naked - Ss RNA
- Icosahedral - Circular - Icosahedral
- Linear - SS RNA - SS
- Ss RNA - 37 nm - Linear
- 45 nm - 30 nm
Other Names Non-A Non-B hepatitis - Defective virus needed genes - N/A - N/A
of Hepatitis B virus to
developed parts, coinfection,
or superinfection
- Specifically Capsid produce

JOHN FERNAN LOS BAÑES


MYCV Lec 8

by the gene of hepatitis B.


Transmission - Parenteral [Blood Transfusion] - Parenteral - Fecal-oral route - Parenteral
- Sexual Intercourse - Sexual intercourse [same with Hepatitis - Sexual Intercourse
- Co-infection with hepatitis B A] [Blood
Transfusion]
Incubation period - 30-50 days - 15-150 days - 2-9 weeks - Not established
Treatment - Supportive care [Both acute and Chronic, - Supportive care - Supportive care, - Supportive care
Subclinical] self-limiting
- Interferon [without taking any
- Ribavirin medication]
- Liver transplant
Prevention/Vaccine - No Vaccine available - No vaccine but it helped when - No vaccine - No vaccine
vaccinated with HBV
Diagnosis - No antigen tests - No antigen tests - HEV Ag -
- Anti-HCV [most common, screening for - Anti-HDV - IgM Anti-HEV
blood donor] - Or possible PCR detecting - HEV RNA [PCR]
- HCV-RNA [PCR] nucleic acid
- 3 generations Serological of hepatitis C
 1st generation: Ouchterlony agar
plate
 2nd generation Counter
electrophoreses
 3rd generation Radio immunoassay,
ELISA or Enzyme link, Reverse
passive heme agglutination, Reverse
passive latex agglutination

JOHN FERNAN LOS BAÑES

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