Principles of Viral

Infections
Viral Hepatitis
& HIV &
AIDS
MPath PartI INTENSIVE COURSE
2022
Associate Prof Dr Zetti Zainol Rashid
Dept of Medical Microbiology & Immunology
MBChB(Manchester), Hospital Canselor Tuanku Muhriz
MPath(Med Microbiology)(UKM)
Faculty of Medicine UKM UKM Medical Centre
56000 Kuala Lumpur
Overview

1. Viral infections – 2. Exposure to viruses & 3. Transmission of viruses:

introduction & modes of transmission. infection prevention &
pathogenesis control
Sites of viral entry into the host

4. Viral infections: 5. Course of infection & 6. Laboratory diagnosis

body system approach outcomes of infection of viral infections
(summary)

7. Viral Hepatitis 8. HIV & AIDS 8. Other examples of

viral infections
Virus Sizes

Figure 13.1
 Virion Structure

• Nucleic acid
• DNA or
RNA
• Capsid
• Capsomeres
• Envelope
• Spikes

Figure 13.2a
 Virus replication cycle
1. Attachment: Viruses attach to cell membrane
4. Biosynthesis: Production of nucleic acid and proteins
2. Penetration by endocytosis or fusion 5. Maturation: Nucleic acid and capsid proteins assemble

3. Uncoating by viral or host enzymes 6. Release by budding (enveloped viruses) or rupture/lysis

 Cell
damage
Virus replication causes

1. Cell damage / death / lysis 2. No cell death (altered function /

– Eg Picornaviruses- cause cell
or loss of function)
lysis and cell death – Eg Retroviruses (eg HIV) do
– damage of enterocytes not generally cause cell death

→ diarrhoea – released from the cell by

budding
– Damage of resp epithelium
→ cause persistent infections.
→ resp tract disease
 Growing Viruses (in the lab)
• Viruses are intracellular organisms.
• Viruses may be grown in cell culture (living cells)
• Cultured viruses are used in viral studies, such as studies
on morphology, pathogenesis and for vaccine production.

Samples are inoculated into the cell culture.

After incubation, CPE is observed using inverted light microscope

Virus-induced injury (cellular) and effects

The host cells that are infected with viruses will display
Cytopathic Effects (CPE)
• Some of these effects consist of: • Other effects shown:

• Altered shape • Formation of Syncytium

• Detachment from substrate • shutting off of cell functions
• Lysis • Immunopathologica
• Membrane fusion; syncytium l lesions.
• Membrane permeability
• Inclusion bodies
• Apoptosis
 Cytopathic Effects of Viruses
(CPE)

eg RSV, CMV, HSV, influenza,

parainfluenza, mumps, measles,
adenovirus

Figure 15.7
Cytopathic Effects of Viruses
(CPE)

Eg CPE of HSV
infection.

A. Uninfected Vero
cells

B. HSV-1-infected Vero cells

showing rounded cells,
multinucleated cells, and loss
of the monolayer. Arrows point
to syncytia.
• Opportunistic infections
 • Pathogenicity: The ability to
cause disease
Majority of viral infections – process by which a viral
are subclinical. It is not in infection
the interest of the virus to leads to disease.
severely harm or kill the – an abnormal situation of no
host.
value to
the virus.
The consequences of viral
• Virulence: The extent of
infections depend on the pathogenicity, or degree of
interplay between a damage caused
number of viral and host
factors.

• Cell tropism /tissue tropism:

Viral affinity for specific
body tissues
Transmission of
viruses
• Human to human only
• Animal to human (zoonotic)
• Animal to human, via arthropods Exposure to viruses
(‘arboviruses’) • Ubiquitous viruses
(respiratory viruses, enteric
viruses)
Shedding & transmission • Crowded living, school,
(from host or infected person) → daycare centres,
dormitories
• Mechanisms (direct or indirect): • Poor hygiene
• Faecal-oral • Sexual contact
• Respiratory (droplets, airborne) • Occupation
• Contact (skin lesions, fomites) • Healthcare workers
• Sexual contact • Travel, camping – contact with
• Blood-borne /parenteral vectors eg mosquitoes,
rodents
• Transplant
• Others
• Vertical (mother to baby)
• Zoonoses (animal, insects)
Transmission of
viruses Droplet (Titisan
pernafasan)
Jarak dekat, 1-2 meter,
terutama ketika
bercakap, batuk, bersin.

Aerosol sprays /
Airborne Transmission
Penyebaran virus
dengan jarak lebih jauh
iaitu melebihi 1-2 meter
atau di seluruh bilik,
wad atau ruang
kawasan.

Contact/Sentuhan -
virus tersebut mendap di
Infection Prevention & Control: atas permukaan atau objek,
• Standard Precautions diikuti dengan sentuhan ke
• Transmission-based precautions mata, hidung, mulut.
1. Contact
2. Droplets
3. Airborne
Transmission of viruses

Indirect contact:
via contaminated
objects or
environment

Portal of entry /mode of transmission vs infection /disease:

There are several portals of entry for viruses, locations through which
viruses gain entry into the body. The mucosal epithelium acts as the
main barrier against pathogen entry.
Portal of entry vs site of infection or dz →
Sites of viral
entry into host
(may not be the same as
site of infection/disease)

Routes:
• Respiratory
• Fecal-oral /GIT
• Urogenital
• Skin
 Portal of entry /mode of transmission vs infection
Portal of/disease
entry / Sources Viruses Infections
Mode of transmission (examples) (examples)

Gastrointestinal / Faeces → contaminated hands and food • Rotaviruses -Gastrointestinal

Faecal-oral • Astroviruses Infections (± systemic
• Norovirus manifestations)
• Adenoviruses

Hepatitis A virus
Hepatitis E virus -Viral hepatitis
-Viral hepatitis
Enteroviruses (eg poliovirus,
echovirus, coxsackievirus) -CNS infections
Respiratory / Respiratory particles >5 µm containing Most respiratory viruses: -Respiratory
Droplets infectious agents • Influenza viruses A & B tract infections
• Parainfluenza viruses
(droplets are larger particles and do • Respiratory Syncytial Virus
not remain suspended in the air or • Human coronaviruses including
travel long distances) SARS-CoV-2
• Enteroviruses
• Rhinoviruses
• Adenoviruses
• Human Metapneumovirus

• Measles -Measles
• Mumps -Mumps
• Rubella -Rubella
• Parvovirus B19 -Fifth Disease
Respiratory / Airborne / aerosol of infectious agents 1. Measles -Measles
Airborne particles <5 µm in size, which remain 2. Varicella zoster virus -Chicken pox
suspended in the air for long periods of 3. SARS-CoV-2 -COVID-19
time. 4. (Mycobacterium tuberculosis – -(TB)
bacteria)
Produced during talking, coughing,
sneezing and some procedures (AGP)
Portal of entry / Sources Viruses Infections
Mode of transmission (examples) (examples)
Skin / Mucous membrane
Contact: Direct contact • Human papillomavirus (HPV) Genital tract infections
(blood, body fluids, lesions etc) • Herpes Simplex Virus-1/2 (HSV-1/2)
• Molluscum contagiosum virus -Mollusca (skin lesion)
• Varicella zoster virus -Chicken pox
• Ebola virus -Ebola disease, VHF

Penetration into dermis or • Parenteral/ blood-borne viruses - (see section below)

subcutaneous • Arthropod-borne viruses e.g. Dengue, -Viral haemorrhagic
Chikungunya, JE virus. fevers, Japanese
encephalitis
• Rabies -rabies

Indirect contact:
Contact with secretions or body
fluids via contaminated objects or
surfaces
→ followed by contact with
mucous membranes
• Respiratory viruses eg Adenovirus, Influenza, -Respiratory tract
Parainfluenza, RSV, Enteroviruses, Rhinovirus, infections
some Coronaviruses e.g. SARS-CoV-2, MERS.
• Gastrointestinal eg Rotavirus, Astrovirus, -Gastrointestinal
Norovirus, Hepatitis A, Hepatitis E virus. infections
• Others eg HSV, VZV, EBV, HPV, Measles, -various diseases
Mumps, Rubella, Parvovirus B19, Ebola

Genital tract Sexual activity • Human papillomavirus (HPV) Sexually transmitted

• Herpes Simplex Virus-2 (HSV-2) diseases (STDs or STIs),
Genital tract infections

• Hepatitis B Viral hepatitis

• HIV HIV /AIDS
Parenteral/ Blood-borne Blood and body fluids • Hepatitis B Viral hepatitis
• Blood • Hepatitis C Viral hepatitis
• Body fluids • Human Immunodeficiency Virus HIV /AIDS

Transplant Transplanted organs or blood • Hepatitis B Viral hepatitis

• solid organ products • Hepatitis C Viral hepatitis
• haemopoetic • Human Immunodeficiency Virus HIV /AIDS
• others eg CMV
Viral infections by body systems
• Respiratory
• Central nervous system – encephalitis, meningitis
• Gastrointestinal
• Hepatitis
• Genitourinary
• Cardiac- myocarditis, pericarditis
• Ocular (eyes)
• Congenital infections
• Skin & mucous membrane
• Viral haemorrhagic fevers
• Viral infections in immunocompromised
 Viral infections by body systems

Restricted to surface epithelium Spread thru body

Eg Eg
• Influenza • SARS-CoV-2
• Common cold viruses • Measles
eg rhinoviruses, some coronaviruses • Mumps
• Parainfluenza • Rubella
• RSV • CMV
• EBV
Viral entry : Respiratory
tract
Viruses that cause skin rashes
(systemic spread)

Structure of the skin

= effective
barrier against
infection
Viral infection : the intestines /
GIT

Viral causes of diarrhoea

• Rotavirus
• Norwalk virus
• Enteric adenovirus
• Astroviruses
 Viral Hepatitis

Most common:

• Hepatitis A virus (HAV) Other viruses can cause

• Hepatitis B virus (HBV) hepatitis-
• Hepatitis C virus (HCV)
• Hepatitis D virus (delta • Epstein-Barr virus (EBV)
• Cytomegalovirus (CMV)
hepatitis, HDV) • Herpes simplex virus (HSV)
• Hepatitis E virus (HEV) -part of disseminated
infection
• Dengue virus
•Yellow fever virus - causse
haemorrhagic fever
 Viral infection : CNS

Meningitis
(viral meningitis- usually self-limited disease,
Encephalitis
compared to bacterial meningitis) (acute, severe illness, high mortality)
• Enteroviruses, echovirus, coxsackievirus • Mosquito-borne @ arboviruses
• Mumps (in non-immune) eg JE, West Nile
• HSV • Animal to human
• EBV
eg rabies
• CMV
• Human to human
• HIV
eg HSV, measles, mumps, VZV
Virus infections : Genitourinary
eg
• HSV (genital ulcers)
• HPV (anogenital warts, cervical cancer)
 Viral haemorrhagic fevers
“Arboviruses” Zoonoses
(via arthropod bite) (animal origin / reservoir,
(mainly Flaviviruses, except contact with animal, exposure
Chikungunya is Alphavirus) to excretions, etc)

• Dengue • Bunyavirus
• Chikungunya - Hantavirus
• Japanese encephalitis - Rift Valley
• Yellow Fever Fever
• Zika - Crimean-
Congo HF
• Arenavirus
– Lassa fever
• Filovirus (+human to human
transmission)
– Marburg disease
– Ebola virus disease
Chikungunya (Alphavirus, Togaviridae
family)
Japanese Encephalitis (JE)
Zika
Congenital viral Viral infections in
infections (mother to immunocompromised
baby)
• Parvovirus – fetal death, • CMV
abortion • EBV
• CMV – congenital defects • VZV
• Rubella virus - congenital • HSV
defects
• Others
• HIV – immunodeficiency
• Zika – congenital defects

Opportunistic infections
 The stages of infectious disease

• Entry into host • Immune response: limit disease or

• Infection at primary site
• Incubation period: virus is amplified,
may spread to secondary site
• Replication: in target tissue, disease
manifestations
immunopathogenesis
• Virus release/ shedding: contagiousness
• Resolution or latency/persistence
Viral infections – Stages of disease
progression
OUTCOMES
Laboratory Diagnosis of Viral Infections – summary for reference
A. Non-culture Methods
1. Cytology
2. Electron microscopy
3. Detection of viral antigen
• Immunofluorescence (IF)
• Enzyme immunoassay (EIA)
• Immunochromatography
B. Viral culture methods
C. Serological Methods
i. Detection of viral antigen
e.g. Hepatitis B virus surface antigen (HBsAg) and HIV p24 core antigen.
ii. Detection of anti-viral antibody
• Serological techniques are used to detect a rise in antibody to a specific virus in serum
collected during acute and convalescent phase of infection, for immunity status or evidence of
exposure to the virus.
• Diagnostic evidence of a recent viral infection:
 IgM seroconversion in paired sera, or
 IgG seroconversion in paired sera, or
 Fourfold IgG titer increase in paired sera (between acute and convalescent serum)
• Detection of virus specific IgM antibody or IgA is indicative of a recent infection.
• Eg Commonly used serological assays to detect IgG or IgM antibody:
 ELISA / EIA eg antiHIV, antiHCV, antiHAV IgM.
 Immunochromatography (ICT):
-Antigen detection: HBsAg
-Antibody detection: Chikungunya IgM, Dengue IgM and IgG, anti-HIV
 Particle agglutination (PA)
 Line immunoassay (LIA)
D. Detection of viral nucleic acids
 Hepatitis B

A. The serologic events associated with

the typical course of acute hepatitis
B disease.

B. Development of the chronic hepatitis

B
virus carrier state.

Anti-HBs: antibody to
HBsAg Anti-HBc: antibody
to HBcAg Anti-Hbe:
antibody to HBeAg.
Spectrum of Hepatitis B Diseases
Serology for diagnosis of Hepatitis B
Serological tests are used for the diagnosis of
acute and chronic hepatitis B:
 Hepatitis B surface antigen (HBsAg):
 Can be detected in high levels in
serum during acute or chronic
hepatitis B virus infection.
 The presence of HBsAg indicates
that
the person is infectious.
 Antibodies to HBsAg as part of
the
normal immune response to
infection.
 HBsAg is the antigen used to make
hep B vaccine.
 Hepatitis B surface antibody (anti-HBs):
 The presence generally indicates
recovery /immunity from hepatitis B
virus infection.
 Anti-HBs also develops in a person
who has been successfully vaccinated
against hepatitis B.
 Protective level of anti-HBs >10
mIU/mL
 Total hepatitis B core antibody (anti-HBc):
 Appears at the onset of symptoms in acute
hepatitis B and persists for life.
 Non-neutralizing antibodies, detected in
both acute and chronic infection
 The presence of anti-HBc indicates previous
or ongoing infection with hepatitis B virus in
an undefined time frame.
 IgM antibody to hepatitis B core antigen (anti-
HBc IgM):
 Positivity indicates recent infection with
hepatitis B virus (<6 mths).
 Its presence indicates acute infection.
 HBeAg - indicates active replication of virus and
therefore infectiveness.
 Anti-Hbe - virus no longer replicating.
However, the patient can still be HBsAg+
 HBV-DNA (viral load) - indicates active replication
of virus, more accurate than HBeAg especially in
cases of escape mutants. Used mainly for
monitoring response to therapy.
Lab tests: EIA
(automated,
routine
serology) Lab tests: rapid tests / ICT
may serve as point-of-care tests
(POCT) for first-line screening
in some circumstances
Hep B serology interpretations
 Terminology in
Terms HBV Definition

Chronic hepatitis B HBsAg seropositive status beyond 6 months.

Subdivided into HBeAg-positive and HBeAg-
negative chronic hep- atitis B (CHB).

HBeAg seroconversion loss of HBeAg and detection of anti-HBe in a

person who was previously HBeAg positive and
anti-HBe negative.

HBeAg reversion reappearance of HBeAg in a person who was

previously HBeAg negative and anti-HBe positive.

Undetectable serum HBV DNA Serum HBV DNA below detection limit of a PCR-
based assay

Resolved hepatitis B infection, Previous HBV infection, but now HBsAg(-) and anti-
‘seroconversion’ HBs
 Serology Results Interpretations

Quiz HBsAg
anti-HBc total
Negative

anti-HBs Negative
:
Q1. Hep B Negative

serology HBsAg
anti-HBc total
Negative
Reactive
anti-HBs Reactive

Interpretations: HBsAg Negative

anti-HBc total
for each anti-HBs Negative
scenario, please Reactive
select the
HBsAg Reactive
appropriate anti-HBc IgM Reactive
interpretations anti-HBs
Negative
from options
A, B, C, D, E HBsAg Reactive
anti-HBc total Reactive
anti-HBc IgM
anti-HBs Negative

Negative

Options:
A. Acutely infected
B. Chronically infected
C. Susceptible
 HCV transmission & risk factors: parenteral, sexual, perinatal
Parenteral
• Transfusion or transplant from infected
donor eg unscreened blood and blood
products
• Received transfusion or organ transplant
before
screening started in 1992
• Injecting drug use, sharing of injection
equipment
• Hemodialysis (yrs on treatment) risk 0.15%
per yr
• HCW
• Accidental injuries with needles/sharps
• Body piercing, tattooing, acupuncture,
cosmetology
• Sharing personal care items eg razors

Sexual exposure to anti-HCV+ contacts,

Multiple sex partners & other high risk, MSM

Vertical / perinatal: born to HCV-infected

mother.
 Hepatitis C

 HCV infection is diagnosed when anti-HCV is present in the

serum (serological evidence of infection)
 Testing for HCV RNA by polymerase chain reaction (PCR)
confirms the diagnosis and documents viremia
Hepatitis C infection is considered to have progressed to chronic
infection when HCV RNA persists in the blood for > 6 mths
 Laboratory Diagnosis of Hep HCV infection is diagnosed
 C
HCV antibody when anti-HCV is present in
 to diagnose hepatitis C infection. the serum (serological
 Not useful in the acute phase evidence of infection)
 takes ≥4 weeks after infection before antibody appears.
 Testing for HCV RNA by
Not useful to monitor disease progression or response to
treatment. polymerase chain reaction
 Anti-HCV is non-protective antibody ie does not indicate (PCR) confirms the diagnosis
immunity, and does not guard against future exposures to and documents viremia
HCV
 Current 3rd generation & 4th generation tests (EIA or CIA)
have a specificity and sensitivity of > 99%.
 HCV-RNA
 various molecular techniques are available e.g. PCR
 Detection of HCV RNA in blood is the currently accepted
“gold standard” for the diagnosis of active HCV infection
 May be used to diagnose HCV infection in the acute phase.
 Monitoring of HCV loads during treatment is important for
response-guided therapy to determine futility, treatment
protocol, and duration
 HCV-antigen
 Detects HCVcAg, using mAb.
 Able to detect early infection (<2 weeks),
 used in the same capacity as HCV-RNA tests but is much
easier to carry out.
Hepatitis C – Treatment
Significant progress, new drugs
• Interferon – 2 types, weekly sc
injections
• Interferon alfa-2a
• Interferon alfa-2b
• Ribavirin
• Daily oral dose
• New: Directly-Acting Antivirals
(DAA) eg
• Harvoni
• Viekira Pak
• Zepatier
• Epclusa
• Vosevi
• Mavyret
Q2. For each of the Hepatitis C infection scenarios below,
indicate the most likely diagnosis from the following options.
A. Acute / active
B. Chronic infection
C. Convalescent
D. Early acute
E. Immunological window period

Patient ALT Anti-HCV PCR Diagnosis

scenario

1. - - +

2. + - +

3. + + +

4. +/- + +

5. - + -
Acute viral hepatitis: ix
Serology - screen for hepatitis viruses A, B, and
C:

• IgM antibody to HAV (IgM anti-HAV)

• Hepatitis B surface antigen (HBsAg)
• IgM antibody to hepatitis B core (IgM anti-
HBc)
• Antibody to HCV (anti-HCV)
• [Hepatitis C RNA (HCV-RNA) PCR if anti-
HCV
pos]

If any test = positive, further serologic testing may be necessary to

differentiate acute from past or chronic infection.

If serology suggests hepatitis B, testing for HBeAg and anti-HBe

help determine the prognosis and to guide antiviral therapy.

If serologically confirmed HBV infection is severe, anti-HDV could

be suspected.

IgM anti-HEV should be tested if the test is available,

if there is history of recent travel to an endemic area.
 HIV infection

Structure of
HIV

Lifecycle of HIV
 HIV infection
Time course and stages of
HIV disease.
The stages in HIV
disease are defined by
the CD4 T-cell levels
and occurrence of
opportunistic diseases.

*ARC- acquired immune

deficiency syndrome
(AIDS)-related
complex.

Lab tests:
• Anti-HIV/ combo
• HIV RNA by PCR
•
Q3. MCQ: Hepatitis B
1. A 19 year-old male enrolling into medical school had a booster dose of hepatitis B
vaccination. One month later, his blood was taken for serology and anti-HBs was
found to be non-reactive. Regarding laboratory tests for hepatitis B:

A. ‘Non-responders’ has non-reactive anti-HBs after completion of 6 doses of

vaccination.
B. Anti-HBs levels of more than 10 IU/ml indicates protection against hepatitis B.
C. Anti-HBe positivity indicates recovery from hepatitis B infection.
D. HBsAg positivity for more than 6 months is defined as chronic infection.
E. Presence of anti-HBc indicates hepatitis B infection.

Q4. OSPE: Hep C

OSPE diagnostic technique in virology- PCR EXHIBIT B
HCV RNA by PCR:
EXHIBIT A HCV RNA detected, 11,000 IU/mL
Anti-HIV : non-reactive
Anti-HCV: reactive
HBsAg : non-reactive
RPR : non-reactive
OSPE diagnostic technique in virology- PCR

A 40-year-old intravenous drug abuser’s blood was taken for viral screening.

Exhibit A shows the serology results.

Exhibit B shows the amplification curve of real-time polymerase chain reaction (rt-
PCR) for HCV RNA.

a. Comment and interpret the results. (3 marks)

b. State the reason for doing the test in Exhibit B. (1 mark)

c. Define real-time polymerase chain reaction. (2 mark)

d. In Exhibit B, state what is represented by the: (1 mark)

x-axis:

y-axis:
e. State another molecular test required before treatment of patient (1 mark)

f. State the new drugs for treatment of this condition with ONE example. (2 marks)
Q5. MCQ: HIV
1. A 40 year-old businessman with HIV is started of anti-retroviral therapy. The
following parameter(s) is/are important in monitoring response to treatment
and disease progression:

A. anti-HIV antibody
B. CD4 lymphocyte count
C. clinical symptoms
D. HIV viral load by polymerase chain reaction
E. p24 antigen by ELISA

Q6 . MCQ: Dengue
1. A 21 year-old student developed fever, rash, headache, retro-orbital pain and
petechiae. He was diagnosed with dengue infection, which is also known as
“breakbone fever”. Regarding laboratory diagnosis of dengue:

A. Nucleic acid tests detect the viral genome within the first 5 days.

B. IgG antibody rises early in secondary infection.

C. NS1 antigen can be detected in the first week of infection

D. Positive IgM and negative IgG indicates primary dengue

E. Presence of IgG indicates immunity

Dengue

• The biggest arbovirus (arthropod-borne) problem

• Found in SE Asia, Africa, the Caribbean, South America.

• Flavivirus, 4 serotypes – DEN1,2,3,4

Presentation
Infection range from mild (‘viral fever’) to severe

a) Classical - high fever, lymphadenopathy, myalgia, bone and joint pains,

headache, retro-orbital pain, maculopapular rash.

b) Severe - Dengue haemorrhagic fever (DHF) and Dengue shock syndrome(DSS)

DHF and DSS appear most often (90%) in patients previously infected by a
different serotype of dengue (secondary dengue) - immunopathological mechanism.
 Clinical Spectrum of Dengue Infection

Dengue infected patients are either asymptomatic or they have 1 of 3 clinical presentations:
Undifferentiated Fever;
Dengue Fever with or without hemorrhage; or
Dengue Hemorrhagic Fever or Dengue Shock Syndrome.
Latest Ministry of Health Malaysia Dengue Clinical Practice Guidelines (3rd Ed) 2015:
http://www.moh.gov.my/index.php/pages/view/136
Clinical course of
DHF
Dengue virus 4 serotypes

DENV1 DENV1

DENV1
DENV2
Recovery from one
serotype gives lifelong
DENV3
immunity to that strain

DENV4

Subsequent infections (secondary

infections) by different serotypes increase
the risk of developing severe dengue/ “Antibody-
DHF dependent
enhancement”
Viral Hepatitis: Key
points
Hepatitis B and C, unlike hepatitis A,
predispose to chronic hepatitis and liver
cancer.
Mode of transmission:
Hepatitis A,E: fecal-oral route.
Hepatitis B and C: parenteral/ bloodborne,
sexual, vertical (perinatal)
Patients with acute viral hepatitis may
be anicteric or even asymptomatic.
Acute hepatitis: treatment is supportive
only (no specific antiviral).
Treatment = for chronic Hep B, chronic
Hep C
Do viral serologic testing (anti-HAV IgM,
HBsAg, anti-HCV) if clinical findings are
consistent with acute viral hepatitis and AST
and ALT are elevated out of proportion to
alkaline phosphatase.
Vaccination for hepatitis A and B.
Hep B vaccination is in Expanded Programme of
Immunisation (EPI) since 1989.
Viral infections: Key points
Viruses – rich in diversity
Viral pathogenesis depends on the
complex interplay of a large number of
viral and host factors.
Classification / types of viral infections:
• Viral infections by body systems
• Viral haemorrhagic fevers
• Congenital viral infections (mother to baby)
• Viral infections in immunocompromised /
Opportunistic infections
• Others?
Mode of transmission:
(May be different within the same virus family) Infection Prevention & Control:
• Human to human only
• Animal to human (zoonotic) • Standard Precautions
• Animal to human, via arthropods • Transmission-based precautions
(‘arboviruses’) 1. Contact
2. Droplets
Transmission / portal of viral entry may or may 3. Airborne
not be the same as site of infection / the body
system involved in disease.
Laboratory diagnosis of viral diseases:
Course of infection & outcomes of Important to know esp for blood-borne
infection: viruses – HIV, HBV, HCV
The immune response is the most
Screening by serology:
important host factor, as it determines
whether the virus is cleared or not. • Anti-HIV ab / combo
• HBsAg
Sometimes, the immune response itself • Anti-HCV
is responsible for the damage and • RPR
manifestations of disease.
 Thanks
& all the best!