SUBJECT CODE: BHCM 3163

SUBJECT NAME: PRINCIPLE OF

HEALTHCARE & DISEASE PREVENTION

WEEK: 2 (LESSON 4)
TOPIC: VIRUS INFECTION

PREPARED BY:
MS. ZAYAN NABILAH
 Virus

Classification of virus

Course Properties of virus

Learning
Outline Structure of virus

Replication of virus

Virus causing disease

Viruses
What is a virus?
‘Infectious particle’

Genetic material

Protein coat
 Properties of a virus
•A virus is a very small, infectious, obligate intracellular parasite
•Virus particles are not living
•Viruses are chemicals, and by themselves cannot reproduce
•A susceptible and permissive cellular host is needed for viruses to reproduce
• All viruses must make mRNA that can be translated by host ribosomes
Basic virus structure
Basic virus structure

DNA

OR

RNA
Basic virus structure
DNA

OR +
RNA
Basic virus structure
DNA

OR + Capsid
Protein
RNA
Basic virus structure
DNA

OR + Capsid
Protein
RNA
Basic virus structure
DNA

OR + Capsid
Protein
Nucleocapsid

RNA
 Basic virus structure
DNA
Capsid
OR
RNA
+ Protein
Nucleocapsid
 Basic virus structure
DNA
Capsid
OR
+ Protein
Nucleocapsid
=
RNA
 Basic virus structure
DNA
Capsid
OR
+ Protein
Nucleocapsid
=
RNA

+
 Basic virus structure
DNA
Capsid
OR
+ Protein
Nucleocapsid
=
RNA

Lipid membrane

Glycoproteins
 Basic virus structure
DNA
Capsid
OR
+ Protein
Nucleocapsid
=
RNA

Lipid membrane

+
Enveloped
virus
Glycoproteins
Capsid symmetry

Icosahedral Helical
Attachment
Attachment: tropism
Lock and key
Penetration
Disassembly
Disassembly
Viral genome
Transcription
Viral genome

Viral
enzymes

mRNA
Translation
Viral genome

Viral
enzymes

mRNA

Viral
proteins
Genome replication
Viral
genome

mRNA

Viral
proteins
Assembly

mRNA

Viral
proteins
Assembly
Viral genome

mRNA

Viral
proteins
Release
Retroviruses
Outcome of cellular infection
Immune response
Cell mediated immunity
◦ Important in the recovery from viral illness

Antibodies
◦ Important in the protection from repeat exposure
Mechanisms of Infection
& Pathogenesis
Viral disease :proliferation of a harmful virus inside the body and cause disease.
Viral pathogenesis interaction of viral and host factors that leads to disease
production
Steps of a virus life cycle that shape pathogenesis

1-Entry of the virus into the body.

2- Local replication in susceptible cells (tissue tropism, modulate the

host innate immune response)

3-Dissemination and spread to secondary tissues and target organs

4-Secondary replication in susceptible cells

5-Shedding of the virus into the environment

6- transmission to new host

Entry of the virus
-Entry via the Respiratory Tract
-attaching to specific receptors
on epithelial cells of mucosa
-remain localized (adenoviruses,
influenza).
-become systemic by disseminated via
lymphatics or bloodstream (rinderpest virus,
Newcastle virus).
 Entry via the Oropharynx and Intestinal Tract

-acquired by ingestion
swallowed ,reach the stomach and intestine directly or may first infect
oropharynx
- esophagus is rarely infected (its tough epithelium and the rapid passage
of swallowed material over its surface)
-rotaviruses, caliciviruses, and enteroviruses
-acid and bile resistant
 Entry via the Skin
- Breaches in skin (e.g. cuts, punctures, abrasions, or wounds)
- bite of arthropods(mosquitoes, ticks, insects)
- bite of an animal (rabies).
- predispose for viral infection
either remain in skin (Papillomaviruses)
or deeper trauma introduce viruses into the dermis with its rich supply
of vessels, lymphatics, nerves ,underlying subcutaneous tissue and
muscle.
 Entry via the Genitourinary Tract

- abrasions to the vaginal, rectal, and urethral

epithelium during sexual activity can facilitate virus
entry
(e.g., papillomaviruses, Herpes simplex virus 2)
- HIV-1 and 2, human T-lymphotropic viruses 1 and 2
and hepatitis B and C viruses, do not produce local
lesions but are sexually transmitted.
 Entry via the Eyes
Virus can reach the eye by aerosol,
Rubbing with contaminated fingers
Ophthalmic procedures with improperly sterilized instruments,
swimming pool water.
(e.g., some adenoviruses, influenza viruses, South American
arenaviruses, and enteroviruses)
Typical sites of virus entry into the

body: The first steps of viral

infection is determined by the site

at which the virus implants into

the body. This would subsequently

dictate the mechanisms of viral

pathogenesis.
 Local replication and spread
Following initial entry to the host:
The virus must modulate the host innate immune response to prevent its
elimination by the body while facilitating its replication.
Replicated virus from the initially infected cell then disperse to infect
neighboring susceptible cells.
This results in a localised infection, like common cold (rhinovirus), flu (
parainfluenza), gastrointestinal infections (rotavirus) or skin infections (
papillomavirus)
 Dissemination and secondary replication
via blood stream (viremia)
Virus can cause systemic disease through a disseminated infection
spread throughout the body via blood or lymphatic system
e.g.,chickenpox (varicella zoster virus), smallpox (variola), HIV (
human immunodeficiency virus).
A minority of viruses can disseminate via the nervous system.
This early viremia is called primary viremia (may be clinically silent).
Virus replication in major target organs leads to the sustained
production of much higher concentrations of virus producing a
secondary viremia which can in turn lead to the establishment of
infection in yet other parts of the body.
Primary and secondary
viremia
 Shedding and secondary transmission
The viruses spread to sites where shedding into the environment can
occur.
The respiratory, alimentary and urogenital tracts and the blood are the
most frequent sites of shedding in the form of bodily fluids, aerosols, skin,
excrement (the same body opening is involved in entry and exit).
The virus would then go on to be transmitted to another person and
establish the infection cycle again.
 Factors affecting pathogenesis
1. Virus tropism
2. Virus factors
3. Host factors

Virus tropism refers to the virus’ preferential site of replication in discrete

cell types within an organ.
In most cases, tropism is determined by the ability of the
viral surface proteins to fuse or bind to surface receptors of specific target
cells to establish infection.
Virus factors
Viral genetics encoding viral factors will determine the degree of viral
pathogenesis which measured as virulence.
In other words, different virus strains possessing different virus factors can
lead to different degrees of virulence.
Virus factors encoded in the genome often control the tropism, routes of virus
entry, shedding and transmission and variety of immunomodulation
mechanisms to subvert the host immune response
Host factors

Several viral infections have displayed a variety of effects, ranging from

asymptomatic to symptomatic or even critical infection, solely based of
differing host factors alone.

In particular, genetic factors, age and immunocompetence play an

important role is dictating whether the viral infection can be modulated
by the host
 Viral Disease Mechanisms

A viral infection does not always cause disease.

A viral infection simply involves viral replication in the host, but disease is the
damage caused by viral multiplication.

An individual who has a viral infection but does not display disease symptoms is
known as a carrier.
Mechanisms by which viruses cause damage
and disease to host cells
 Damage caused by the Virus

Viruses can destroy cells through a variety of mechanisms.

Viruses often induce direct cytopathic effects to disrupt cellular functions
through releasing enzymes to degrade host metabolic precursors, or
releasing proteins that inhibit the synthesis of important host factors,
proteins, DNA and/or RNA
 Viral
Infections
Importantly, viral infections can differ by the “lifestyle strategy”.
Persistent infections happen when cells continue to survive despite a viral
infection and can be further classified into latent (only the viral genome is
present, there is no replication occurring) and chronic (basal levels of viral
replication without stimulating an immune response).
In acute infections, lytic viruses are shed at high titres for rapid infection to
a secondary tissue/host, whereas persistent viruses undergo shedding at
lower titres for a longer duration of transmission (months to years)
 Lifestyle Strategies of Viruses in Host Cells
-Acute infections occur for short duration
-persistent infections (virus is not completely cleared from the body).
-latent infections, reactivation of disease occur a long time after the initial
infection
 Damage caused by Host Immune System
Sometimes, instead of cell death or cellular dysfunction caused by the virus, the host
immune response can mediate disease and excessive inflammation.
The stimulation of the innate and adaptive immune system in response to viral
infections destroys infected cells, which may lead to severe pathological
consequences to the host.
This damage caused by the immune system is known as virus induced
immunopathology.
Specifically, immunopathology is caused by the excessive release of antibodies,
interferons and pro-inflammatory cytokines, secretion of interferons and other
cytokines can trigger cell damage, fever and flu-like symptoms.
In severe cases of certain viral infections, as in avian H5N1 influenza in 2005,
aberrant induction of the host immune response can elicit a flaring release of
cytokines known as a cytokine storm
 Parvoviridae
Erythrovirus is human pathogen.
Causes lace like rash that lasts a few days.
Children 4-10 years old most affected.
Transmission occurs during incubation period.
No longer infectious by appearance of rash.
 Papovaviridae
Papilloma virus
◦ Skin warts and genital warts
◦ Various strains of Human Papilloma Virus (HPV). Each have
preference for different body sites.
◦ Grouped into 2 main categories:
◦ 1) cutaneous
◦ 2) mucosal
◦ Incubation can be up to 2 years before signs or symptoms
are detected.
◦ Genome can persist in cells for years without outward signs.
◦ Early genes stimulate proliferation of basal cells which
causes the protruding papilloma (visible tissue or wart).
Cutaneous (plain old warts)
◦ Transmission through skin abrasions
◦ Commonly picked up from wet floors of public swimming pools and
bathrooms
◦ Subsequent spreading through scratching, picking, digging of wart.
◦ Reaction
◦ Wart regresses spontaneously.
◦ Cryotherapy (freezing with liquid Nitrogen) or injectable anti-cancer
drugs are occasionally effective.
Mucosal
◦ Transmission through abrasions during sexual intercourse
◦ Can cause cancer by inactivation tumor suppressor gene products.
The tumor suppress gene prevents the uncontrolled growth of cells.
When it’s function is compromised uncontrolled cell growth is
allowed causing tumors.
◦ Cervical carcinomas may develop 20-50 years post infection because
the genome of the virus persists in the infected cells.
◦ Reaction
◦ Laser
◦ Surgery
◦ Vaccination: currently testing vaccine against mucosal strains
◦ On average, there are 9,710 new cases and 3,700 deaths from cervical
cancer in the United States each year.
◦ HPV is the most common sexually transmitted infection in the United
States, More than 20 million men and women in the United States are
currently infected with HPV and there are 6.2 million new infections
each year. HPV is most common in young women and men who are in
their late teens and early 20s. By age 50, at least 80 percent of
women will have acquired HPV infection.

◦ “Although an effective vaccine is a major advance in the prevention of

genital HPV and cervical cancer, it will not replace other prevention
strategies, such as cervical cancer screening for women or protective
sexual behaviors,” said Dr. Schuchat “Women should continue to get
pap tests as a safeguard against cervical cancer.”’ www.cdc.gov
 Herpesviridae
◦ 2 types of Herpes Simplex Virus
◦ 1) Herpes Simplex Virus 1 (HSV-1): cold sores, shed in saliva,
contaminated hands, eating utensils, etc.
◦ 2) HSV-2: sexual intercourse, through infected birth canal to infants
◦ Varicella Zoster, Chickenpox/Shingles: to be covered in the group
presentations.
Signs and Symptoms
◦ infection causes groups of small,
painful blisters. The fluid in the
blisters may be clear or cloudy.
The area under the blisters will
be red. The blisters break open
so easily that they quickly
become open sores.
◦ It may hurt to urinate. You may
run a fever and have other flu-
like symptoms.
Transmission
◦ Spread by close person to person contact w/ lesions or mucosal
secretions
◦ Infects sensory neurons and remains for in the sensory neurons life,
causing recurrent infections.
◦ Initial infection is usually more severe w/ subsequent infections
decreasing in frequency, duration, and severity.
Prevention and Reaction
◦ Avoid contact when lesions are present.
◦ Use condoms during sexual intercourse whether or not lesions are
present.
◦ Acyclovir
◦ Inhibits DNA polymerase
◦ Helps to further decrease the frequency and duration of
subsequent outbreaks.
 Calicivirida
e
Norwalk virus
◦ Responsible for most gastroenteritis cases
◦ Signs and symptoms:
◦ mild fever, nausea, vomiting, malaise, myalgia (muscle aches)
◦ Transmission: Contact with infected body fluids, fomites.
◦ Prevention: wash your hands frequently.
 Picornavirida
e
Poliovirus: Will be discussed at a later time.
Enteroviruses
◦ Commonly infect children, produce life-long immunity
◦ Can cause meningitis, carditis, rashes (very common),
sometimes colds or sore throats during summer, as well as
other types of disease.
◦ Transmitted mainly by close contact via fecal-oral route,
droplet spread can also occur.
Rhinoviruses
◦ Over 100 different rhinoviruses, which cause 50% of all colds
◦ No possibility for vaccine yet
◦ 3 or 4 rhinovirus types circulate among community
simultaneously.
◦ Virus shed in nasal secretions for 2-3 days.
Transmission
◦ Spread through sneezing, coughing, contamination of hands,
handkerchiefs, any other fomites, to nose or eye.
◦ Because generally acquire cold during cold weather, has generated
myth that if exposed to cold weather will get a cold. Remember
that it is the organism that causes the cold, not the weather or
how little clothing one is wearing. However, the weather and
clothing can be predisposing factors for acquiring an illness.
Hepatitis A
◦ Similar symptoms to Hepatitis B
◦ Preicteric phase: malaise, anorexia, nausea, and lethargy aren’t as
bad, don’t last as long
◦ Icteric phase: Hepatomegaly may produce pain in the right upper
abdominal quadrant, followed by bilirubinuria, then pale feces and
jaundice.
◦ Convalescent phase: signs and symptoms decrease, virus is
eliminated from body.
◦ Transmission
◦ Oral-Fecal route. Virus passed in the feces of an infected person. It
is transmitted when an infected individual fails to wash his hands
after going to the bathroom, etc.
◦ Multiplies in intestinal cells before entering blood stream and
infecting liver
 ◦ Incubation period is about 4 weeks
◦ Most infections occur in children (usually subclinical)
◦ Illness usually last 4 weeks
◦ Reaction and prevention
◦ Good public and personal hygiene
◦ Vaccine for children, especially those exposed to other children on a
daily basis such as in daycare
 Orthomyxoviridae
Influenza
◦ Signs and symptoms
◦ Fever, sore throat, nonproductive cough, myalgia, headache, and
malaise
◦ Lasts 3-7 days
◦ Complications depend on age of patient
◦ Possible pneumonia, middle ear infection, croup
◦ Susceptible to secondary bacterial infections
Transmission
◦ Droplet (sneezing and coughing)
◦ Short incubation period (1-4 days)
◦ Antigens frequently mutate causing new strains, this is called an
antigenic shift.
◦ Influenza Type A undergoes an antigenic shift every 10-40
years.
◦ Flu season is generally Oct. to Mar each year.

◦ Note: The vaccine given to infants called Hemophilus

influenzae is not the same as the flu vaccine. The bacteria
mentioned above causes meningitis, not influenza.
Vaccine
◦ Develop according to prevalent strain in other part of world
◦ Recommend that elderly and under 2 receive vaccine as well as
those more likely to be exposed such as care givers of young
children.
◦ The vaccine is made according to the strains that affect the other
side of the world when it is not our flu season. The most prevalent
strains are then used to manufacture the virus for our flu season.
◦ If the strain mutates or if a new strain is introduced into the
population after the virus has been manufactured, the vaccine
probably won’t provide adequate protection against all strains of
the virus.
◦ Each year a new flu vaccine is recommended because the strains
change from year to year.
REFERENCES

Merrill, Ray M. (2021). Introduction to Epidemiology (8th ed.).

Jones and Bartlett Learning Publisher.
THANK YOU