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Virology Note

Viruses are non-cellular infectious agents composed of proteins and nucleic acids, lacking independent metabolic processes and relying on host cells for replication. They can cause various effects on host cells, including cell death and malignant transformation, and can be classified based on their morphology and biochemical properties. Viral infections can be localized or disseminated, and some viruses can persist in the body, leading to chronic or latent infections.

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0% found this document useful (0 votes)
15 views23 pages

Virology Note

Viruses are non-cellular infectious agents composed of proteins and nucleic acids, lacking independent metabolic processes and relying on host cells for replication. They can cause various effects on host cells, including cell death and malignant transformation, and can be classified based on their morphology and biochemical properties. Viral infections can be localized or disseminated, and some viruses can persist in the body, leading to chronic or latent infections.

Uploaded by

sa'di Osman
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Introduction to Viruses
Viruses are complexes consisting of protein and an RNA or DNA genome. They lack
both cellular structure and independent metabolic processes.

A virus is an autonomous infectious particle that differs widely from other


microorganisms in a number of characteristics.

Characteristics of Viruses
The essential characteristics of viruses are:

They have no cellular structure, consisting only of proteins and nucleic acid
(DNA or RNA)
They have no metabolic systems of their own
They depend on the synthetic mechanism of a living host cell
They exploit normal cellular metabolism by delivering their own genetic
information into the host cell

Morphology and Structure


A mature virus particle, also known as a virion, consists of:

1. A genome of DNA or RNA


Double-stranded or single-stranded, linear or circular, and in some cases
segmented
A single-stranded nucleic acid can have plus or minus polarity
2. The capsid
Enclosing the genome of the virus and determining its antigenicity
Can have a cubic rotational, helical, or complex symmetry
Made up of subunits called capsomers
3. In some cases, an envelope
Surrounds the capsid and is always derived from cellular membranes

Classification of Viruses
The taxonomic system used for viruses is artificial and based on the following
morphological and biochemical criteria:

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Criteria Description

Genome DNA or RNA genome


Capsid symmetry Cubic, helical, or complex symmetry
Presence or absence of an envelope Envelope surrounds the capsid
Diameter of the virion Size of the virion or nucleocapsid

Replication of Viruses
The steps in viral replication are:

Adsorption of the virus to specific receptors on the cell surface


Penetration by the virus and intracellular release of nucleic acid
Proliferation of the viral components: virus-coded synthesis of capsid and
noncapsid proteins, replication of nucleic acid by viral and cellular enzymes
Assembly of replicated nucleic acid and new capsid protein
Release of virus progeny from the cell

Host-Cell Reactions
Possible consequences of viral infection for the host cell:

Cytocidal infection necrosis: viral replication results directly in cell destruction


Apoptosis: the virus initiates a cascade of cellular events leading to cell death
Noncytocidal infection: viral replication per se does not destroy the host cell
Latent infection: the viral genome is inside the cell, resulting in neither viral
replication nor cell destruction
Tumor transformation: the viral infection transforms the host cell into a cancer
cell

Pathogenesis
The ability of viruses to cause disease can be viewed on two distinct levels:

1. The changes that occur within individual cells


2. The process that takes place in the infected patient

The Infected Cell


There are four main effects of virus infection on the cell:

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1. Death
2. Fusion of cells to form multinucleated cells
3. Malignant transformation
4. No apparent morphologic or functional change

Effects of Virus Infection on the Cell


Inhibition of host cell protein synthesis frequently occurs first and is probably
the most important effect
Inhibition of DNA and RNA synthesis may be a secondary effect
Inclusion bodies are discrete areas containing viral proteins or viral particles
Cytopathic effect CP E is a change in the appearance of the infected cell,
usually beginning with a rounding and darkening of the cell

The Infected Patient


Pathogenesis in the infected patient involves:

1. Transmission of the virus and its entry into the host


2. Replication of the virus and damage to cells
3. Spread of the virus to other cells and organs
4. The immune response## Stages of a Typical Viral Infection The stages of a
typical viral infection are the same as those described for a bacterial infection,
namely:
5. An incubation period during which the patient is asymptomatic
6. A prodromal period during which nonspecific symptoms occur
7. A specific-illness period during which the characteristic symptoms and signs
occur
8. A recovery period during which the illness wanes and the patient regains good
health

Transmission and Portal of Entry


Transmission of viruses can occur through:

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Person-to-person spread by transfer of respiratory secretions, saliva, blood, or


semen and by fecal contamination of water or food
Vertical transmission from mother to offspring in utero, at the time of delivery,
or during breast feeding
Horizontal transmission that is not from mother to offspring
Zoonotic transmission from animals to humans, either directly or indirectly
through an insect vector

Localized or Disseminated Infections


Most viral infections are either localized to the portal of entry or spread systemically
through the body. Examples of localized infections include:

The common cold caused by rhinoviruses, which involves only the upper
respiratory tract
Influenza, which is localized primarily to the upper and lower respiratory tracts
Examples of systemic infections include:
Poliomyelitis and measles, which have a long incubation period due to viremia
and secondary sites of replication

Pathogenesis and Immunopathogenesis


The signs and symptoms of most viral diseases are the result of cell killing by virus-
induced inhibition of macromolecular synthesis.

Cell killing by virus-induced inhibition of macromolecular synthesis occurs


when a virus infects a cell and inhibits the cell's ability to produce
essential proteins and other molecules, leading to cell death.

However, some diseases are not caused by the virus damaging or killing the infected
cell, but rather by:

Stimulation of the enteric nervous system, as seen in rotavirus-induced


diarrhea
Immunologic attack by cytotoxic T cells and antibodies, as seen in
lymphocytic choriomeningitis and hepatitis

Virulence

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Virulence refers to the ability of a virus to cause disease. Strains of viruses differ
greatly in their ability to cause disease, with some strains being attenuated and used
in vaccines. The viral genes that control virulence are poorly characterized, and the
process of virulence is poorly understood.

Evasion of Host Defenses


Viruses have several ways to evade host defenses, including:

Synthesis of receptors for immunemediators, such as interleukin-1 and tumor


necrosis factor
Reduction of expression of class I MHC proteins
Production of cytokine decoys, which bind to immune mediators and block
their ability to interact with receptors on immune cells

Multiple Antigenic Types


Some viruses have multiple antigenic types, also known as multiple serotypes. This
allows a patient to be infected with one serotype, recover, and have antibodies that
protect against infection by that serotype in the future, but still be susceptible to
infection by another serotype of the same virus. Examples of viruses with multiple
serotypes include:

Rhinovirus, which has over 100 serotypes


Influenza virus, which has multiple serotypes and is responsible for severe
worldwide epidemics

Persistent Viral Infections


In most viral infections, the virus does not remain in the body for a significant period
after clinical recovery. However, in certain instances, the virus persists for long
periods either intact or in the form of a subviral component. The mechanisms that
may play a role in the persistence of viruses include:

Integration of a DNA provirus into host cell DNA, as occurs with retroviruses
Immune tolerance, because neutralizing antibodies are not formed
Formation of virus-antibody complexes## Persistent Viral Infections
Persistent viral infections can be categorized into three main types: Chronic-
Carrier Infections, Latent Infections, and Slow Virus Infections. These types
are distinguished by whether the virus is produced by the infected cells and the
timing of the appearance of the virus and symptoms of the disease.

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Chronic-Carrier Infections
In Chronic-Carrier Infections, patients continue to produce significant amounts of the
virus for long periods. This can occur after an asymptomatic infection or an actual
disease, and can be either asymptomatic or result in chronic illness. Examples of
chronic-carrier infections include:

Chronic hepatitis hepatitisBandhepatitisCviruscarriers


Neonatal rubella virus and CMV infections

Latent Infections
Latent Infections are characterized by the recovery of the patient from the initial
infection, followed by a stop in virus production. The symptoms may recur,
accompanied by the production of virus. The Herpesvirus group is a prime example
of latent infections.

A latent infection is a type of infection where the virus is present in the


body, but not actively replicating, and can reactivate at a later time.

Examples of latent infections include:

Herpes Simplex Virus Type 1: latent in the trigeminal ganglion, causing


infections primarily of the eyes and face
Herpes Simplex Virus Type 2: latent in the lumbar and sacral ganglia, causing
infections primarily of the genitals
Varicella-Zoster Virus: latent in the trigeminal or thoracic ganglion cells,
causing Varicella chickenpox as its initial manifestation and Zoster shingles as
a recurrence

Slow Virus Infections


Slow Virus Infections are characterized by a prolonged period between the initial
infection and the onset of disease, usually measured in years. The virus has a normal
growth cycle, but the incubation period and disease progression are prolonged.
Examples of slow virus infections include:

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Subacute Sclerosing Panencephalitis: caused by Measles Virus, occurring


several years after the initial infection
Progressive Multifocal Leukoencephalopathy P ML: caused by JC Virus, a
papovavirus, occurring primarily in patients with lymphomas or
immunosuppression

Pathogenesis
Pathogenesis refers to the development of a disease. In the context of viral
infections, pathogenesis involves:

Transmission of the virus and its entry into the host


Replication of the virus and damage to cells
Spread of the virus to other cells and organs
The immune response, both as a host defense and as a contributing cause of
certain diseases
Persistence of the virus in some instances

The Infected Cell


The effects of virus infection on the cell can be categorized into four main types:

1. Death: due to inhibition of macromolecular synthesis


2. Fusion of cells: to form multinucleated cells, characteristic of Herpesvirus and
Paramyxovirus infections
3. Malignant transformation: characterized by unrestrained growth, prolonged
survival, and morphologic changes
4. No apparent morphologic or functional change: the cell survives and
multiplies despite the replication of the virus

Transmission and Portal of Entry


Viruses can be transmitted to an individual through various routes, including:

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Person-to-person spread: through respiratory secretions, saliva, blood, or


semen, and fecal contamination of water or food
Vertical transmission: from mother to offspring, either in utero, at the time of
delivery, or during breast feeding
Horizontal transmission: person-to-person transmission that is not from mother
to offspring
Animal-to-human transmission: either directly from the bite of a reservoir host
or indirectly through the bite of an insect vector

Localized or Disseminated Infections


Viral infections can be either Localized or Disseminated. Localized infections are
confined to the portal of entry, while disseminated infections spread systemically
through the body. Examples of localized infections include the common cold and
influenza, while examples of disseminated infections include poliomyelitis and
measles.

The following table summarizes the characteristics of localized and disseminated


infections:

Type of
Characteristics Examples
Infection

Confined to the portal of entry, short incubation Common cold,


Localized
period Influenza
Spreads systemically through the body, long Poliomyelitis,
Disseminated
incubation period Measles

Pathogenesis and Immunopathogenesis


The signs and symptoms of most viral diseases are the result of cell killing by virus-
induced inhibition of macromolecular synthesis. However, some diseases are not
caused by the virus damaging or killing the infected cell, but rather by the stimulation
of the enteric nervous system, as seen in Rotavirus-induced diarrhea. The immune
response can also contribute to the development of certain diseases.

The following table summarizes the stages of a typical viral infection:

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Stage Characteristics

Asymptomatic, virus
Incubation period
replication and spread
Nonspecific symptoms,
Prodromal period such as fever and
headache
Characteristic symptoms
Specific-illness period
and signs of the disease
Illness wanes, and the
Recovery period patient regains good
health
Virus persists in the body,
and the patient may
Chronic carrier state or latent infection
experience recurring
symptoms
Cytotoxic T cells and antibodies play a crucial role in the
pathogenesis of various diseases. For instance, in
hepatitis caused by hepatitis A, B, and C viruses,
cytotoxic T cells recognize viral antigens on the surface of
hepatocytes, leading to damage and disease.

The process by which the immune system causes tissue damage and
disease is known as immunopathogenesis.

Virulence
Virulence refers to the ability of a virus to cause disease. Different strains of viruses
can have varying levels of virulence. For example, some strains of poliovirus have
mutated to become attenuated, meaning they have lost their ability to cause disease
in immunocompetent individuals.

Evasion of Host Defenses


Viruses have developed several mechanisms to evade the host's immune system,
including:

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Encoding receptors for immune mediators such as interleukin-1 IL − 1 and


tumor necrosis factor T NF
Reducing the expression of class I MHC
Blocking the synthesis of IL-12
Synthesizing proteins that block the induction or action of interferon

These viral proteins are often referred to as cytokine decoys or virokines.

Persistent Viral Infections


In some cases, viruses can persist in the body for long periods, either intact or as a
subviral component. The mechanisms that contribute to persistent infections include:

Integration of a DNA provirus into host cell DNA


Immune tolerance
Formation of virus-antibody complexes
Location within an immunologically sheltered sanctuary
Rapid antigenic variation
Spread from cell to cell without an extracellular phase
Immunosuppression

Chronic-Carrier Infections
Some individuals can become chronic carriers of a virus, producing significant
amounts of the virus over long periods. This can occur after an asymptomatic
infection or actual disease and can result in chronic illness. Examples include chronic
hepatitis caused by hepatitis B and C viruses.

Latent Infections
In latent infections, the virus remains dormant in the body, and symptoms may recur
periodically. This is often seen in herpesvirus infections, where the virus enters a
latent state in the cells of the sensory ganglia.

Slow Virus Infections


Slow virus infections are characterized by a prolonged period between initial
infection and the onset of disease, often measured in years. Examples include
HIV/AIDS and subacute sclerosing panencephalitis.

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Classification of Medically Important Viruses


The classification of viruses is based on chemical and morphologic criteria, including
the type of nucleic acid and the structure of the capsid.

DNA Viruses
The following table summarizes the characteristics of medically important DNA
viruses:

Virus Family Size nm Shape Envelope Nucleic Acid

Parvoviruses 22 Icosahedral Naked Single-stranded linear DNA


Polyomaviruses 45 Icosahedral Naked Double-stranded circular DNA
Papillomaviruses 55 Icosahedral Naked Double-stranded supercoiled DNA
Adenoviruses 75 Icosahedral Naked Double-stranded linear DNA
Hepadnaviruses 42 Icosahedral Enveloped Double-stranded circular DNA
Herpesviruses 100 Icosahedral Enveloped Double-stranded linear DNA
Poxviruses - Brick-like Enveloped Double-stranded linear DNA

RNA Viruses
The following table summarizes the characteristics of medically important RNA
viruses:

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Size
Virus Family Shape Envelope Nucleic Acid
nm

Single-stranded
Picornaviruses 28 Icosahedral Naked
linear RNA
Single-stranded
Hepeviruses 30 Icosahedral Naked
linear RNA
Single-stranded
Caliciviruses - Icosahedral Naked
linear RNA
Single-stranded
Flaviviruses - Icosahedral Enveloped
linear RNA
Single-stranded
Togaviruses - Icosahedral Enveloped
linear RNA
Single-stranded
Retroviruses - - Enveloped
linear RNA
Single-stranded
Orthomyxoviruses - Helical Enveloped
linear RNA
Single-stranded
Paramyxoviruses - Helical Enveloped
linear RNA
Single-stranded
Rhabdoviruses - Helical Enveloped
linear RNA
Single-stranded
Filoviruses - Helical Enveloped
linear RNA
Single-stranded
Coronaviruses - Helical Enveloped
linear RNA
Single-stranded
Arenaviruses - Helical Enveloped
linear RNA
Single-stranded
Bunyaviruses - Helical Enveloped
linear RNA
Single-stranded
Deltavirus - - -
circular RNA
The main human pathogens in this
category include:

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Hepatitis E virus: a type of Calicivirus


Norovirus: a type of Calicivirus
Rotavirus: a type of Reovirus
Hepatitis C virus: a type of Flavivirus
Dengue virus: a type of Flavivirus
West Nile virus: a type of Flavivirus
Rabies virus: a type of Rhabdovirus
Ebola virus: a type of Filovirus
Marburg virus: a type of Filovirus
Coronaviruses: cause respiratory tract infections, such as the common cold,
SARS, and COVID-19

Characteristics of Viruses with Single-Stranded RNA


Genomes
The following table summarizes the characteristics of these viruses:

Virus Family Diameter Capsid Genome

Single-stranded, linear,
Caliciviruses 38 nm Icosahedral nonsegmented, positive-polarity
RNA
Two icosahedral 10 or 11 segments of double-
Reoviruses 75 nm
capsid coats stranded linear RNA
Single-stranded, linear,
Flaviviruses Enveloped Icosahedral nonsegmented, positive-polarity
RNA
Single-stranded, linear,
Bullet-shaped, Helical
Rhabdoviruses nonsegmented, negative-polarity
enveloped nucleocapsid
RNA
Single-stranded, linear,
Helical
Filoviruses Enveloped nonsegmented, negative-polarity
nucleocapsid
RNA
Single-stranded, linear,
Helical
Coronaviruses Enveloped nonsegmented, positive-polarity
nucleocapsid
RNA

Viruses with Double-Stranded DNA Genomes

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The main human pathogens in this category include:

Papillomaviruses: cause warts and cervical cancer


Adenoviruses: cause respiratory tract infections, eye infections, and intestinal
infections
Hepatitis B virus: causes hepatitis B

Characteristics of Viruses with Double-Stranded DNA


Genomes
The following table summarizes the characteristics of these viruses:

Virus Family Diameter Capsid Genome

Papillomaviruses 55 nm Icosahedral Linear, 8 kbp dsDNA


Adenoviruses 70-90 nm Icosahedral Linear, 36-38 kbp dsDNA
Hepadnaviruses Enveloped Icosahedral Partially double-stranded DNA

Definitions
Oncogene: a gene that has the potential to cause cancer Tumor
suppressor gene: a gene that helps to prevent cancer Ambisense RNA: a
type of RNA that contains both positive-polarity and negative-polarity
sequences Reverse transcription: the process of converting RNA into
DNA

Prevention and Treatment


Papillomaviruses: prevention includes vaccination and hygienic measures,
treatment includes topical chemotherapy and surgical removal of tumors
Adenoviruses: prevention includes hygienic measures and vaccination,
treatment includes antiviral medication and supportive care
Hepatitis B virus: prevention includes vaccination and safe sex practices,
treatment includes antiviral medication and liver transplantation in severe
cases

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Epidemiology
Papillomaviruses: transmitted through direct contact and autoinoculation
Adenoviruses: transmitted through droplet infection, smear infection, and
fecal-oral route
Hepatitis B virus: transmitted through blood and bodily fluids, mother-to-
child transmission, and unsafe sex practices## Hepatitis B Virus HBV The
Hepatitis B Virus HBV is a member of the Hepadnaviridae family. The
complete, infectious virion is also known as the Dane particle, named after its
discoverer. It has a diameter of 42 nm, with an inner structure of 27 nm. The
virus replicates in liver cells.

The HBV antigens include:

HBs antigen: present in two different forms, a filamentous particle


approximately 22x100 nm and a spherical form with a diameter of about 22 nm
HBc antigen: not released into the bloodstream
HBe antigen: a posttranslational, truncated form of the HBc antigen, released
from the hepatic cells into the blood

Hepatitis D Virus HDV


The Hepatitis D Virus HDV is an unclassified RNA virus that codes for the delta
antigen. Its capsid consists of HBs antigen, which is HBV-coded material. For this
reason, the virus can only replicate in persons infected with HBV thehelpervirus.

The Hepatitis D Virus HDV is a small, single-stranded RNA virus that


requires the presence of HBV to replicate.

The HDV has a size of 36 nm and possesses a very short viral RNA containing 1683
nucleotides. Its transcription and replication take place in the cell nucleus by means
of a cellular polymerase.

Pathogenesis and Clinical Picture


The incubation period of hepatitis B is 4 to 12 weeks, followed by the acute infection
phase, which can be icteric or anicteric. The hepatic cell damage resulting from an
HBV infection is not primarily due to cytopathic activity of the virus, but rather to a
humoral and cellular immune response directed against the virus-induced membrane
antigens (HBs, HBc) on the surface of the infected hepatocytes.

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The clinical course of hepatitis B can be:

Fulminant: often lethal, experienced by 0.51% of those infected


Benign: complete recovery and elimination of the HBV from the body,
experienced by 80-90% of cases
Chronic: develops in 5-10% of cases, with three forms differentiated:
Healthy HBV carriers
Chronic persistent hepatitis CP H without viral replication
Chronic aggressive hepatitis CAH with viral replication and a
progressive course

Diagnosis
Hepatitis B is diagnosed by identifying the various HBV antigens or the antibodies
directed against them. Both antigens and antibodies can be detected in patient blood
using ELISA. The Hepatitis D Virus HDV is diagnosed by detection of delta antigen
or possibly antibodies to delta IgM in the blood.

Epidemiology and Prevention


The global distribution of hepatitis B is widespread. Humans are the sole reservoir of
HBV. Transmission is parenteral, either with blood or body fluids containing HBV
sexualintercourse that come into contact with mucosa, lesions, or microlesions in the
skin.

The WHO recommends general hepatitis B prophylaxis in the form of active


immunization with HBs antigen. In response to a sudden high-level infection risk
accidentalinoculationwithinfectiousmaterial, persons whose immune status is
uncertain should also be passively immunized with human anti-HBs antiserum.

Properties of Hepatitis Viruses


The following table summarizes the properties of hepatitis viruses:

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Virion Genome
Virus Family Genus Envelope Genome
Size Size kb

Hepatitis
Picornaviridae Hepatovirus 27 nm No ssRNA 7.5
A
Hepatitis Yes
Hepadnaviridae Orthohepadnavirus 42 nm dsDNA 3.2
B HBsAg
Hepatitis
Flaviviridae Hepacivirus 60 nm Yes ssRNA 9.4
C
Hepatitis Yes
Unclassified Delta virus 35 nm ssRNA 1.7
D HBsAg
Hepatitis 30-32
Hepeviridae Hepevirus No ssRNA 7.2
E nm

Picornaviruses
The picornaviruses are a family of small, single-stranded RNA viruses that include:

Enteroviruses: e.g., polioviruses, coxsackieviruses, echoviruses


Parechoviruses: e.g., types 1 and 2
Hepatoviruses: e.g., hepatitis A virus
Rhinoviruses: e.g., common cold viruses

Enteroviruses
The enteroviruses are transmitted perorally through saliva and replicate in the
lymphoid tissue of the pharyngeal space and intestinal wall. They can cause a range
of diseases, including:

Poliomyelitis: caused by polioviruses


Meningitis: caused by coxsackieviruses and echoviruses
Myocarditis: caused by coxsackieviruses

Hepatoviruses HepatitisAV irus


The hepatitis A virus is a member of the picornaviridae family. It differs from
enteroviruses in some characteristics and requires long adaptation to grow in cell
cultures. Only one serotype is known to date.

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The clinical picture of hepatitis A is similar to that of hepatitis B, with a benign


course in most cases. The disease is transmitted through food and water or by smear
infections, and active immunization with an inactivated HAV vaccine is available.##
Hepatitis Viruses Hepatitis viruses are a group of viruses that cause hepatitis, a
disease characterized by inflammation of the liver. The main types of hepatitis viruses
are Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E.

Nomenclature and Definitions


The following are definitions of the different components of hepatitis viruses:

Hepatitis A virus HAV is the etiologic agent of infectious hepatitis.


Hepatitis B virus HBV is a common etiologic agent of posttransfusion
hepatitis. Hepatitis C virus HCV is a flavivirus that causes hepatitis C.
Hepatitis D virus HDV is the etiologic agent of delta hepatitis. Hepatitis E
virus HEV is an enterically transmitted hepatitis virus.

Epidemiologic and Clinical Features


The following table summarizes the epidemiologic and clinical features of the
different types of hepatitis viruses:

Feature Hepatitis A Hepatitis B Hepatitis C

Incubation
10-50 days 50-180 days 15-160 days
period
Principal age
Children, young adults Adults Adults
distribution
Seasonal Throughout the year,
Throughout the year Throughout the year
incidence peaks in autumn
Route of
Fecal-oral Parenteral Parenteral
infection
Occurrence of 2 weeks before to 1
Months to years Months to years
virus in blood week after jaundice
Abrupt onset, fever, Insidious onset, fever, Insidious onset, fever,
Clinical and
elevated elevated elevated
laboratory
aminotransferase aminotransferase aminotransferase
features
levels levels levels

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Transmission and Outcomes


The transmission and outcomes of the different types of hepatitis viruses are as
follows:

Hepatitis A: transmitted through the fecal-oral route, outcomes include


inapparent infection, icteric disease, complete recovery, and rare mortality.
Hepatitis B: transmitted through parenteral and sexual routes, outcomes
include recovery from acute infection, progression to chronic infection, and
chronic carriers.
Hepatitis C: transmitted through parenteral and sexual routes, outcomes
include recovery from acute infection, progression to chronic infection, and
chronic carriers.

Measles Virus
Measles virus is a paramyxovirus that causes measles, a disease characterized by a
maculopapular rash.

Important Properties
The measles virus has the following important properties:

The genome of the measles virus is composed of RNA and nucleocapsid.


The virion has two types of envelope spikes, one with hemagglutinating
activity and the other with cell-fusing and hemolytic activities. The
measles virus has a single serotype, and the hemagglutinin is the antigen
against which neutralizing antibody is directed.

Replicative Cycle
The replicative cycle of the measles virus involves the following steps:

Adsorption to the cell surface via its hemagglutinin


Penetration and uncoating of the virus
Transcription of the viral genome into mRNA
Translation of the mRNA into specific viral proteins
Assembly and release of the new virions

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Transmission and Epidemiology


The measles virus is transmitted through respiratory droplets produced by coughing
and sneezing. The virus occurs worldwide, usually in outbreaks every 2-3 years,
when the number of susceptible children reaches a high level.

Clinical Findings
The clinical findings of measles include:

Prodromal phase: characterized by fever, conjunctivitis, running nose, and


coughing
Kopliks spots: bright red lesions with a white, central dot that are located on
the buccal mucosa
Maculopapular rash: appears on the face and proceeds gradually down the
body to the lower extremities

Complications
The complications of measles can be severe and include:

Encephalitis: occurs at a rate of 1 per 1000 cases of measles


Pneumonia: both primary measles giantcell pneumonia and secondary
bacterial pneumonia
Bacterial otitis media: common in children with measles
Subacute sclerosing panencephalitis SSP E: a rare, fatal disease of the central
nervous system that occurs several years after measles

Prevention
Prevention of measles rests on immunization with the live, attenuated vaccine. The
vaccine is effective and causes few side effects. It is given subcutaneously to children
at 15 months of age, usually in combination with rubella and mumps vaccines MMR
.## Introduction to Influenza Influenza, also known as the flu, is a highly contagious
respiratory illness caused by the influenza virus. The virus is spread from person to
person through respiratory secretions, either as droplets or through airborne
infection.

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Characteristics of Influenza Virus


The influenza virus has the following characteristics:

Diameter: 80-120 nm
Pleomorphic, spherical, filamentous particles
Single-stranded RNA
Segmented genome, 8 segments in A and B
Hemagglutinin and Neuraminidase on the surface of the virion

Causative Agent of Influenza


The causative agent of influenza is a virus belonging to the MYXOVIRUS group,
which comprises:

1. Orthomyxovirus
2. Paramyxovirus Influenza virus is an Orthomyxovirus, classified as Baltimore
Group V C−SSRNA).

Structure of Influenza Virus


The structure of the influenza virus consists of:

Nucleoprotein
Neuraminidase
RNA
Lipid bilayer membrane
Hemagglutinin
Matrix protein M1
Matrix protein M2

Hemagglutinin
Hemagglutinin is a homotrimeric glycoprotein found on the surface of
influenza viruses and is integral to its infectivity. It functions as an
attachment factor, binding the influenza virus to sialic acid on the surface
of target cells, and as a membrane fusion protein, fusing the viral
envelope with the late endosomal membrane.

Neuraminidase

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Neuraminidase is a type of enzyme found on the surface of influenza


viruses that enables the virus to be released from the host cell. It cleaves
sialic acid groups from glycoproteins, allowing the virus to spread.

Types of Influenza Virus


There are three types of influenza virus:

Type Description

A Causes worldwide epidemics pandemics of influenza


B Causes major outbreaks of influenza
Causes mild respiratory tract infections, but does not cause outbreaks of
C
influenza

Pandemics
Pandemics occur when a variant of influenza A virus that contains a new
hemagglutinin against which people do not have pre-existing antibodies is
introduced into the human population.

Antigenic Variation
Influenza viruses tend to undergo changes from time to time, resulting in two types
of changes:

Antigenic shift: Major changes in hemagglutinin and neuraminidase resulting


from reassortment of gene segments involving two different influenza viruses.
Antigenic drift: Minor changes in hemagglutinin and neuraminidase resulting
from mutation in the RNA segments coding for either the HA or NA.

Control Measures
Control measures for influenza include:

Immunoprophylaxis with vaccine


Chemoprophylaxis and chemotherapy
Types of vaccine: Inactivated, live attenuated
Antiviral drugs: Amantadine, rimantadine, zanamivir, oseltamivir

Coronaviruses

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Coronaviruses were discovered in the 1960s and are believed to cause a significant
percentage of all common colds in human adults and children. They can cause:

Pneumonia
Bronchitis
Severe acute respiratory syndrome SARS

Human Coronaviruses
Human coronaviruses can cause:

Fever
Dry cough
Sore throat
Headache
Throat swollen adenoids

SARS-CoV
SARS-CoV is a human coronavirus that causes severe acute respiratory
syndrome SARS , characterized by both upper and lower respiratory tract
infections.

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