You are on page 1of 34

Rhinovirus

Rhinovirus infections are chiefly limited to the upper


respiratory tract but may include otitis media and
sinusitis.
Rhinovirus plays a role in exacerbations of asthma,
cystic fibrosis, chronic bronchitis, and serious lower
respiratory tract illness in infants, elderly persons,
and patients who are immunocompromised.
Although infections occur year-round, the greatest
incidence is in the fall and spring.
Of persons exposed to the virus, 70-80% have
symptomatic disease.

Rhinovirus
Belong to the picornavirus family the smallest (pico) RNA
viruses (24-30 nm)
ssRNA virus
Acid-labile
Rhinovirus Capsid consists of 4 proteins VP1, VP2, VP3& VP4
At least 100 serotypes are known
Intercellular Adhesion Protein-1 (ICAM-1)
Receptor for most human rhinovirus serotypes

Rhinovirus bonded to
a CAM 1 receptor

Antibodies bonded
to a rhinovirus

Functions of Viral RNA


RNA genome is mRNA Positive strand.
A viral-coded peptide (VPg) is attached to the 5 end.
When introduced into cells, viral RNA can produce
infectious virus.
Viral RNA serves as a template for its replication
Optimum growth occurs between 33 and 34 oC
Viruses replicate rapidly in the cytoplasm
do not require DNA for reproduction

Functions of Viral Proteins


Derived from one polyprotein precursor
Processed by post-translational cleaving
Structural proteins
Responsible for host tropisms
Protection of genome
Antigenicity
Non-structural proteins
Proteases
RNA polymerase
Inhibitors of normal host cell functions

Virus Replication Cycle

Internal ribosome entry segment (IRES)

Coronavirus

ssRNA Virus
Enveloped,
pleomorphic
morphology
2 serogroups:
OC43 and 229E

Transmission
Routes
Cold viruses may be transmitted
by three routes:
Large-particle droplets, which
can travel a short distance to
directly inoculate another
person
Small-particle aerosols, which
can travel longer distances
and deposit
directly in alveoli of other individuals
Secretion, which are transmitted by direct physical
contact

How does it spread?


Very contagious
Spread from person to person
Usually from nasal secretions and
from fingers of the affected person
Most contagious in the first 3 days
after symptoms begin
Viruses can last up to 5 hours on the
skin and hard surfaces

Rhinovirus
Higher rates occur in humid,
crowded conditions, as found in
nurseries, day care centers, and
schools, especially during cooler
months in temperate regions and
rainy season in tropical regions.

Pathogenesis
The offending virus invades the epithelial cells of
URT.
Inflammatory mediators are released.
They alter the vascular permeability and cause
tissue edema and stuffiness.
Stimulation of cholinergic nerves in the nose and
URT leads to increased mucus production
(rhinorrhea) and occasionally to bronchocontriction
Injury to cilia in the nasal epithelial cells may
decrease ciliary function and impair clearance of
nasal secretions.

Pathophysiology
Rhinoviruses are transmitted to
susceptible individuals by :
Direct contact
Aerosol particles
infecting both ciliated areas of the nose and nonciliated
areas of the nasopharynx through receptors, most
frequently ICAM-1 (found in high quantities in the posterior
nasopharynx).
Few cells are actually infected by the virus, and the
infection involves only a small portion of the epithelium.

Pathophysiology
Symptoms develop 1-2 days
after viral infection, peaking 2-4
days after inoculation, although
reports have described
symptoms as early as 2 hours
after inoculation with primary
symptoms 8-16 hours later.

Pathophysiology
Detectable histopathology causing the

associated nasal obstruction, rhinorrhea, and


sneezing is lacking:
which leads to the hypothesis that the host immune
response plays a major role in rhinovirus pathogenesis .

Infected cells release interleukin-8 (IL-8), which is a potent


polymorphonuclear (PMN) chemoattractant.
Concentrations of IL-8 in secretions correlate proportionally with the
severity of common cold symptoms.
Inflammatory mediators, such as kinins and prostaglandins, may
cause vasodilatation, increased vascular permeability, and exocrine
gland secretion.
These, together with local parasympathetic nerve-ending
stimulation, lead to cold symptoms

Pathophysiology

Viral clearance is associated with the host response


and is due, in part, to the local production of nitric
oxide.
Serotype-specific neutralizing antibodies are found
7-21 days after infection in 80% of patients.
Although these antibodies persist for years, providing
long-lasting immunity, recovery from illness is more
likely related to cell-mediated immunity.
Persistent protection from repeat infection by that
serotype appears to be partially attributable to
immunoglobulin A (IgA) antibodies in nasal
secretions, serum immunoglobulin G (IgG), and,
possibly, serum immunoglobulin M (IgM).

Pathophysiology
The virus has a limited temperature
range in which it can grow (33-35C)
and cannot tolerate an acidic
environment.
Thus, finding the virus outside of the nasopharynx
is unlikely because of the acidic environment of
the stomach and the temperature elevation in both
the lower respiratory and gastrointestinal tracts.

The Common Cold


Chemical
Mediators
of Inflammation

VIRAL
INFECTION
OF NAZAL
CELLS

SNEEZING
SORE THROAT

Vascular
Dilatation

Increased
Vascular
Permeability

Tissue
Edema

Serum
Transduction
Increased
Mucus
Production

Sensitization
of Irritated of
Airways Receptors

NASAL OBSTRACTION

Cholinergic
Stimulation

RHINORRHEA

Bronchoconstriction

COUGH

Physical examination
Red nose with dripping nasal discharge may
be present.
Nasal mucous membranes have a
glistening, glassy appearance without
obvious erythema and edema.
Yellow or green nasal discharge does not
indicate bacterial infection because a large
number of white blood cells migrate to the
site of viral infection.

Physical Examination
If marked:
1. erythema, edema, exudates, or small
vesicles are observed in the oropharynx
2. conjunctivitis
3. polyps in the nasal mucosa occur, consider
other etiologies, including: adenovirus, herpes

simplex virus, mononucleosis, diphtheria, Coxsackie


A virus, or group A streptococcus (GAS).

Clinical characteristics
Incubation period 12-72 hours
Nasal obstruction, drainage,
sneezing, scratchy throat
Median duration 1 week but 25% can
last 2 weeks
Pharyngeal erythema is commoner
with adenovirus than with rhino or
coronavirus

Symptoms
Begins with a feeling of dryness and stuffiness in the

nasopharynx (nose)
Nasal secretions (usually clear and watery)
Watery eyes
Red and swollen nasal mucous membranes
Headache
Generalized tiredness
Chills (in severe cases)
If the pharynx and larynx
(throat) becomes involved:
Fever (in severe cases)
Sore throat
Hoarseness
Exhaustion (in severe cases)

ICEBERG CONCEPT INFECTION

Sever Symptoms
Mild Symptoms

Infection but no Symptoms


Exposure but no Symptoms

Features

Influenza

Common
cold

Onset

Abrupt

More gradual

Fever

Common

Uncommon

Myalgia

Severe,
common
Severe,
common
Common

Uncommon

Severe,
common

Mild,
uncommon

Arthralgia
Anorexia
Headache

Uncommon
Uncommon

Cough (dry)

Common, severe

Mild to
moderate

Malaise

Severe

Mild

Fatigue,
weakness

More common
than with the
common cold;
lasts 2 to 3
weeks

Very mild, short


lasting

Chest discomfort Common, severe

Mild to
moderate

Stuffy nose

Occasional

Common

Sneezing

Occasional

Common

Sore throat

Occasional

Common

RISK FACTOR FOR MORE SEVER


COMMON COLD
LOW NEUTRALIZING Ab
CHRONIC LUNG DISEASE
EXTREMES AGE
ASTHMA
ALLERGY
Ig E
CYTOKINE PRODUCTION
I F N -gamma
I L-5

Complications

Acute otitis media


Paranasal sinusitis
Neck lymphonoditis
Retropharyngeal abscess
Laryngitis
Lower respiratory tract disease
Acute glomerulonephritis and rheumatic
fever

Laboratory Test
White cell count

The viral infections is normal to low.


The bacterial infections or viral-bacterial infection
is high.

Laboratory diagnosis of viral


infections

Antigen or nucleic acid detection


Serologic testing

Isolation of viruses by culture of the throat

or nasopharynx
Use of monoclonal antibodies
Polymerase chain reaction (PCR)

TREATMENT

Treatment of common cold


Antihistamines
Decongestants
Pain Relievers
Cough suppressants
Nasal Strips
Antibiotics are ineffective!!!

MEDICATION
Drugs used in the symptomatic treatment
include:

Nonsteroidal anti-inflammatory drugs


(NSAIDs)
Antihistamines
Anticholinergic nasal solutions

These agents have no preventive activity


and appear to have no impact on
complications.

TREATMENT
Rhinovirus infections are predominately mild
and self-limited:

thus, treatment is generally focused on symptomatic relief


and prevention of person-to-person spread and
complications.

The mainstays of therapy include:


Rest,
Hydration,
Antihistamines,
Nasal decongestants

Antibacterial agents are not effective unless


bacterial superinfection occurs.

TREATMENT
Development of effective antiviral medications has

been hampered by the short course of these


infections.
Because peak symptom severity occurs at 24-36
hours after inoculation, only a narrow window of
time exists in which antivirals could positively impact
upon this infection.
In addition, the cause of the common cold is not
always rhinovirus.
Therefore, rapid and accurate diagnostic tests would
be needed if a specific antiviral therapy were
developed.

VACCINATION
Because of the large number of rhinovirus
immunotypes and the inaccessibility of
the conserved region of the viral capsid
(the most likely effective site for targeting
a vaccine), no rhinovirus vaccine is on
the horizon.

PREVENTION
Because infection is spread by:
hand-to-hand contact,
autoinoculation,
possibly, aerosol particles,
emphasize appropriate hand washing,
avoidance of finger-to-eyes or finger-tonose contact, and use of nasal tissue.
Cough and sneeze into arm or tissue,
not into your hand

SUMMARY