Ita an overview on RSV and its associated factor.

1. Respiratory Syncytial
Virus (RSV)

2. Classification
• Family: Paramyxoviridae
• Sub-family: Pneumovirinae
• Genus: Pneumovirus

3. Morphology
• irregular spherical particles that
range in diameter from 150 to 300
nm
• consists of a nucleocapsid contained
within a lipid envelope
• non-segmented, single-stranded,
negative-sense genome of helical
symmetry

4. • has four nucleocapsid proteins
packaged in the virion: the major
nucleocapsid protein N, the
phosphoprotein P, the antitermination
factor M2-1, and the large
polymerase subunit L.
• envelope contains three virally
encoded transmembrane surface
glycoproteins, the attachment
protein G, the fusion protein F, and
the small hydrophobic SH protein

5. • The viral glycoproteins are organized
separately into virion “spikes,” which
are visualized as short (11–20 nm),
closely spaced (intervals of 6 to 10
nm) surface projections
• There also is a matrix M protein that
is thought to form a layer on the
inner envelope face

6. • RNA genome is 15-16 kb long
• Genome encodes 11 proteins
• Nine are structural (L, G, F, N, P, M,
M2-1, M2-2 and SH)
• Two are non-structural (NS1 and
NS2)
[RSV is divided into two antigenic
subgroups (A and B) on the basis of G
surface glycoprotein]

8. Epidemiology
• RSV infection is prevalent worldwide
• Highly contagious in nature
• Highly prevalent in young children
with a peak incidence in 2-8 months
of age
• Virtually all children are infected by
RSV by the age of 4 years.
• Usually seasonal, mostly occuring
during winter

9. • Shed in respiratory secretions for
several days, sometimes weeks
• Nosocomial infections are frequent.
• Outbreaks occur in neonatal wards of
maternity hospitals, sometimes
inflicting high mortality

10. Replication
• All events in the RSV replicative
cycle occur in the cytoplasm without
nuclear involvement
• Attachment is mediated by G
glycoprotein with specific cellular
receptor (suggested to be cellular
GAGs, “glycosaminoglycans”)
• Replication is similar to that of
Paramyxoviruses

11. Transmission
• Droplet inhalation
• Direct contact with contaminated
hands and fomites

12. Pathogenesis
• RSV is restricted to the respiratory
tract
• Inoculation of the virus occurs
through the upper respiratory tract
and initiates infection in the
epithelial cells.
• The virus subsequently spreads along
the epithelium of the respiratory
tract, mostly by cell-to-cell transfer
of the virus along intracytoplasmic
bridges (or syncytia formation).

13. • The virus usually does not cause any
viremia or systemic spread.
• As the virus spreads to the lower
respiratory tract it may produce
bronchiolitis and/or pneumonia.
• Virus causes necrosis of the small
airway epithelium, plugging of the
lumens with exudates, and edema,
leading to obstruction of the normal
airways.

14. Immune response
• Antibodies of IgA, IgM and IgG
classes are produced but plays the
minimal role in the host immunity
against RSV.
• Systemic and local cell-mediated
immune responses appear to be key
to the severity and recovery from
RSV infection
• Reinfection occurs, but of low
severity than that of primary
infection

15. • Maternal antibody does not protect
infant from infection.
• Natural infection does not prevent
reinfection
• Improper vaccination increases
severity of disease

16. Clinical manifestations
• The incubation period from time of
infection to onset of illness for RSV
is 4 to 5 days
• In the normal infant who encounters
RSV for the first time at age 6
weeks to 9 months, RSV infection
usually causes upper respiratory
symptoms.

17. • In 25% to 40% of such infections,
however, the respiratory tract below
the larynx also becomes involved.
• Bronchiolitis and pneumonia are the
primary manifestations of lower
respiratory tract disease
• RSV has been reported in various
studies as causing 10% of croup
cases, 5–40% of the pneumonias and
bronchitis in young children, and 50–

18. • Clinically, the condition presents as
cough, coryza, wheezing, rales and
low-grade fever.
• Reinfection with the virus occurs
throughout the life.
• However, in advancing age, the RSV
infection is confined more to the
URT than the LRT.

19. Complications
• Secondary bacterial complications are
rare.
• Approximately 20% of children with RSV
bronchiolitis develop a viral otitis media.
• Small children with bronchiolitis during
their first year of life may develop
chronic respiratory disease, in particular
asthma.

20. Laboratory diagnosis
• RSV infection may be diagnosed by
identification of the viral antigen by
rapid diagnostic techniques, viral
isolation or serology
• The gold standard is isolation of
virus in cell culture
• Specimens are best obtained by
aspiration or gentle washing out of
nasal or nasopharyngeal secretions or
by nasal swab

21. • Rapid antigen detection
• Viral antigens can be detected by direct
immunofluorescence or enzyme immunoassy
using specific monoclonal antibodies.
• Virus culture
– HeLa cells, Hep-2 cells or monkey kidney
cell lines can be used
– After 3-10 days of inoculation and
incubation, RSV is identified by the
characteristic synsytium formation
– DFA test can be employed for viral
detection in earlier days

22. • Serodiagnosis
– ELISA can be used for the
demonstration of antibodies in the
serum
– Demonstration of fourfold or more
increase in the antibody titer of acute
and convalescent sera
• Molecular diagnosis
– PCR

23. Prophylaxis and control
• Supportive and symptomatic care
• Ribavirin has been recommended for the
aerosolized treatment of childern with
severe RSV disease.
• Parenterally administration of RSV-
neutralizing antibodies is suggested as an
antiviral therapy against established
infection of high-risk infants and young
children.

24. • Development of effective vaccine
against RSV have not succceed to
date.