RESPIRATORY SYNCYTIAL VIRUS

Structure & Property	Transmission	Pathogenesis	Clinical findings	Laboratory diagnosis	Treatment	
Family: paramyxovirus

Genome: one piece of single-stranded RNA

Nucleocapsid: helical

Lipoprotein envelope:
- only fusion proteins
- cause cells to fuse, forming syncytia

Only one antigenic type

Antibody against fusion protein neutralizes infectivity.	Humans and chimpanzees are natural hosts.

Transmission occurs via respiratory droplets and by direct contact of contaminated hands with nose or mouth.

Causes outbreaks of respiratory infections every winter.

Causes outbreaks of respiratory infections in hospitalized infants.

Infected children shed virus in respiratory secretions for 3-8 days. 

	Invade lower respiratory tract.

Infants:
- more severe
- involves lower respiratory tract
- localized infection
- viremia does not occur

Immunopathogenesis:
- maternal antibody passed to infant react with virus & damage respiratory tract cells
- immune complexes (IgG + virus), IgE, and histamine may be involved.

Multiple RSV infections – incomplete immunity	Bronchiolitis:
- young children with peak at age 3 months.
- fever
- cough
-dyspnea
- tachypnea
-wheezing
- cyanosis

Complications:
- pneumonia
- secondary bacterial infections
- otitis media
- cardiac failure
-apnea

Up to 5% mortality in bronchiolitis & pneumonia

High mortality associated with CNS malformations, congenital disease of heart and lung

Upper respiratory tract infection in older children and adults	Tissue culture:
- inoculate HeLa or Hep-2 cells
- highly characteristic refractile syncytium formation of multinucleated giant cells

Immunofluoresence:
on smears of respiratory epithelium or by isolation in cell culture.

A rise in antibody titer of at least 4-fold

Does not haemagglutinate

Isolation:
- mouth washings
- nasal secretions	Ribavirin aerosol therapy

Ventilatory support

No effective vaccine

Isolate infected hospitalized children