Respiratory Syncytial Virus (RSV)

Respiratory Syncytial Virus (RSV)

Discovered in 1956 Morris, Blount and Savage described a Chimpanzee Coryza Virus Accidental human infection lead to recognition of role in human infections

RSVRSV- syncytium formation

Respiratory Syncytial Virus

Family Paramyxoviridae Genus Pneumovirus Subgroups A and B

RSVRSV- Structure
   

100100-350nm enveloped virus Spherical or pleomorphic shape Single stranded negative sense RNA 2 non-structural and 8 structural proteins non-

RSVRSV- Structure

RSVRSV- Structure

RSVRSV- Structure (contd.)

  

Envelope Glycoproteins:- F and G Glycoproteins:G protein lacks H/N activity Subgroups A and B based on variations in G protein

Pathogenesis
Entry Cell

through mucosa of nose and eye

to cell spread within respiratory tract

Pathogenesis (contd.)
 Attachment via G protein to respiratory

epithelium  Fusion with cell membrane - F protein



Syncytium formation (tissue culture) with multinucleated giant cells

Pathogenesis

RSVRSV- syncytium formation

RSVRSV- syncytium formation

Pathology
Mucosal

edema mucin secretion sloughing

Increased Cell

necrosis within mucosa

Obstruction

of lumina-debris, mucin luminalymphocytic infiltration

Peribronchial

ImmunityImmunity-role in pathogenesis

Host immune response contributes to pathology (T cells, cytokines)

IgE response in some people is linked to airway hyperhyper-reactivity CellCell-mediated immunity limits infection

Epidemiology

Important cause of lower respiratory disease in young infants (bronchiolitis and pneumonia) Worldwide distribution Most children infected at least once by age 4 years

Epidemiology
75,00075,000-125,000 infants are hospitalized each year in U.S.

Account for 50-90% of hospitalizations for 50bronchiolitis

SeasonalSeasonal- fall through spring

Epidemiology - transmission

Incubation Period- 2-8 days PeriodVirus survives on surfaces for up to 6 h. Transmission via droplets, fingers, fomites Nosocomial spread is common

Epidemiology (contd.)
Asymptomatic viral shedding Viral shedding lasts for <1 to 3 weeks Infants show high titer nasal shedding, especially initially (107 /mL) Prolonged viral shedding in immunecompromised hosts

Clinical Features
Upper Respiratory Infection
  

Lower Respiratory Infection

(Bronchiolitis, Pneumonia)

Fever Rhinitis Pharyngitis

    

Cough Poor feeding, lethargy Hypoxemia Respiratory Distress

(tachypnea, retractions)

Apnea

RSV Bronchiolitis- clinical Bronchiolitisfeatures

Diagnosis - specimens

Nasal and tracheo-bronchial secretions tracheoSwabs, or aspirates Transport in viral culture medium and on ice Process immediately

DiagnosisDiagnosis- methods

Viral isolation
PRMK, LLLC-MK-2 LLLC-MKCPE in 2-5 days 2Shell vial technique with immunofluoresence

Antigen detection
EIA (Binax NOW/Quick lab RSV) (Binax NOW/ RSV) RIA, IF

Antibody detection- not useful clinically detection-

DiagnosisDiagnosis- RSV in Hep-2 cell culture Hep(immunofluoresent stain)

Treatment
Supportive
Fluids, oxygen, respiratory support, bronchodilators

Antiviral Agents Ribavirin (Virazole), a synthetic guanosine (Virazole),

analogue, given as an aerosol

Preventing Spread

Handwashing Disinfection of surfaces Gloves, masks, goggles, gowns Isolation, and cohort nursing Immunization

Prevention of Disease

Active Immunization Formalin inactivated vaccine resulted in enhanced disease Subunit vaccines being studied

Prevention of Disease(contd.)

Passive immunization (immunoprophylaxis) Pooled hyperimmune globulin (RespiGam) RespiGam) Monoclonal antibody to F proteinproteinPalivizumab (Synagis)