Paramyxoviruses by Dr. Rakesh

1. Paramyxoviruses
By Dr. Rakesh Prasad Sah
Associate Professor, Microbiology

2. Myxo = affinitiy to mucin
Orthomyxo
viruses
Paramyxo
viruses
Myxoviruses
•Smaller
•Segmented RNA genome
•Liable to Antigenic
variation
•Larger
•Single piece of RNA genome
•Not liable to Antigenic
variation

3. Myxo = affinitiy to mucin
Orthomyxo
viruses
Paramyxo
viruses
Myxoviruses
•Smaller
•Segmented RNA genome
•Liable to Antigenic
variation
•Larger
•Single piece of RNA genome
•Not liable to Antigenic
variation

4. Introduction
• Paramyxoviruses resembles Orthomyxoviruses in morphology bt
differ from other properties 
S.No.
Property Orthomyxovirus Paramyxovirus
1 Size of virion 80-120nm 100-130nm
2 Shape Spherical; filamentous Pleomorphic
3 Genome Segmented; eight pieces* of
negative sense single
stranded RNA
Single piece of negative
sense, single stranded
RNA
4 Nucleocapsid (diameter) 9nm 18nm
5 Site of ribonucleoprotein
synthesis
Nucleus Cytoplasm
6 Genetic recombination Common Absent
7 DNA-dependent RNA
synthesis
Necessary for multiplication Not required
8 Rate of Agenic change High Low
9 Haemolysin Absent Present
*Influenza virus type C contains seven pieces of RNA

5. • Parainfluenza virus
• Mumps virus
• Measles virus
• Respiratory syncytial virus (RSV)
Important for human
infections
Parainfluenza & Mump Both have HA & NA
Measles Has HA but no NA
RSV &
Metapneumovirus
Do not have any of two

6. Morphology
• Spherical enveloped particles
• 100-300nm
• Envelop  lipoprotein & covered by
projections
• Projections  HN
(Haemagglutinin, neuraminidase)
and F (fusion protein)  12-14nm
long and 2-4nm wide.
• Inner surface of envelope is lined
by matrix (M) protein.
• Nucleocapsid  helical symmetry
 -veSSRNA and RNA-dependent
RNA polymerase.

8. Parainfluenza Viruses
• Causes respiratory infections in children and less often in adults
• Five serotypes 1,2,3,4a and 4b.
• Spherical 125-250nm, enveloped RNA viruses.

9. Pathogenesis
Acquired by droplets and contact with respiratory secretions
Incubation period  2-6days
Are ubiquitous and produce URTI
In infants and young children, cause severe respiratory disease 
laryngotracheobronchitis or croup (an infection of the upper airway, which
obstructs breathing and causes a characteristic barking cough).
Fever
Cough
Respiratory obstruction  swelling of larynx and related structures
Pneumonia or bronchiolitis  occur especially with type 3.
Type 4  only mild illness

11. Laboratory Diagnosis
• Direct demonstration
– Immunofluorescence: Viral Ags 
demonstrated in exfoliated cells aspirated from
respiratory tract by immunofluorescence using
monoclonal Abs.
– ELISA

12. Laboratory Diagnosis
• Isolation
– Mouth washing samples  posterior pharynx or nasopharynx and throat
swabs  inoculated in primary human or monkey kidney cells or in
continuous cell lines such as H292.
– Visible cytopathic effect is minimal except with type 2  induces syncytia
formation.
– By haemadsorption or guinea pig red cells or by use of specific
immunofluorescent Ab.
• Serology
– Rising Ab titre by neutralisation, ELISA and CFT.
• PCR

13. Mumps Virus
Pathogenesis
Mumps or parotitis  ds of childhood
Acquired from direct contact with infected saliva or aerosols from infected patients
Mode of entry  Respiratory tract
I.P.  16-18 days
Enters bloodstream and spreads to the salivary glands, testes, ovaries, pancreas,
kidney and brain.
Virus multiplies URT and local lymph nodes
Shed in saliva  six days before to one week after onset of clinical parotitis.
Non-suppurative inflammation of the parotid glands (95%)

14. • Complications
– Meningitis
– Meningoencephalitis
– Orchitis (common complication in
– postpubertal male patients)
– Oophoritis
– Pancreatitis
– Nephritis

15. Laboratory Diagnosis
• Direct demonstration
– Immunofluorescence  secretions of throat and saliva  demonstration of
viruses.
• Isolation
– Virus isolated from
• Saliva
• Throat swab
• CSF
• Urine
• Serology
• IgM Ab
• ELISA
• PCR
•Primary monkey kidney
cells
•H292
•Hep-2 cell cultures.
Little CPE but can be
demonstrated by
haemadsorption
(guinea pig red cells)
By Immunofluorescence testing of infected cell cultures.

16. Prophylaxis
• Live attenuated vaccine
• Derived by passage in chick fibroblasts
• Jeryl-Lynn strain of mump virus  used for
manufacturing of vaccine.
• MOD  subcutaneously in combination with
attenuated measles and rubella vaccine (MMR
vaccine).
• Given to children aged 12-15 months.
• Provides effective protection for at least
10years.
• Contraindication
– Pregnancy
– Immunodeficiency
– Hypersensitivity to egg protein.

17. Measles Virus
• Highly infectious ds of childhood.
• Spread by respiratory secretions.
• Caused by measles virus.
• Morphology
– Resembles paramyxoviruses
– Spherical 120-250nm
– Helical nucleocapsid surrounded by lipoprotein envelop
– Haemagglutinin (H) spikes but neuraminidase spikes  absent.
– Envelop has the F protein.
– Matrix M protein  located below lipoprotein envelope.

18. Pathogenesis
Acquired by inhalation
I.P.  10-12 days
Viruses multiplies in lymhoid tissue of RT and invades bloodstream  Primary
viraemia
Viruses spreads to R.E. system through blood.
Virus enters to epithelial surfaces  skin, mouth, RT, conjunctiva
Multiplies there  secondary viremia
Koplik’s spots (on 12th day of infection)  seen on buccal mucosa and are
pathognomonic of measles.
Characterised by high fever (on 10th day of infection), cough and conjunctivitis.

19. Pathogenesis
With decline of acute symptoms in 1-2 days  wide spread of maculopapular rash
(on 14th day of infection) appears first on neck and then spreads to rest of body.
Rash fades in a week and patient recovers by 10-14th days.

20. Pathogenesis
Complications
– Due to decrease in resistance of Respiratory epithelium
• Secondary bacterial infections
• Otitis media
• Bronchopneumonia
• Croup (an infection of the upper airway, which obstructs breathing
and causes a characteristic barking cough)
– Giant cell pneumonia  in impaired CMI
– Post-measles encephalitis and subacute
slerosing panencephalitis (SSPE) a progressive
neurological disorder of children and young adults that
affects the central nervous system (CNS).

22. Lab Diagnosis
• Specimens
– Nasopharyngeal swab
– Throat washings
– Conjunctival swab
– Blood and urine
• Direct demonstration
– Multinucleate Gaint cells  Geimsa stained nasal secretions.
Dacron, Rayon or
polyester swab

23. Lab Diagnosis
• Ag detection
– Detected in exfoliated respiratory cells in nasal secretions by
immunofluorescence.
• Virus isolation
– Cultured on primary human or monkey kidney cells  CPE takes 7-10
days to develop  multinucleated gaint cells (CPE) containing
intranuclear and intracytoplasmic inclusion bodies  suggestive of
+ce of measles virus.
• Serology
– IgM Ab
– ELISA
– High titre of IgG Ab in CSF  suggestive of SSPE.
• PCR

24. Prophylaxis
• Active immunisation
– Live attenuated vaccine is used.
– Schwartz strain, Moraten strain and Edmonston-
Zagreb strain.
– Prepared in chick embryo cell line.
– Available in lyophilised form.
– Reconstituted with D.W. and should be used
within 4hrs.
– Vaccine must be stored at -200C and is thermolabile.
– Dose 0.5ml.
– Route  Subcutaneous route.
– Is used in combination with Rubella (MR vaccine)
with mumps and rubella (MMR vaccine) and with
varicella (MMR-V vaccine).

25. • Indications
– Under National Immunisation Programme of India, 0.5ml of MR
(measles, rubella)  administered subcutaneously at right upper
arm at age of 9-12months  along with vitamin A supplement.
– 2nd dose  16-24 months.
• Passive Immunisation
– Measles immunoglobulin (IgG)  3 days to susceptible contacts for
protection against measles.
– Dose  0.25mg/kg body weight
– Post exposure prophylaxis (PEP)

26. Respiratory Syncytial Virus
• Pleomorphic
• 150-300nm
• Envelope lacks both HA & NA
• Contains a surface glycoprotein G  virus attaches to cell surfaces &
• F (fusion) protein  induces fusion of infected cells into large
multinucleated syncytia  so named RSV….
• Nucleocapsid  13nm diameter
• Impt cause of bronchiolitis and pneumonitis in infants  6 months of age.
• Infection in older children and adults  rhinitis or common cold.
• Is highly labile and inactivated at RT.
• Lyophilisation  for preservation.
• Ag-enically stable.

27. Pathogenesis
Highly contagious, transmitted by contact with contaminated hands and surface.
Nosocomial infections  nurseries and paediatric ward
I.P.  4-6 days.
Virus multiplies  mucous membranes of nose and throat
Spread into lower respiratory tract causing bronchiolitis and pneumonitis
Viruses shed in respiratory secretions for several days or weeks.

30. Laboratory Diagnosis
• Direct demonstration
– Immunofluorescence in nasopharyngeal
aspirates.
– Viral Ag by ELISA
• Virus isolation
– HeLa, Hep-2 or monkey cell cultures
– Characteristic giant cells and syncytia
formation.
– In 2-10 days.
– Definitive identification by
immunofluorescence.
• Serology
– ELISA for Ab
• PCR