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PARAMYXOVIRUS
PARAMYXOVIRUSES
 Family Paramyxoviridae
 ssRNA – single piece
 Helical nucleocapsid, enveloped
 Spherical, 100-300nm diameter
Classification
Five genera-
1. Respirovirus- human parainfluenza v-1,3
2. Rubulavirus- human parainfluenza V-2,4
3. mumps virus
4. Morbillivirus- measles virus
5. Pneumovirus- Human respiratory synctial virus
6. Metapneumovirus- human metapneumo virus
PROPERTIES OF ORTHOMYXOVIRUS
AND PARAMYXOVIRUS
Property orthomyxovirus paramyxovirus
viruses Influenza A,B,C Measles,mumps,
RSV,& parainfluenza
genome Segmented Non segmented
Virion RNA
polymerase
yes yes
Capsid helical helical
Envelope yes yes
size Smaller(110 nm) Larger( 150 nm)
Surface spikes H&N diff. spikes H&N same spikes
Giant cell formation no yes
Parainfluenza Virus
 Surface spikes: H & N same spike, fusion on different
spike
 Both humans and animals infected
 Four serotypes: 1, 2, 3 & 4
 MOT: respiratory droplet
Parainfluenza infections spreads
through respiratory tract…
 The infection is acquired
through inhalation of
infected droplet nuclei or
directly through contact
with infected secretions.
The incubation period is
generally 2-6 days
Parainfluenza virus causes
Respiratory infection in young
 They are the second most common cause of
respiratory tract infection in younger children
 No viremia
 Clinical:
 1&2- major cause of group; children < 6 y/o
 Laryngitis
 Pneumonia
 Common cold- 4
 Pharyngitis
 Otitis media
LAB DIAGNOSIS
 1. direct demonstration- immunofluorescence
ELISA
2. isolation –primary human or monkey kidney cells
continous cell lines(H292)
haemadsorption of guinea pig RBC
3. Serology- CFT, ELISA
MEASLES VIRUS
 Single serotype
 H- target of neutralizing Ab
 Humans are the natural
host
 MOT –RT and conjunctiva.
 1-5 year age group.
 MOT-respiratory secretions
 Spherical,helical nucleocapsid, no
neuraminidase spikes
 I.P- 10-12 days
 PATHOGENESIS- lymphoid tissue
of RT-bloodstream(primary
viremia)- RE system (secondary
viremia)- epithelial surfaces.
 High fever, cough, conjunctivitis.
KOPLIK’S SPOTS
 Maculopapular rash- neck, then rest
of the body
 Recovery- 10-14 days
LAB DIAGNOSIS
 1. Direct demonstration-nmultinucleated giant cells
virus particles in exfoliated
nasal cells by IF
 2. Isolation- during prodromal phase till upto 2 days
post rash.
primary human embryo kidney, monkey
kidney cells- CPE- MNGC with both intracytoplasmic
and intranuclear IB
3. Serology- specific IgM Ab by ELISA, HI and CFT
for paired sera- 4 fold rise is diagnostic.
PROPHYLAXIS
 1. Active immunisation
live attenuated- at 9 months
Firstly Edmonston strain- vaccination measles, then
schwartz strain- effective only after 15 months
Edmonston –Zagreb strain- passage in human diploid
cells- 1 dose, S/C route
MMR vaccine-single dose, S/C
LA vaccine- intranasal aerosol
2. Passive immunisation-pooled sera containing Ab
 Both live and killed vaccines exist.
 In India Measles vaccination is a part of
universal vaccination programme of
Government of India since 1990 with a
dramatic decline in the incidence of the
disease.
Prevention
Mumps virus
 H and N + fusion protein on envelope spikes
 Humans are the natural host
 thermolabile
Mumps
 Nasal or URT epithelial cells- blood-
salivary glands, testes,ovaries,
pancreas, meninges and kidneys
 Shed in the saliva 2 days before to 9
days after the onset of salivary gland
swelling
 (+) virus in urine up to 14 days after
onset of symptoms
 Malaise and fever is followed within a day by painful swelling
of one or both of the parotid (salivary) glands
 A possible complication in males after puberty is orchitis -
painful swelling of one or both testicles.
 Inflammation of the ovary and pancreas can also occur.
 Disease is usually self-limiting within a few days
 Aseptic meningitis (usually resolving without problems) or
postexposure encephalitis (can prove fatal) are the most
serious complications associated with mumps.
Mumps virus
Diagnosis
 1. cell culture
 Specimen-saliva, spinal fluid or urine
 Monkey kidney cell
 CPE- cell rounding and giant syncytia formation
 2. serology- 4 fold rise in Ab titer in HI or CF
 Ab vs S antigen- current infection
 Ab Vs V antigen- past infection
 Prevention: vaccine, attenuated vaccine
Prevention and treatment
 Treatment: none
 Prevention: live attenuated vaccine, used with
measles and rubella virus vaccines (MMR)
 Not a part of universal immunization programme.
Respiratory Syncytical Virus
 Most important cause of pneumonia and
bronchiolitis in infants
 Fusion proteins- syncytia formation
 Humans and chimpanzees- natural host
 2 serotype: A & B
 MOT: respiratory droplet
Clinical
 1. infants- bronchiolitis,
pneumonia
 2. young children- otitis
media
 3. older children and adults-
common cold
 Diagnosis:
immunofluorescence
 Isolation in cell culture- + CPE
 serology
Treatment
 Aerosolized Ribavirin
 Ribavirin + hyperimmune globulins
 Prevention
 NO VACCINE
 Palivizumab-prophylaxis, monoclonal ab vs. fusion protein
Rubella Virus
General Concepts
 Enveloped virus ss-positive-sense RNA.
 Belongs to Togavirus family
 Replication in cytoplasm and bud at
plasma membrane
 Cause Rubella( German measles, 3-days
measles)
Epidemiology
 Occurrence: worldwide in prevalence
 Mode of Transmission: Droplet infection;
fomites;
 Mild infection (3 day fever) with
maculopapular rash post-auricular and
cervical lymphadenopathy. In adults it gives
joint pains. Antibodies give life long
immunity.
 In India 85% get infection by adolescence.
 Incubation period: 2-3 weeks
32
Pathogenesis
Rubella enters and infects the
nasopharynx and then spreads
to the lymph nodes and RE
system. The resulting viremia
spreads the virus to other
tissues and the skin. In
susceptible (seronegative)
pregnant woman, the virus
infects the placenta and then
spreads to developing fetus.
Virus
Congenital
infection
Lab Diagnosis
 Current rubella infection, particularly in
pregnant women can be confirmed by
- Presence of virus specific IgM antibodies in
acute phase serum; or
- 4-fold rise in virus specific antibody (IgG)
titers between acute and convalescent-phase
serum specimens by ELISA
MMR vaccine
• Composition : live attenuated virus
Measles / Mumps / Rubella
• Vaccination schedule: at 15-24 months and
at 4 to 6 years or before high school
• Efficiency: 95% lifelong immunization with a
single dose

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paramyxovirus.ppt

  • 2. PARAMYXOVIRUSES  Family Paramyxoviridae  ssRNA – single piece  Helical nucleocapsid, enveloped  Spherical, 100-300nm diameter
  • 3. Classification Five genera- 1. Respirovirus- human parainfluenza v-1,3 2. Rubulavirus- human parainfluenza V-2,4 3. mumps virus 4. Morbillivirus- measles virus 5. Pneumovirus- Human respiratory synctial virus 6. Metapneumovirus- human metapneumo virus
  • 4. PROPERTIES OF ORTHOMYXOVIRUS AND PARAMYXOVIRUS Property orthomyxovirus paramyxovirus viruses Influenza A,B,C Measles,mumps, RSV,& parainfluenza genome Segmented Non segmented Virion RNA polymerase yes yes Capsid helical helical Envelope yes yes size Smaller(110 nm) Larger( 150 nm) Surface spikes H&N diff. spikes H&N same spikes Giant cell formation no yes
  • 5.
  • 6. Parainfluenza Virus  Surface spikes: H & N same spike, fusion on different spike  Both humans and animals infected  Four serotypes: 1, 2, 3 & 4  MOT: respiratory droplet
  • 7. Parainfluenza infections spreads through respiratory tract…  The infection is acquired through inhalation of infected droplet nuclei or directly through contact with infected secretions. The incubation period is generally 2-6 days
  • 8. Parainfluenza virus causes Respiratory infection in young  They are the second most common cause of respiratory tract infection in younger children  No viremia  Clinical:  1&2- major cause of group; children < 6 y/o  Laryngitis  Pneumonia  Common cold- 4  Pharyngitis  Otitis media
  • 9. LAB DIAGNOSIS  1. direct demonstration- immunofluorescence ELISA 2. isolation –primary human or monkey kidney cells continous cell lines(H292) haemadsorption of guinea pig RBC 3. Serology- CFT, ELISA
  • 10. MEASLES VIRUS  Single serotype  H- target of neutralizing Ab  Humans are the natural host  MOT –RT and conjunctiva.  1-5 year age group.
  • 11.  MOT-respiratory secretions  Spherical,helical nucleocapsid, no neuraminidase spikes  I.P- 10-12 days  PATHOGENESIS- lymphoid tissue of RT-bloodstream(primary viremia)- RE system (secondary viremia)- epithelial surfaces.  High fever, cough, conjunctivitis. KOPLIK’S SPOTS  Maculopapular rash- neck, then rest of the body  Recovery- 10-14 days
  • 12.
  • 13.
  • 14.
  • 15. LAB DIAGNOSIS  1. Direct demonstration-nmultinucleated giant cells virus particles in exfoliated nasal cells by IF  2. Isolation- during prodromal phase till upto 2 days post rash. primary human embryo kidney, monkey kidney cells- CPE- MNGC with both intracytoplasmic and intranuclear IB 3. Serology- specific IgM Ab by ELISA, HI and CFT for paired sera- 4 fold rise is diagnostic.
  • 16. PROPHYLAXIS  1. Active immunisation live attenuated- at 9 months Firstly Edmonston strain- vaccination measles, then schwartz strain- effective only after 15 months Edmonston –Zagreb strain- passage in human diploid cells- 1 dose, S/C route MMR vaccine-single dose, S/C LA vaccine- intranasal aerosol 2. Passive immunisation-pooled sera containing Ab
  • 17.  Both live and killed vaccines exist.  In India Measles vaccination is a part of universal vaccination programme of Government of India since 1990 with a dramatic decline in the incidence of the disease. Prevention
  • 18. Mumps virus  H and N + fusion protein on envelope spikes  Humans are the natural host  thermolabile
  • 19. Mumps  Nasal or URT epithelial cells- blood- salivary glands, testes,ovaries, pancreas, meninges and kidneys  Shed in the saliva 2 days before to 9 days after the onset of salivary gland swelling  (+) virus in urine up to 14 days after onset of symptoms
  • 20.  Malaise and fever is followed within a day by painful swelling of one or both of the parotid (salivary) glands  A possible complication in males after puberty is orchitis - painful swelling of one or both testicles.  Inflammation of the ovary and pancreas can also occur.  Disease is usually self-limiting within a few days  Aseptic meningitis (usually resolving without problems) or postexposure encephalitis (can prove fatal) are the most serious complications associated with mumps. Mumps virus
  • 21. Diagnosis  1. cell culture  Specimen-saliva, spinal fluid or urine  Monkey kidney cell  CPE- cell rounding and giant syncytia formation  2. serology- 4 fold rise in Ab titer in HI or CF  Ab vs S antigen- current infection  Ab Vs V antigen- past infection  Prevention: vaccine, attenuated vaccine
  • 22. Prevention and treatment  Treatment: none  Prevention: live attenuated vaccine, used with measles and rubella virus vaccines (MMR)  Not a part of universal immunization programme.
  • 23.
  • 24. Respiratory Syncytical Virus  Most important cause of pneumonia and bronchiolitis in infants  Fusion proteins- syncytia formation  Humans and chimpanzees- natural host  2 serotype: A & B  MOT: respiratory droplet
  • 25.
  • 26. Clinical  1. infants- bronchiolitis, pneumonia  2. young children- otitis media  3. older children and adults- common cold  Diagnosis: immunofluorescence  Isolation in cell culture- + CPE  serology
  • 27. Treatment  Aerosolized Ribavirin  Ribavirin + hyperimmune globulins  Prevention  NO VACCINE  Palivizumab-prophylaxis, monoclonal ab vs. fusion protein
  • 29. General Concepts  Enveloped virus ss-positive-sense RNA.  Belongs to Togavirus family  Replication in cytoplasm and bud at plasma membrane  Cause Rubella( German measles, 3-days measles)
  • 30. Epidemiology  Occurrence: worldwide in prevalence  Mode of Transmission: Droplet infection; fomites;  Mild infection (3 day fever) with maculopapular rash post-auricular and cervical lymphadenopathy. In adults it gives joint pains. Antibodies give life long immunity.  In India 85% get infection by adolescence.  Incubation period: 2-3 weeks
  • 31. 32 Pathogenesis Rubella enters and infects the nasopharynx and then spreads to the lymph nodes and RE system. The resulting viremia spreads the virus to other tissues and the skin. In susceptible (seronegative) pregnant woman, the virus infects the placenta and then spreads to developing fetus. Virus Congenital infection
  • 32. Lab Diagnosis  Current rubella infection, particularly in pregnant women can be confirmed by - Presence of virus specific IgM antibodies in acute phase serum; or - 4-fold rise in virus specific antibody (IgG) titers between acute and convalescent-phase serum specimens by ELISA
  • 33. MMR vaccine • Composition : live attenuated virus Measles / Mumps / Rubella • Vaccination schedule: at 15-24 months and at 4 to 6 years or before high school • Efficiency: 95% lifelong immunization with a single dose