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ST.PIOUS X DEGREE & PG COLLEGE
FOR WOMEN
M.SC MICROBIOLOGY I SEMESTER
VIROLOGY
SEMINAR TOPIC
INFLUENZA VIRUS
By: P.DHARANI
121220518029
INTRODUCTION
 Belongs to orthomyxoviridae family & has 4 genera, they are influenza A, B, C&
thogotoviruses.
 Influenza A can infect a variety of different host species & cause pandemic infection in
man &1st isolated in 1933 by intranasal inoculation.
 Influenza B infects only humans and isolated along with type A in cell culture in 1940.
 Influenza C is a primary human infection but also isolated from pigs in china.
 Thogotoviruses is newly discovered 4th genus of orthomyxoviridae & are found in
mosquitoes ,ticks & the banded mongoose.
 Most predominant feature of influenza virus is the ability to change antigenically either
gradually(antigenic drift) or suddenly(antigenic shift).
 Only influenza A has the potential of antigenic shift.
 Influenza A, B, C can drift antigenically but minor changes are seen in ‘C’.
MORPHOLOGY
 Viruses are spherical, 80-120nm in diameter and may be filamentous.
 They have helical nucleocapsid comprising of A& B with 8 segments of ssRNA.
 Also contains viral RNA dependent RNA polymerase, which is essential for
infectivity as viral RNA is of negative sense. Therefor it need to be transcribed as
viral messenger RNA(mRNA).
 The nucleocapsid is surrounded by M1 protein shell and out of this shell there is a
lipid layer derived from the host cell.
 The M2 protein projects through the envelop forming ion channels which allow
pH changes in endosome.
 There are 2 types of species they are, haemagglutination(H) & neuraminidase(N).
 The haemagglutinin is called because the virus agglutinates certain erythrocytes.
 They are of 10nm in length & contains glycoprotein subunits, each contain polypeptide
chains HA1 & HA2.
 The 2 polypeptides are joined by a linkage site i.e., by single base or multibase.
 This virus binds to c ell by haemagglutinin by interacting with cell membrane receptor
containing N –acetylneuramic acid (sialic acid).
 Epitopes show great variability due to mutation in RNA cause a.a substitutions at several
sites of an HA1 molecule.
 Between ‘H’ spikes, mushroom like projection is called as neuraminidase & is important in
final stage of release of new virus particles from infected cell.
 It can withstand slow drying at room temperature & can survive in cold sea H2O for several
weeks.
 It can be preserved for long period at -70⁰ & remain viable when freeze dried.
 Exposure to heat for 30mins at 50⁰ is sufficient to inactivate strain & 90mins to kill.
 Virus can be inactivated by 20% ether in cold, phenol, formaldehyde, salt of heavy metals,
detergents, soaps ,etc.
PATHOGENISIS
 Pathogenicity of influenza is multifactorial & involve viral, host & environmental factors.
 Avian strains is identified host receptor & protease as determinants of tropism.
 Human strains are monobasic with HA1/HA2 joints with trypsin like proteases .
 Neuraminidase allows the virus to break the bond.
 IgA antibodies if present from previous infection, may neutralize the virus before it
attaches.
 The interferon’s produced from infected cell diffuse into both adjacent & distinct cells
before virus arrives & protects them.
 There are 3types of influenza: they are
I. Influenza A: incubation period is short and symptoms are like chill, fever, headache,
Myalgia & anorexia.
 Many patients show upper & lower respiratory infection. Fever last for 3-5days, during
2nd & 3rd day of illness, the systematic effects diminish, 4th & 5th day respiratory signs &
symptoms are seen.
 In adults, systematic illness without respiratory symptoms is common.
II. Influenza B: symptoms closely resemble associated with influenza A.
 It shows 3days febrile illness with systemic symptoms.
III. Influenza C: causes afebrile upper respiratory infection confined to young children
and outbreaks are not recognized.
DIAGNOSIS
1. Viral association & detection: for isolation, 2⁰ baboon kidney cells (or) Madin -
Darby canine kidney cells are used.
• The presence of virus maybe detected in baboon kidney cells when incubated at 33⁰C
after 18hrs if incubation by haemadsorption with human ‘O’ group (or) guinea pig RBC.
• In clinical specimens, virus can be isolated with in 7days by immunofluorescence method.
2. Rapid diagnosis: immunofluoroscent detection of influenza antigen in respiratory
system either directly after amplification in cell culture for 24hrs.
• Nasal aspirates or nasal washes are best specimens.
EPIDEMOLOGY
 Epidemics caused by influenza virus have been described for more than 2000yrs.
 Pandemic are recognized at various intervals.
 The great pandemic of 1918-1919 was severe, killing 20-40 million people.
 It is possible to deduce which viral antigen circulated before virus isolation became possible.
 Major pandemics are associated with antigenic shifts i.e. when the viral H (or) N (or) both
change.
 If a cell is infected with 2 different strains, the progeny will include both the parental RNA
molecules.
 All the H & N antigen subtypes are formed in aquatic birds.
INFLUENZA B: this virus do not undergo antigenic shift as there is no animal reservoirs.
Epidemic occurs every 3-6yrs interval and they do not become pandemic.
INFLUENZA C: they are not associated with epidemics but give rise to respiratory infections
in young children and are asymptomatic.
TREATMENT
 Oral amantadine hydrochloride was derived from rimantadine in early 1980’s & worked
only on influenza A, this will block ion channels &thus prevent pH changes.
 Amantadine is effective when given prophylactically & therapeutically when given within
24hrs of administration.
 Zanamivir & oseltamivir are the neuraminidase inhibitors & are effective against
influenza A & B.
 These are effective against amantadine or rimantadine resistant strains.
Influenza

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Influenza

  • 1. ST.PIOUS X DEGREE & PG COLLEGE FOR WOMEN M.SC MICROBIOLOGY I SEMESTER VIROLOGY SEMINAR TOPIC INFLUENZA VIRUS By: P.DHARANI 121220518029
  • 2. INTRODUCTION  Belongs to orthomyxoviridae family & has 4 genera, they are influenza A, B, C& thogotoviruses.  Influenza A can infect a variety of different host species & cause pandemic infection in man &1st isolated in 1933 by intranasal inoculation.  Influenza B infects only humans and isolated along with type A in cell culture in 1940.  Influenza C is a primary human infection but also isolated from pigs in china.  Thogotoviruses is newly discovered 4th genus of orthomyxoviridae & are found in mosquitoes ,ticks & the banded mongoose.  Most predominant feature of influenza virus is the ability to change antigenically either gradually(antigenic drift) or suddenly(antigenic shift).  Only influenza A has the potential of antigenic shift.  Influenza A, B, C can drift antigenically but minor changes are seen in ‘C’.
  • 3. MORPHOLOGY  Viruses are spherical, 80-120nm in diameter and may be filamentous.  They have helical nucleocapsid comprising of A& B with 8 segments of ssRNA.  Also contains viral RNA dependent RNA polymerase, which is essential for infectivity as viral RNA is of negative sense. Therefor it need to be transcribed as viral messenger RNA(mRNA).  The nucleocapsid is surrounded by M1 protein shell and out of this shell there is a lipid layer derived from the host cell.  The M2 protein projects through the envelop forming ion channels which allow pH changes in endosome.  There are 2 types of species they are, haemagglutination(H) & neuraminidase(N).
  • 4.  The haemagglutinin is called because the virus agglutinates certain erythrocytes.  They are of 10nm in length & contains glycoprotein subunits, each contain polypeptide chains HA1 & HA2.  The 2 polypeptides are joined by a linkage site i.e., by single base or multibase.  This virus binds to c ell by haemagglutinin by interacting with cell membrane receptor containing N –acetylneuramic acid (sialic acid).  Epitopes show great variability due to mutation in RNA cause a.a substitutions at several sites of an HA1 molecule.
  • 5.  Between ‘H’ spikes, mushroom like projection is called as neuraminidase & is important in final stage of release of new virus particles from infected cell.  It can withstand slow drying at room temperature & can survive in cold sea H2O for several weeks.  It can be preserved for long period at -70⁰ & remain viable when freeze dried.  Exposure to heat for 30mins at 50⁰ is sufficient to inactivate strain & 90mins to kill.  Virus can be inactivated by 20% ether in cold, phenol, formaldehyde, salt of heavy metals, detergents, soaps ,etc. PATHOGENISIS  Pathogenicity of influenza is multifactorial & involve viral, host & environmental factors.  Avian strains is identified host receptor & protease as determinants of tropism.  Human strains are monobasic with HA1/HA2 joints with trypsin like proteases .  Neuraminidase allows the virus to break the bond.  IgA antibodies if present from previous infection, may neutralize the virus before it attaches.
  • 6.  The interferon’s produced from infected cell diffuse into both adjacent & distinct cells before virus arrives & protects them.  There are 3types of influenza: they are I. Influenza A: incubation period is short and symptoms are like chill, fever, headache, Myalgia & anorexia.  Many patients show upper & lower respiratory infection. Fever last for 3-5days, during 2nd & 3rd day of illness, the systematic effects diminish, 4th & 5th day respiratory signs & symptoms are seen.  In adults, systematic illness without respiratory symptoms is common. II. Influenza B: symptoms closely resemble associated with influenza A.  It shows 3days febrile illness with systemic symptoms. III. Influenza C: causes afebrile upper respiratory infection confined to young children and outbreaks are not recognized.
  • 7. DIAGNOSIS 1. Viral association & detection: for isolation, 2⁰ baboon kidney cells (or) Madin - Darby canine kidney cells are used. • The presence of virus maybe detected in baboon kidney cells when incubated at 33⁰C after 18hrs if incubation by haemadsorption with human ‘O’ group (or) guinea pig RBC. • In clinical specimens, virus can be isolated with in 7days by immunofluorescence method. 2. Rapid diagnosis: immunofluoroscent detection of influenza antigen in respiratory system either directly after amplification in cell culture for 24hrs. • Nasal aspirates or nasal washes are best specimens.
  • 8. EPIDEMOLOGY  Epidemics caused by influenza virus have been described for more than 2000yrs.  Pandemic are recognized at various intervals.  The great pandemic of 1918-1919 was severe, killing 20-40 million people.  It is possible to deduce which viral antigen circulated before virus isolation became possible.  Major pandemics are associated with antigenic shifts i.e. when the viral H (or) N (or) both change.  If a cell is infected with 2 different strains, the progeny will include both the parental RNA molecules.  All the H & N antigen subtypes are formed in aquatic birds. INFLUENZA B: this virus do not undergo antigenic shift as there is no animal reservoirs. Epidemic occurs every 3-6yrs interval and they do not become pandemic. INFLUENZA C: they are not associated with epidemics but give rise to respiratory infections in young children and are asymptomatic.
  • 9. TREATMENT  Oral amantadine hydrochloride was derived from rimantadine in early 1980’s & worked only on influenza A, this will block ion channels &thus prevent pH changes.  Amantadine is effective when given prophylactically & therapeutically when given within 24hrs of administration.  Zanamivir & oseltamivir are the neuraminidase inhibitors & are effective against influenza A & B.  These are effective against amantadine or rimantadine resistant strains.