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  • Spherical, pleomorphic, 80-120 nm, Enveloped
  • Single stranded RNA, negative sense, segmented (A,B: 8 segments, C: 7 segments) 
a. Influenza virus
  1. Affects both upper & lower respiratory tracts
  2. Outbreaks in winter
  3. Divided into A, B & C depending on antigenic characteristics of nucleoprotein (NP) & Matrix (M)-type specific antigens
  4. Influenza A further divided on the basis of hemagglutinin (H) & neuraminidase (N)- strain specific antigens
  5. lipid envelope, from the surface of which H & N glycoprotein projects
  6. Hemagglutinin is the site at which virus binds to cell receptor. Antibodies to H Ag are major determinants of immunity to Influenza virus
  7. Neuraminidase degrades the receptor & also causes release of virus from infected cells Antibodies to N Ag limits viral spread
  8. M protein present on surface of lipid envelope causes virus assembly and stabilizes lipid envelope
  9. Segmentation of genome leads to increased chances of genetic reassortment
b. Epidemiology :
  1. Localized epidemics occur every 1 - 3yrs
  2. Pandemics occur every 10 - 15yrs
  3. Epidemics occur mainly due to Influenza A virus due to Antigenic variation in H & N Ag
  • Antigenic Shift : Major antigenic variation , due to genetic reassortment. They are  associated with pandemics and are restricted to Influenza A
  • Antigenic drift - Minor antigenic variations due to point mutation
  1. Influenza B causes less severe outbreaks
c. Pathogenesis :
  1. Infection spreads by aerosols
  2. Virus multiplies mainly in ciliated columnar respiratory epithelium. Virus not found in any extrapulmonary site   
  3. Severity of illness is related to quantity of virus shed in secretions. Virus shedding lasts for 2 - 5days after appearance of symptoms
  4. Incubation period 18 - 72 hrs
  5. Serum antibodies appear after 2 weeks of primary infection
  6. IgA antibodies are found in respiratory secretions
  7. Interferons appear in respiratory secretion shortly after virus shedding begins & rise of interferons coincides with decrease in virus shedding
d. Clinical features :
  1. Abrupt onset of symptoms- Moderate fever, sore throat, myalgia
  2. Ocular signs eg : Photophobia and burning of eyes
  3. Mild cervical lymphadenopathy
  4. Acute illness lasts for 2 - 5days
e. Complications :
  1. Pneumonia - Most common complication
  2. Primary viral pneumonia is severe with scanty sputum production. Secondary bacterial pneumonia is commonly caused by Streptococcus pneumoniae, Staphylococcus aureus & Hemophilus influenzae
  3. Mixed bacterial & viral pneumonia commonly occurs
  4. Worsening of COPD & exacerbation of chronic bronchitis and asthma
  5. Reye's Syndrome: Mainly associated with Influenza 'B', especially with the use of aspirin for viral infection      
  6. Myositis, myoglobinuria, rhabdomyolysis
  7. Myositis leads to increase in CPK & aldolase and Myoglobinuria may cause renal failure
  8. Pericarditis, Myocarditis
f. Laboratory diagnosis :
  1. Demonstration of viral antigen: Immunofluorescence staining
  2. Virus is isolated from throat swabs, nasopharyngeal washes or sputum through tissue culture or amniotic cavity of chick embryo within 48 - 72hrs of inoculation
  3. Antibody detection: CFT, HAI, Nt
  4. RT-PCR and probes
g. Treatment :
  1. Salicylates & acetaminophen are used for symptomatic relief
  2. Amantadine & Rimantadine are active only against influenza A
  3. Ribavirine is effective against both Influenza A & Influenza B
  4. Maintenance of oxygenation and fluid is done in viral pneumonia
  5. Secondary bacterial pneumonia is treated with antibacterial drugs
h. Prophylaxis :
  1. Vaccines against Influenza A & B are effective in 50 - 80% cases
  2. Live attenuated vaccine against Influenza A is given intranasally
  3. Commercially available vaccine is the killed vaccine
  4. Amantadine & Rimantadine are 70 - 100% effective in prophylaxis of illness
  5. During outbreaks amantadine & vaccine can be given simultaneously

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