INFLUENZA VIRUSES

 

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Structure & Property

Transmission

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment

Family:

- only members of orthomyxovirus family

- ‘myxo’: interact with mucins

 

Size: 80-100 nm

 

Genome: segmented single-stranded RNA, negative polarity

 

Nucleocapsid:

- helical, surrounded by protein capsomeres.

- 8 discrete RNA segments

- group-specific antigen that distinguishes influenza A, B, and C

 

Envelope:

- lipoprotein

- covered with spikes:

- hemagglutinin: virus attachment to host cells

- neuraminidase: cleaves neuraminic acid to release virus from infected cell

Transmitted by airborne respiratory droplets

 

Ability of influenza A to cause epidemics is dependent on antigenic changes in hemagglutinin and neuraminidase

 

Antigenic changes:

- antigenic shifts: recombination of RNA segments of two antigenic types (major).

- antigenic drifts: mutations (minor)

 

Occurs primarily in the winter months, when it and secondary bacterial pneumonia cause a significant number of deaths, esp. in old people.

Primary site of multiplication: superficial epithelium of lower respiratory tract.

 

Inhalation of virus.

 

Degradation of mucus layer by neuraminidase

 

Virus gain access to cells of upper and lower respiratory tract

 

Infection limited to this area; viremia is rare.

 

Systemic symptoms such as myalgias, are due to cytokines circulating in the blood.

 

Necrosis of superficial layers of respiratory epithelium.

 

Immunity:

- mainly IgA in respiratory tract

- IgG

- cytotoxic T cells

Incubation period: 24-48 hours.

 

Fever, myalgias, headache, and cough develop suddenly.

 

Symptoms resolve in 4-7 days

 

Secondary bacteria infections after damage of bronchial mucosa:

- streptococcus pneumoniae

- haemophilus influenzae

- staphylococcus aureus

 

Reye’s syndrome:

- encephalopathy & liver degeneration

- associated with influenza B, chicken-pox and aspirin intake.

Antibody staining:

- virus grown in cell culture from throat washings

- identified by fluorescent-antibody staining of infected cells

- by using antisera to influenza A and B.

- takes several days

 

Serology:

- rise in antibody titer of at least 4-fold in paired serum samples taken early in illness

- either the hemagglutination inhibition or complement fixation test is used to assay the antibody titer.

Amantadine:

- effective against influenza A not B

- used to prevent influenza in a confined, elderly, unimmunized population.

- effective in treatment if given early in infection.

 

Inactivated vaccine (grown in chick embryos) prophylaxis for high risk groups during winter – problems of timely preparation, short-lived immunity, incomplete protection.

 

Guillain-Barre syndrome is a complication of vaccine.

 

Minimize spread by respiratory route.

 

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