human influenza virus.pptx disease causing virus

Human influenza virus

1. Human Influenza Virus BOOMIKA. S I MSc Microbiology

2. INTRODUCTION: Family – Orthomyxoviridae Virus – Human influenza virus Genera – Influenza A, B & C Cause – They are not major cause of morbidity & mortality Responsible – Responsible for several epidermic and pandamic of respiratory for in the last two centuries. MORPHOLOGY: Shape – Spherical Size – 80-120 nm in diameter Symmetry – Helical nucleocapsid (9nm). Envelope – present Viral RNA segments – Multiple segments of (- ve ) sense as SS stranded RNA, Influenza A & B – Eight segments Influenza C - seven segments (Neuraminidase absent)

3. REPLICATION: SITE OF REPLICATION: RNA replication occurs typically in the nucleus VIRAL PROTEINS : 8 structural proteins(PB1, PB2, PA, NP, HA, NA, M1 & M2) PB1, PB2 & PA(Polymerase protein) – RNA transcription and replication NP( Nucleoprotein) – Major capsid protein Non structural proteins: NS1- interferon antagonist and inhibits pre- mRNA splicing and NS2 helps in export of molecules. ENVELOPE : MATRIX PROTEINS : M1- Major viral protein. M2 – help transport of molecules. Hemagglutinin(HA)&Neuraminidase(NA) :Glycoprotein inserted into the lipid envelope.

4. STRUCTURE: Negative sense, single stand RNA, Eight segments. Matrix protein (M1 And M2) Hemagglutinin (HA) Nucleoprotein (NP)

5. ANTIGENIC SUBTYPES AND NOMENCLATURE: THREE GENERA: Based on RNP and M proteins, A, B, and c SUBTYPES: Based on HA and NA antigens, Influenza A; distincT 16H subtypes (H1 TO H16) and 9N subtypes (N1 to N9. *Subtypes infect animals, birds, but occasionally undergo genetic changes and infect humans to cause major epidermic and pandemic . Influenza B and C viruses through have subtypes ;but are not designated. The standard nomenclature system for influenza virus: Influenza virus type/host(indicated only for non- human origin)/geographic origin/strain number/year of isolation/(HA/NA subtype). EXAMPLE: HUMAN STRAIN-Influenza A/Hong Kong/03\1968(H3N2). NON HUMAN STRAIN-Influenza A/swine/ lowa /15\1930(H1N1).

6. ANTIGENIC VARIATION: TWO TYPES ANTIGENIC DRIFT: Minor change occurring due to point mutations in the HA/NA gene, resulting in alteration of amino acid sequence of the antigenic sites on HA/NA. Such that virus can escape recognition by the host’s immune system. The new variant must sustain two or more mutations to become epidermologically significant. Seen in both influenza virus type-A and B. Resulting in outbreak and minor periodic epedermics . Antigenic drift occurs more frequently, every 2-3 years. ANTIGENIC SHIFT: Major drastic, discontinuous variation in the sequence of a viral surface protein HA/NA , that occurs due to genetic ressortment between genomes of two or more influenza viruses infecting the same host cells, resulting in a new virus strain. Unrelated antigenically to proceduressor strains. Occurs only in influenza A virus. Resulting in pandemics and major epidemics-e.g. H1N1 pandemics of 2009. Antigenic shift occurs less frequently every 10-20years.

7. PATHOGENESIS: TRANSMISSION: Infected aerosols generated by coughs and sneezes, rarely via contacts. Or by fomites, small-particle aerosols(less than 10 micro meter) are more efficient in the transmission. INCUBATION PERIOD : It is about 18-72 hours. TARGET CELL ENTRY: Viral HA attaches to specific sialic acid receptors on the host cell surface that leads to viral entry. Ciliated columnar epithelial cells are most commonly infected but it may also infect other cells including alveolar cells, mucus gland cells and alveolar macrophages. MULTIPLY LOCALLY: Virus replicates in the infected cells and infections daughter virions spread to the adjacent cells to involve large number of respiratory epithelial cells over several hours .

8. PATHOGENESIS: SPREAD: Very rarely, virus spreads to the lower respiratorytract or spills over blood stream to involve extra pulmonary sites. LOCAL DAMAGE: Influenza virus infection causes cellular destruction and desquamation of superficial mucosa of the respiratory tract, but it does affect the basal layer of the epithelium . Edema and mononuclear cell infiltrations occur at local site leading to cytokinase influx which accounts for local symptoms. Local damage predisposes to secondary bacterial invasion.

9. TRANSMISSION:

10. CLINICAL MANIFESTATIONS: UNCOMPLECATED INFLUENZA: Chills, headache, dry cough, sore throat, high grade fever, myalgia and anorexia. Indistinguishable from the infections caused by other upper respiratory tract pathogens. COMPLECATED INLUENZA: Pneumoia ; Secondary bacterial pneumonia. Other pulmonary complications; Chronic bronchitis and osthma . Reye’s syndrome; Encephalopathy, Influenza B, Varicella-A High risk groups; Aging, underlying chronic lung, cardiac, renal hepatic & CNS conditions. Low immunity, older children.

11. LABORATORY DIAGNOSIS: SPECIMENS:- Nasopharyngeal swab, Kept at 4*c ISOLATION OF VIRUS :- Primary monkey kidney cell lines. VIRAL ANTIGENS DETECTION: Direct IF test. MOLECULAR METHODS:- RT-PCR detects viral RNA ANTIBODY DETECTION:- HAI, Neutralisation test, ELISA DETECTION OF VIRAL GROWTH IN EMBRYONATED EGG OR CELL LINE:- Hemabsorption test Hemagglutinin Direct immunofluroscence test

12. TREATMENT AND DOSAGE: TREATMENT: Neuraminidase inhibitors such as zanamivior , oseltamivir and peramivir. It is the drug of choice for A/H1N1 2009 flu,A /H5N1 Avian flu and influenza B. DOSAGE: Oseltamivir(Tamiflu 75 mg tab) Zanamivir(10 mg, inhalation form) Matrix protein M2 inhibitor such as amantadine and rimantadine.

13. REFERENCE: Medical virology(MBBS materials) Slide share ppt(Human influenza virus) Fenner and White’s medical virology (Book)

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