SWINE FLU NEHA SRIVASTAVA M.PHARM (PHARMACOLOGY)

Evolution 1918–19 H1N1 influenza A appeared in pigs, affected 50 million people worldwide 1930 Isolation of H1N1 from pigs for the first time 1970 Transmission of H3N2 virus to swine in Asia 1976 New strain of swine flu variant of H1N1, affected soldiers at Fort Dix in the US 1984 Reassortment between human H3N2 and avian H1N1 in swine

1988 Women exposed to pigs at country fair exhibition in Wisconsin died of H1N1 infection from swine 1994 H1N2, isolated from pigs in the UK. Example of human–avian reassortment 1998 H3N2 virus caused severe disease in North America. Triple reassorted (avian–human–swine) distinct from earlier strains 1958–2005 37 cases of swine influenza reported among humans 2005–2009 Triple reassortant swine flu virus in human, in United States 2009 New strain of swine influenza H1N1, reported from Mexico and the United States shows sustained human-to-human transmission

Swine flu Gene = Swine + Avian + human flu virus Introduction Swine Influenza (swine flu) is a- Respiratory disease of pigs Type A influenza virus [orthomyxoviridae] High morbidity and low fatality Swine flu Gene = Swine + Avian + human flu virus Scientist call this “Quadruple Re-assortment Virus”. Incubation : 2-7 days

Symptoms

Transmission Between pigs. The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing Between humans Direct transmission Contact between sick and healthy animals. Indirect transmission Feeding with garbage containing infected meat. Biological vectors: soft ticks of the genus Ornithodoros. Fomites: premises, vehicles, implements,clothes.

MORPHOLOGY OF VIRUS -Hemagglutinin (H) -Neuraminidase (N) Pleomorphic Two surface antigen- -Hemagglutinin (H) -Neuraminidase (N) Contain 16 hemagglutinin antigen & 9 neuraminidase antigen 8 pieces of segmented negative sense RNA Matrix protein (M1)-strength & rigidity to envelope Matrix protein (M2)-target for antiviral Neuraminidase enzyme that support the virus to cell wall is known as Sialidase

Pathogenesis Step 1- H bind onto sialic acid sugar which is cleaved by protease enzyme and cell import virus Step 2- Due to acidic endosome viral envelope fuses with vacuole’s membrane and M2 ion channel releases viral RNA & core protein Step 3- Core protein form complex with viral RNA and transported into nucleus where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense vRNA Step 4- vRNA either transported to cytoplasm or remain in nucleus Step 5- Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface or transported back into the nucleus to bind vRNA and form new viral genome particles. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane Step 6- The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion. Step 7- The mature virus buds off from the cell

Different steps of pathogenesis 1 2 3 4 5 6 7

Diagnosis A) IDENTIFICATION OF THE AGENTS Culture -cell culture isolation -egg inoculation test -haemagglutination test Swine influenza virus isolates -haemagglutination inhibition test -neuraminidase inhibitionn test Fluorescent test Polymerase chain reaction test B) SEROLOGICAL TESTING Haemagglutination Inhibition test Enzyme-Linked Immunosorbent Assay

Treatment Allopathic Oseltamivir [TAMIFLU] Zanamivir [RELENZA] Rimantidine [FLUMADINE] Herbal Therapy Tulsi Garlic Ginger Gooseberry Aloe-vera Camphor

Prevention

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