orthomyxoviridae
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detailed information about influenza viruses(A,B,C)
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orthomyxoviridae
- 2. Influenza viruses The Influenza viruses are a major determinant of morbidity & mortality caused by respiratory diseases. Outbreaks of infection some times occur in world wide epidemics. Influenza has been responsible for millions of deaths world wide during the twentieth century. Control of influenza is difficult due to it’s high frequency of genetic reassortment. Influenza A is highly variable antigenically & is responsible for most cases of epidemic influenza. Influenza type B may exhibit antigenic changes & some times causes epidemics. Influenza type C is antigenically stable & causes only mild illness.
- 3. Properties of Orthomyxoviruses: All known Orthomyxoviruses are influenza viruses, three immunologic types are known, A,B& C Antigenic changes continually occur within type A & to lesser degree in type B , type C is antigenically stable.
- 4. Influenza A strains are also known for pigs, horses, birds & some of them are antigenically similar to strains circulating in human population. Virion: Spherical, pleomorphic 80- 120 nm Single stranded negative sense, RNA virus, genome consists of 8 segments, Enveloped.
- 5. Classification: Antigenic differences exhibited by two of the internal structural proteins. The NP & M proteins are used to divide influenza viruses into types A,B & C. Theses proteins possess no cross reactivity among the three types. Antigenic variations in the surface glycoproteins HA & NA are used to subtype the viruses. 16 subtypes of HA (H1- H16) & 9 subtypes of NA (N1-N9) in many different combinations have been recovered from birds, animal or humans.
- 6. Influenza virus infections in humans : Epidemiology : The types of influenza vary markedly in their epidemiologic patterns. Influenza C is least significant, it causes mild, sporadic respiratory disease but not epidemic influenza. Influenza B some times causes epidemics, but influenza type A causes massive epidemic & can cross around the world causing pandemics. The incidence of influenza peaks during winter. There is no evidence of latent infection, continuous person – to person chain transmission must exist for viral survival. Periodic outbreaks appear because of antigenic changes in one or both surface glycoprotein of the virus. Avian influenza ranges from highly lethal infections in chickens & turkeys to in apparent infections. It is possible that influenza is a water born infection ( virus is shed in duck faeces & remains viable in water for days or weeks).
- 7. Influenza epidemic occurs in waves (every 2-3 years). Every 10-40 year when a new subtype of influenza virus appears, a pandemic results Past Antigenic Shifts 1918 H1N1 “Spanish Influenza” 20-40 million deaths 1957 H2N2 “Asian Flu” 1-2 million deaths 1968 H3N2 “Hong Kong Flu” 700,000 deaths 1977 H1N1 Re-emergence No pandemic At least 16 HA subtypes and 9 NA subtypes occur in nature. Up until 1997, only viruses of H1, H2, and H3 are known to infect and cause disease in humans.
- 8. Theories Behind Antigenic Shift 1. Reassortment of the H and N genes between human and avian influenza viruses through a third host. 2. Recycling of pre-existing strains – this probably occurred in 1977 when H1N1 re-surfaced. 3. Gradual adaptation of avian influenza viruses to human transmission. There is some evidence that this occurred in the 1918 H1N1 pandemic.
- 9. Transmission : From person to person by air born droplets or by contact with contaminated hands or surfaces.
- 10. Pathogenesis : Few of respiratory cells are firstly infected, virus spread to adjacent cells, where replication cycles repeated. Viral NA lowers the viscosity of mucous film in the respiratory tract, within a short time many cells in the respiratory tract are infected & killed. Virus shedding starts one day before onset of symptoms, peaks within 24 hrs – 2 days then declines rapidly. Interferon is detectable in respiratory secretions one day after viral shedding, this aids in the recovery of the host. Specific Ab & cell mediated response can not be detected for another 1-2 weeks. Influenza virus causes cellular destruction & desquamation of superficial mucosa of the respiratory tract, this lowers it’s resistance to secondary bacterial infections ( Staph, Strept, Haemophilus).
- 11. Incubation period : 1 – 4 days. Clinical signs : A :Uncomplicated influenza (type A & B). Symptoms appear abruptly, (chills, headache, dry cough followed by high fever, generalized muscular aches, malaise, anorexia). The fever lasts for 3 days, respiratory symptoms lasts another 3-4 days. The cough & weakness may persist for 1-3 weeks after subsides of major symptoms. In children, symptoms are similar to adults & influenza is an important cause of Croup in under one year of age. Type C rarely cause these symptoms.
- 12. B : Pneumonia : Serious complications usually occur only in the elderly & debilitated individuals (specially with cardiopulmonary or other chronic disease). Pregnancy appeared to be a risk factor for lethal complications in some epidemics ( mainly due to pneumonia, cardiovascular & renal diseases). Lethal pneumonia is mainly viral, secondary bacterial or combined infection which is three times more common than primary influenza pneumonia. Staph aureus co infection has been reported to cause 42 % fatality rate. C : Reye’s syndrome :It is an acute encephalopathy of children & adolescent ( 2- 16 years of age), fatty liver degeneration is associated with this syndrome. Mortality rate is high (10-40 %).
- 13. The cause of Reye’s syndrome is unknown but it is recognized as complication of influenza B, A & herpes virus (Varicella zoster) infections. Epidemic cases of Reye’s syndrome have been associated with influenza B outbreaks. Immunity : Antibody against HA & NA are important in immunity to influenza, resistance to initiation of infection is related to HA Abs Where decrease of the disease severity & it’s transmission to contacts is related to NA Abs. Protection correlates with both serum antibodies & secretory IgA antibodies in nasal secretions. No cross protection is seen between the three influenza types. Serum antibodies persists for months – years & secretory Abs lasts for several months only).
- 14. Laboratory diagnosis : Detection of Antigen by ELISA Isolation & identification of the virus : and inoculation in embryonated eggs & monkey kidney cells. Identified by CF, FAT Serology : HI, CF, ELISA .
- 15. Treatment : Amantadine hydrochloride, rimantadine antiviral drugs are useful to prevent influenza A infections (they block uncoating). NSAIDs (other than asprin) is used for fever & headache Control : Amantidine is effective against influenza A if given early in the illness. However, resistance to amantidine emerges rapidly. Neuraminidase inhibitors are becoming available. They are highly effective and have fewer side effects than amantidine. Moreover, resistance to these agents emerge slowly .
- 16. Oseltamivir (Tamiflu)R is neuraminidase inhibitors serving as competitive inhibitors of the activity of viral neuraminidase enzyme upon sialic acid found on glycoprotein on the surface of the normal host cells. By blocking the activity of the enzyme, oseltamivir prevent new viral particles from being released by infected cells.