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| <big><center>[[Viruses|'''BACK TO VIRUSES''']]</center></big> | | <big><center>[[Viruses|'''BACK TO VIRUSES''']]</center></big> |
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| + | -Introduction- |
| + | Influenza is a largely species-specific infection, but the threat of zoonotic potential is real. Virulence varies between strains, but all are spread by aerosol routes. They are typified by rhinitis, pyrexia, and anemia. Flu presents a particular challenge to vaccination as antigenic drift within the virus means that strains can vary from one year to the next. As such, vaccine produced from this year's virus may not give protection against next year's virus. |
| + | |
| + | -Morphology- |
| + | *Enveloped, single-stranded RNA negative sense virus with a different gene on each of its 8 segments |
| + | *Each gene codes for one protein: |
| + | **Haemagglutinin ('''H''') spike |
| + | **Neuraminidase ('''N''') spike |
| + | **Matrix, which lines the envelope and acts as scaffolding |
| + | **Nucleic acid |
| + | **3 viral polymerases |
| + | **1 large non-structural protein |
| + | *Each strain of flu is named according to it's '''H''' and '''N''' number, eg. H5N1 |
| + | **Haemagglutinin binds virus to respiratory epithelia via sialic acid |
| + | **Neuraminidase is a sialidase enzyme that prevents reattachment to the same host cell upon detachment |
| + | |
| + | -Virulence- |
| + | Virulence depends on the tropism of the H molecule involved: |
| + | *H is formed by the cleavage of a precursor protein H0 |
| + | *Cleavage typically happens in respiratory or enteric epithelia |
| + | *However, a virulent virus has more basic amino acids at it's H0 cleavage site, leaving it open for cleavage by other cells, such as neurons |
| + | |
| + | -Types and Subtypes- |
| + | *Three genuses of Flu exist: A, B, and C, of which only A is of veterinary interest |
| + | *The subtype of a flu virus is described in terms of H (of H1-H15) and N (of N1 to N9) |
| + | *Subtype by species: |
| + | **Ducks: H1-H15 |
| + | **Equine: H7 (previously Equine type 1) and H3 (previously Equine type 2) |
| + | **Harp seals: H4 and H7 |
| + | **Pigs: H1, H3, H4, H5 (Asian), H9 |
| + | **Human: H1-3, H7, H( |
| + | *Vaccines cannot cross protect against different subtypes within the same species |
| + | |
| + | -Antigenic Shift and Drift- |
| + | Flu continues to be a feared disease because of it's ability to evolve, both within a particular strain and into new and undefined strains. The flu epidemics of history show that antigenic variation of influenza should not be taken lightly, hence the great concern over the recombination of the H5N1 virus in asia through infection of a pig with human and avian strains of flu. |
| + | *'''Shift''' is the more serious of antigenic movements and is definied by: |
| + | **Gene reassortment |
| + | **Change of species specificity |
| + | *'''Drift''' is the evolution of a virus within its subtype, evidenced by the changing strains of human flu from year to year |
| + | **Each H spike carries 4 antigenic region, and a change in any region results in drift |
| + | **Viral RNA is constantly evolving to evade immune detection and destruction |
| + | *Vaccination schemes are affected by both shift and drift: |
| + | **Complete change of H spike renders current vaccinations useless, and is the cause of an epidemic |
| + | **Current vaccines are always modeled on the most recent outbreaks of the flu in question, and cannot therefore protect against the evolution of the virus from year to year |
| + | **Partial protection can be provided against strains within the same ''subtype'', hence the continuation of vaccination shemes |
| + | |
| + | -Influenza by Species- |
| + | --Equine Influenza-- |
| + | ---Subtypes--- |
| + | *Two subtypes of Equine Influenza have been described: |
| + | **H7N7 (Equine 1), which was prevalent in the UK between 1963-1977 |
| + | **H3N8 (Equine 2), or the European strains, have been circulating since 1965 |
| + | *Some drift has occurred, causing outbreaks of North-American-like strains of H3N8 in 1998 (EU) and 2003 (South America) |
| + | ---Pathogenesis--- |
| + | *Aerosol transmission infects the epithelium of the upper respiratory tract, resulting in cell necrosis |
| + | *This manifests a bronchiolitis and serous exudation |
| + | *1-3 day incubation period |
| + | *Excretion of the virus in nasal secretions peaks at 3-4 days and finishes by 10 days |
| + | *Clinical signs: |
| + | **Harsh dry cough |
| + | **Pyrexia (103-106F) |
| + | **Depression |
| + | **Loss of appetite |
| + | **Enlarged submandibular lymph nodes |
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| *Swine influenza virus in [[Nasal Cavity Inflammatory - Pathology#Infectious causes of rhinitis|rhinitis]], may progress to [[Lungs Inflammatory - Pathology#Infectious causes of pneumonia|pneumonia]] - see [[Respiratory Viral Infections - Pathology#Swine influenza|respiratory viral infections]] | | *Swine influenza virus in [[Nasal Cavity Inflammatory - Pathology#Infectious causes of rhinitis|rhinitis]], may progress to [[Lungs Inflammatory - Pathology#Infectious causes of pneumonia|pneumonia]] - see [[Respiratory Viral Infections - Pathology#Swine influenza|respiratory viral infections]] |
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| *Equine influenza virus in [[Nasal Cavity Inflammatory - Pathology#Infectious causes of rhinitis|rhinitis]], see [[Respiratory Viral Infections - Pathology#Equine influenza|respiratory infections]] | | *Equine influenza virus in [[Nasal Cavity Inflammatory - Pathology#Infectious causes of rhinitis|rhinitis]], see [[Respiratory Viral Infections - Pathology#Equine influenza|respiratory infections]] |