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Influenza Virus

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Influenza Virus 1 | P a g e Influenza virus Introduction: The name Myxovirus is a group of enveloped viruses characterized by their ability to adsorb onto mucoprotein receptors on erythrocytes, causing hemagglutination. They are spherical and filamentous RNA viruses. They are now classified into two separate families: 1. Orthomyxoviridae- consisting of the influenza viruses 2. Paramyxoviridae- consisting of Newcastle disease virus, mumps virus, parainfluenza viruses, measles and respiratory syncytial viruses. Influenza viruses are classic respiratory viruses. Morphology: The influenza virus is typically spherical or filamentous with a diameter of 80-120 nm but pleomorphism is common. The virus consists of ribonucleoprotein in helical symmetry. The negative sense single-stranded RNA genome is segmented and exists as eight pieces. These segments code for different proteins which are NS1, NS2, NP, M1, M2, M3, HA and NA. The genome consists of an RNA-dependent RNA polymerase, which transcribes the negative-polarity genome into mRNA. The genome, therefore, is not infectious. The nucleocapsid is surrounded by an envelope, which has an inner membrane protein layer and an outer lipid layer. The membrane protein is also known as the matrix or ‘M protein’ composed of two components, M1 and M2. The protein part of the envelope is virus coded but the lipid layer is derived from the modified host cell membrane, during the process of replication by budding. Projecting from the envelope are two types of spikes (peplomers): Hemagglutinins (HA) spikes which are triangular in cross-section and 2 | P a g e the mushroom-shaped neuraminidase (NA) peplomers which are less numerous. Viability characteristics: The virus is inactivated by heating at 50 ͦC for 30 minutes. It remains viable at 0-4 ͦ C for about a week. It can be preserved for years at -70 ͦC or by freeze drying. Influenza viruses are resistant to slow drying. The virus survives slow drying and may remain viable on fomites such as blankets for about two weeks. They remain viable in dust up to 2 weeks. Ether, formaldehyde, phenol, salts of heavy metal and many other chemical disinfectants destroy infectivity. Iodine is particularly effective. Hemagglutinating, enzymic and complement-fixing activities of the virus are more stable than infectivity. Antigenic and genomic properties: The antigens of the influenza virus can be classified into two types: 1) Internal Antigens: . The internal antigen is the ribonucleoprotein and is hence called the RNP antigen. Because it is found free in infected tissues and occurs in the supernatant when the virus containing fluidis centrifuged, it was also called as ‘soluble’ (S) antigen. The RNP antigen is type specific and based on its nature, influenza viruses are classified into types A, B and C. The RNP antigens of types A, B and C are distinct but all strains of any one type possess the same antigen. The RNP antigen is stable and does not exhibit any significant antigenic variation. M protein antigen, like the RNP antigen is also type specific and distinct for A, B and C types of influenza viruses. The envelope lipid antigen is 3 | P a g e host specific and is determined by the species in which virus replication takes place. 2) Surface antigen: The term ‘viral’ or V antigen was used to describe the surface antigen of the influenza virus. The V antigen is actually composed of at least two virus-coded proteins, hemagglutinins and neuraminidase. Hemagglutinin is a glycoprotein. It is a trimer. It is strain specific. It undergoes antigenic variation. It is composed of two polypeptides, HA 1 and HA 2. It is responsible for hemagglutination and hemadsorption. It enables the virus to adsorb to mucoprotein receptors on red cells as well as on respiratory epithelial cells. Anti-hemagglutinin antibodies are produced following infection and immunization. This antibody is protective by preventing adsorption of the virus to cells. Hemagglutinins is a strain- specific antigen and is capable of great variation. Fifteen distinct HA subtypes, H1-H15, have been identified in avian influenza viruses, but only four of them have been found in human isolates so far. The hemagglutinin consists of 500 spikes, each measuring 12 nm in length. The triangular shaped HA is inserted into the virus membrane by its tail end. The distal end, which contains five antigenic sites (designated HA1-HA5), is responsible for binding of virion to host cells. Neuraminidase is a glycoprotein enzyme which destroys cell receptors by hydrolytic cleavage. It is a tetramer. It consists of 100 mushroom-shaped spikes. The mushroom-shaped NA is inserted into the virus membrane by its hydrophobic tail end. The distal end contains antigenic as well as enzymatically active sites. The anti-neuraminidase antibody is formed following infection and immunization. It is not as effective in protection as the anti-hemagglutinin antibody. It does not prevent the adsorption of virus onto cells but can inhibit the release and spread of progeny virions and may thus contribute to limiting the infection. It is a strain specific antigen and exhibits variation. Nine different subtypes have been identified (N1-N9). Neuraminidase is an isoenzyme. The function of neuraminidase is to cleave the neuraminic acid and to release progeny virions from the infected host cells. The neuraminidse also degrades the 4 | P a g e mucus layer, thereby exposing the epithelial membrane of the respiratory tract for infection by the virus. Difference between HA and NA: Sr.No. Hemagglutinin (HA) Neuraminidase (NA) 1. It is a trimer. It is a tetramer. 2. It consists of 500 spikes. It consists of 100 spikes. 3. HA is triangular in shape. NA is mushroom-shaped. 4. There are 15 distinct subtypes of There are 9 distinct subtypes of NA HA designated as H1-H15. designated as (N1-N9). 5. Anti-hemagglutinin antibodies are The anti-neuraminidase antibody is produced following infection and formed following infection and immunization and this antibody is immunization which is not as protective by preventing effective in protection as the anti- adsorption of the virus to cells. hemagglutinin antibody. It does not prevent the adsorption of virus onto cells. Antigenic variations: Antigenic variation is a unique feature of influenza virus. The surface antigens HA and NA show variations and are primarily responsible for antigenic variations exhibited by influenza viruses. The internal RNP antigen and M protein are stable, hence do not contribute to the antigenic variations. Antigenic variations are of two types: 1) Antigenic shift and 2) Antigenic drift. 1) Antigenic shift: The abrupt, drastic, discontinuous change is called the antigenic shift. This occurs due to major antigenic changes in HA or NA antigens, and is caused by replacement of the gene for HA by one coding for a completely different amino acid sequence. The antigenic shift is 5 | P a g e characterized by alteration of virtually all the antigenic sites of the HA. This occurs independently in the HA and NA. 2) Antigenic drift: The gradual, sequential, regular antigenic change in influenza virus is known as antigenic drift. This occurs due to minor antigenic changes in the HA or NA occurring at frequent intervals. This is caused by a single mutation affecting HA glycoprotein. The antigenic drift is characterized by changes in certain epitopes in the HA, while others are being conserved. Difference between antigenic shift and antigenic drift: Sr. Antigenic shift Antigenic drift no. 1. Abrupt, drastic and Gradual, sequential and regular discontinuous variation in the variation at periodic intervals antigenic structure 2. Results in a different strain Results in a new strain Related to predecessor strain Not related to predecessor strain 3. Antigenic drift is due to Antigenic shift is due to gene mutation and selection reassortment 4. Responsible for epidemics of Responsible for epidemics as well influenza as pandemics of influenza. Gene Reassortment: Because the influenza virus genome is segmented, genetic reassortment can occur when a host cell is infected simultaneously with viruses of two different parent strains. This process of genetic reassortment accounts for the periodic appearance of the novel types of influenza A strains that cause influenza pandemics. Influenza viruses of animals, such as aquatic birds, chickens, swine, and horses show high host specificity. These animal viruses are the source of the RNA segments that encode the antigenic shift variants that cause epidemics among humans. For example, if a person is infected simultaneously by an avian and 6 | P a g e human influenza strains, then it is possible that a genetic reassortment could occur in infected cells in humans. The reassortment could lead to emergence of a new human influenza A virus, the progeny of which will contain a mixture of genome segments from the two strains (e.g. a new variant of human influenza A virus bearing the avian virus HA). Many studies have conclusively demonstrated that the aquatic birds (such as water fowl) are a common source of these new genes. The pigs act as mixing vessels, where these virulent genes of water fowl mix with the genome of influenza virus giving rise to new variant of influenza virus. Designation of influenza viruses: Influenza virus type A can be classified into subtypes based on the variations in their surface antigens. The WHO proposed a new system of classification in 1971 and was later modified, which takes into account Pathogenicity: The route of entry is the respiratory tract. In experimental infection in volunteers, very small doses (approximately three viable particles) can initiate infection when given as aerosols. Larger doses are required when infection is by intranasal instillation. The viral neuraminidase facilitates infection by reducing the viscosity of the mucus film lining the respiratory tract and exposing the cell surface receptors for virus adsorption. The ciliated cells of the respiratory tract are the main sites of viral infection.
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