History Causes And Types Of Influenza Biology Essay

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INFLUENZA is also known as grippe or flu. A number of viruses are found responsible for flu. Entry into to the body is through mouth and nose. Viruses belong to orthomyxoviridae family. The virus is covered by a coat which encloses seven to eight ssRNA. Based on its structural protein such as internucleotide protein and matrix protein, the virus can be divided into three types INFLUENZA A, INFLUENZA B, INFLUENZA C. Two proteins namely hemagluttinin and neuraminidase help the virus influenza A to bind to any cell and cause the viral infection. Influenza has sloppy character which means that influenza from one strain can incorporate genetic material from other strain. The organism which easily gets infected by any type of influenza becomes mixing site for all the influenza virus and leads to the formation of novel strain. Cytotoxic T lymphocytes (CTLs) specific for conserved viral antigens can respond to different strains of virus, in contrast to antibodies, which are generally strain-specific. The generation of such CTLs in vivo usually requires endogenous expression of the antigen, as occurs in the case of virus infection. This resulted in the generation of nucleoprotein-specific CTLs and protection from a subsequent challenge with a heterologous strain of influenza A virus. Based on their antigenicity influenza A are also sub-divided and currently the class H1N1 and H3N2 are in circulation[1,3,5].

Fig.1: 3-D model of influenza virus [1]


There are RNA viruses which lead to influenza in human and also in animals and birds. Influenza is found to be more severe than common cold and has led to a mortality rate of 0.1% in human [6].

Influenza has been divided into two types known as conventional influenza and seasonal influenza. However, there are situations in which some flu outbreaks are severe. These severe outbreaks occur when the human population is exposed to a flu strain against which the population has little or no immunity because the virus has become altered in a significant way. Unusually severe worldwide outbreaks (pandemics) have occurred several times in the last hundred years since influenza virus was identified in 1933. By an examination of preserved tissue, the worst influenza pandemic (also termed the Spanish flu) occurred in 1918 when the virus caused between 40-100 million deaths worldwide, with a mortality rate estimated to range from 2%-20%.[6]

In April 2009, a new influenza strain against which the world population has little or no immunity was isolated from humans in Mexico. It quickly spread throughout the world so fast that the WHO declared this new flu strain (termed novel H1N1 influenza A swine flu, often shortened to H1N1 or swine flu) as the cause of a pandemic on June 11, 2009. This was the first declared flu pandemic in 41 years [6].


The influenza A virus is an enveloped particle containing eight separate gene segments of single stranded, negative sense RNA which code for seven viral and three non structural proteins. Only two of the viral proteins, the haemagluttanin and neuraminidase are found on the surface of the virion. Both are anchored in the viral membrane and project out from viral surface, both are glycosylated and both exhibit major and minor changes in antigenecity during the evolution of new virus strains. the primary and secondary structural changes associated with antigenic reactions are to be established [2].


Fig.03 Detailed molecular structure of the influenza virus

Fig.4: Genomic structure of the influenza virus.


HA is a homotrimeric membrane glycoprotein. It is shaped like a cylinder, and is approximately 13.5 nanometers long. The three identical monomers that constitute HA are constructed into a central α helix coil; three spherical heads contain the sialic acid binding sites. HA monomers are synthesized and then cleaved by protease into HA1 and HA2 subunits [1]. .Influenza B virus is responsible for causing disease in human and it is found in human only.

Arginine removed and the two domains combine to form a double bonded disulphide protein domain

Two proteins from HA1 and HA2 fuse to form a protein which will allow fusion to change the confirmation to allow viral infectivity.

Translated in cell as a single protein

Haemagluttinin as a trimmer with receptor binding pockets.

Fig.5: showing the pathway for the formation of HA (haemagluttanin acid)


Fig.1: Pathway showing the pathogenecity of influenza virus

The virus attaches itself to the host cell wall. With the help of attachment site on surface of the virus known as virus receptor and receptor sites on the host cell surface known as host cell receptor. [3]

Cells lacking receptor for a certain virus are resistant to the virus and so cannot be infected.

Attachment can be blocked by antibody molecules that bind to the viral attachment sites or host cell receptors to influenza haemagglutinin .There are 16 known haemagglutinin types H1 to H16.

HA (haemogluttaminic acid) binds to the sialic acid which is present on the surface of the target host cells. [3]

HA are proteins that possess specific affinity for certain sugar molecules. Since carbohydrates moieties exist in most animal cell membranes, they may attach themselves to receptor groups if the specific structure of the later is suitable.Haemaglutinins or lectins can be characterized and detected by their capability of agglutinating the red blood cells. The interaction of haematogglutinin with the glycoprotein on the cell surface is manifested in vitro by agglutination of cells. [1]

Entry of the cell is guided by the binding of virus receptor protein to host receptor protein (HA spikes) to mucoproteins containing N-acetylnuraminic acid groups. After binding, the particle is engulfed by endocytosis via coated pits into endocytotic vesicles and finally endosomes. After the virion attaches to sialic-acid(neuraniminc acid) containing receptors on the cell surface, the formation of this complex and the virus is engulfed in the cell which is known as endocytosis.After entering the cell the endosomal vesicles contain virus particles that move toward the cell nucleus. Now there is a fusion peptide on the HA is formed that insert in the endosomal membrane and fuses with the membrane of virus. When this occurs the viral RNA is released in the environment. Then this RNA material is sent to the cell nucleus where the RNA replication starts occurring. The viral RNAs are not naked, but bound to a number of viral proteins. One of these proteins is M1 protein. If the RNAs bound to M1protein, they are not able to enter the nucleus. Then that time they uses anew protein on their cell surface known asM2 .these viral protein forms a channel in the membrane that actively pumps proton from the endosome into the interior of the virion.These proton lower the ph in the interior of the virion,releasing the viral RNAs from M1.in this way RNA can enter the nucleus.

Viruses may replicate widely throughout the body without any disease symptoms, if they do not cause significant cell damage or death. Although retroviruses (e.g. HIV) do not generally cause cell death, being released from the cell by budding rather than by cell lysis, they cause persistent infections and may be passed vertically to offspring if they infect the germ line.  Conversely, most other viruses, referred to as virulent viruses, ultimately damage or kill their host cell by several mechanisms, including inhibition of synthesis of host cell macromolecules, damage to cell lysosomes, alterations of the cell membrane, development of inclusion bodies, and induction of chromosomal aberrations.[3,4]

Fig: 06 process occurring in the endosome

Fig.08: Process of replication of virus inside the host cell.


[1]. http://www.unu.edu/unupress/food/8F083e/8F083E04.htm


Lectin is haemogglutinin.

It has affinity for sugar

That is why it tends to bind with glycoprotein of cells.

[2]. http://www.sinobiological.com/Influenza-Hemagglutinin-General-Information-a-145.html


The genetic composition of neuraminidase gene is found

Nucleotide sequences between 150 to 300 residues long from the 3' end of the neuraminidase gene has been used to partially characterize the antigenic drift and shift.

"Drift" refers to the constant mutation in the strain which alters the strain much.

"Shift" refers to the little mutation in any strain which still makes it to resemble to other strain



The pathway of viral influenza infection is found.



3-D diagram of influenza virus.

[5]Infectious cell entry mechanism of the influenza virus, journal of virology, july 1982


The uncoating mechanism of influenza virus (orthomyxovirus), however, has not yet been made clear.

Most of the morphological studies have shown uptake of the virus by endocytosis

One study has suggested envelope fusion method.

Fusion of liposomes containing the viral glycoprotein with cells has also been reported.

Moreover, the uncoating mechanism after endocytosis has not been clarified.

The viral RNA is passes into the cytoplasm using the process of fusion.

[6]. (Flu) Influenza, conventional, H1N1, Charles Davis, MD, PhD, Melissa Conrad Stöppler,


In general strains can be divided into two type's i.e. conventional and seasonal strain.

Flu outbreaks occur only in severe conditions.

The condition is formed when the community is not resistant to a certain strain.

In 1933 the influenza virus was found.

Several flu outbreaks have occurred because of this virus.

In2009, H1NI influenza A swine flu virus was found, to which world was not immuned to.



Several viruses are found responsible for common cold .Among which rhinovirus is most common. In addition to common cold it is also found responsible for acute asthma. Till now it is found to cause upper respiratory tract infection. It belongs to:

Family- picornaviridae.

Genera- enterovirus.

Rhinoviruses are of 30nm in length, nonenveloped, single stranded RNA genome, within the capsid. Diseases caused by Rhinoviruses are nasopharyngitis, croup, pneumonia and also otitis media and asthma exacerbations. 101 serotypes are known till now. In temprate region people are found to be suffering from common cold during the month of September to April. The month between October to march is found responsible for common cold but not only by rhinovirus but also parainfluenza virus, coronavirus, respiratory syncytial virus and influenza virus. Adenovirus is found to be in infecting state throughout the year and in every season [1].

Fig.1: Seasonal variation of selected upper respiratory tract infection pathogens.

PIV: parainfluenza virus RSV: respiratory syncytial virus MPV: metapneumovirus

Common cold is common among younger children. Children are found to have 3 to 8 colds per year and adults are found to have 2 to 4 colds per year. Preterm infants are also very much susceptible to rhinovirus. One interesting point to be noted here is that native Americans and Eskimos are more prone to common cold with the complication of otitis. The name common cold and cause seem to be unrelated to each other because common cold is not caused by any cold environment, chilled wet feet or drafts .Coming in contact to any infected person is found to be the main cause of common cold[1,2].


Symptoms of Rhinovirus infection:

Dryness and irritation in nose, nasal congestion and sneezing.

Sore throat.

Malaise, headache and cough.

Nasal secretions become thicker and colored after certain days of illness.

Post tussive vomiting can also occur.

Preceding rhinovirus infection can lead to preceding bacterial super infection [2].

Genetics of rhinovirus:

HRVs (human rhinoviruses) are composed of a protein shell which is made up of 60 copies of each of the four capsid proteins VP1, VP2, VP 3, and VP4. VP4 is internal and in close proximity to the RNA. The envelope surrounds a single-stranded RNA genome of roughly 7100 bases. Upon arrival in the cytosol, the RNA becomes translated into a polyprotein that is auto catalytically and co-translationally cleaved by the viral proteinases, a protease found responsible to break up VP0 into VP2 and VP4, this is done with the help of an unknown protease [3,4].

Fig.2: structure of the rhinovirus


The main cause of rhinovirus infection is its binding to the receptor ICAM1. The structure of ICAM1 comprises of membranous protein with five immunoglobulin(Ig) like extracellular domains, a hydrophobic transmembrane domain and a short cytoplasmic domain. The binding site for the virus is located in the N-terminal domains 1 and 2. A recombinant soluble form of ICAM-1 (sICAM-1) truncated at the membrane that contains all five Ig-like domains has been shown to inhibit rhinovirus infection and induce irreversible modification of the viral capsid in vitro. After binding of rhinovirus and other picornaviruses to the receptor on the cell membrane, the viral RNA is released from the capsid (uncoating) and delivered to the cytoplasm. It has been proposed that penetration of picornaviruses into the cell involves conformational changes in the viral particle that increase the hydrophobicity of the capsid, promoting the binding of the viral capsid to the lipid bilayer and the penetration of the lipid bilayer by viral RNA. Lysosomal acidification and receptor binding have both been proposed to be important in inducing changes in the viral capsid that lead to productive infection. Human rhinovirus (HRV) infections induce epithelial cell production of chemokines that may contribute to the pathogenesis of exacerbations of chronic obstructive pulmonary disease (COPD) and asthma. Cigarette smoking is the predominant risk factor for the development of COPD and also aggravates asthma symptoms. We examined whether cigarette smoke extract (CSE) modulates viral inflammation by altering the profile of HRV-induced epithelial chemokine production. Thus, CSE differentially modulates HRV-16-induced chemokine production from human airway epithelial cells in a manner that might be expected to alter inflammatory cell profiles.


Fig.3: The figure showing the mechanism for uncoatting of the virus capseed and then the penetration of the unenveloped viruses by the process of endosome rupture or pore formation.

(A) Endosome rupture in the host cell takes place which results in the release of co-internalized fluid phase genomes in the cytosol [6].

(B) Formation of virus induced pore takes place in the endosome which leads to the release of low density mass[6].