Influenza Virus Life Cycle

When we hear the word virus, we usually think of something that makes us sick. A virus is an ultramicroscopic infectious organism that, having no independent metabolic activity, can replicate only within a cell of another host organism. A virus consists of a core of nucleic acid, either RNA or DNA, surrounded by a coating of antigenic protein and sometimes a lipid layer surrounds it as well. The viral genome provides the genetic code for replication, and the host cell provides the necessary energy and raw materials. To fight viruses, we use vaccines. While some may infect a broad range, other viruses can only infect certain kinds of cells. Vaccines are made of inactive, dead or weakened virus cells or protein antigens that can no longer infect

Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.

RSV enters a cell through fusion at the plasma membrane. Initiation emerges when the G protein of the RSV binds to a specific long unbranched polysaccharide of the

On encountering a host cell, the retrovirus attaches itself to receptors on the surface of the host cell’s membrane. Once inside the cell, the capsid opens, releasing RNA and reverse transcriptase into the cell’s cytoplasm.

The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.

The SH (small hydrophobic) protein, matrix protein (M), and the M2 protein are envelope-associated proteins that are not involved in viral attachment or syncytium formation (3). Other proteins such as the nucleoprotein (N), phosphoprotein (P), and the large nucleoprotein (L) are in the nucleocapsid. NS-1 and NS-2 are non-structure protein that is only found in the infected cells but not present in virions (3).

Our project revolved around two major ideas, the first idea that detected the expression of the Hemagglutinin glycoprotein of Measles virus (MV-H) on the surface of helper virus (Vesicular Stomatitis Virus) in our tissue culture. The second idea that identified the effect of Axl antibodies on the penetration processes of VSV-ΔG-MV-H virus The manner of this project represented in three major stages, the first stage that generated the VSV-ΔG-MV-H pseudovirion. This stage required to remove the VSV G glycoprotein gene from VSV and replace with gene for the green fluorescent in helper virus, however, this process was more complex so we skipped this step. The next step that was extraction the plasmid from the bacteria by following a specific protocol and then started working with PEI Transfection.

The virus starts by getting a host cell and either uses it right away then kills it or kills right away usually they use it first. When the virus invades a body, It collides with the cell that spicks and propherances then they brush against each other and it if they fit together become one. The viruses is also able to hide from the immune system therefore avoiding being killed so it can reproduce. Then the virus gains control of a cell by injecting its genes into the cell and makes it do whatever it wants for the benefits of the virus not the cell. Of course while you have a cell doing the dirty work for you. The viruses make is own offspring/ copies of itself and takes of over and invading surrounding cells.

Some viruses also have an outer bag of lipo-protein called an envelope. After a virus attaches to a living cell, it either enters the cell to release the genetic information, or, the virus injects the information through the cells outer lining. Thus changing the cells natural functions and forcing the cell to spend its energy to create copies of the virus. The cell will go on making copies of the virus until the cell is used up and dies. The virus then leaves the dead cell and invades a nearby cell and the process starts all over. There are five types of human herpes virus: Varicella zoster which causes chickenpox, Epstein Barr virus which causes infectious mononucleosis, cytomegalovirus which can cause cytomegalic inclusion disease in infants, and herpes simplex viruses 1 and 2.

(Silverstein: 13) There are three types of influenza, depending on their activity: type A, which is usually the cause of outbreaks; type B, which is linked to sporadic cases, and type C, which rarely causes disease reactions. (Silverstein: 54) The virus which causes influenza enters the host through the respiratory tract, and binds itself to epithelial cells. The virus causes the cell to engulf it by endocytosis, and then fuses to the wall of the endocytic vesicle, injecting the contents of the virus into the cytosol of the cell. The RNA of the virus enter the nucleus of the cell, and spur the creation of new copies of the genes. These genes, as well as new viral proteins that are created in the cell, leave the cell as fresh viruses, budding off the plasma membrane of the cell.

Influenza is an acute condition that results in high fever, a dry cough and sore throat, body aches, headache, runny nose and malaise upon contracting the influenza virus (1). These symptoms often progress into more severe conditions and in certain populations; infection with influenza can lead to death. The influenza virus is an RNA virus that belongs to the family orthomyxoviridae. There are three types of influenza virus and they are classified as type A, type B and type C (2).

Once tightly bound the virus is endocytosed via coated vesicles. The virus is transported into late endosomes which acidify their content and hence induce conformational rearrangement of HA exposing the fusiogenic peptide sequence. The loop region of the HA becomes a coiled coil that mediates membrane fusion. The release of viral genome into the cytoplasm also requires protons that are pumped from the acidic endosome into the virion interior via the matrix protein M2 that acts as a proton channel. Viral RNA dissociates from M1 and is then imported in an ATP-dependent manner into the nucleus for transcription and translation. In humans, the replication of the influenza virus is usually restricted to the airways epithelial cells due to the limited expression of a serine protease, produced by nonciliated bronchial epithelial cells and which cleaves the HA precursor in HA1 and HA2 polypeptides, rendering the virions infectious. Replication and virions production occurs within hours after virus entry. The viral ribonucleoprotein (vRNP) complexes are released from the endosomes into the cytoplasm and subsequently transported to the nucleus, where replication and transcription take

Structure: The influenza virus looks like a sphere covered with spike like proteins for grip ready to latch on to a healthy human cell. “The H spike (hem agglutinin) and the N spike (neuraminidase) are called proteins and exist in the envelope and they are used for antigenic typing” (Pearson 2004). These proteins allow the virus to enter and exit the host (our cells). Once the virus is inside the cell, the virus can begin reproducing. Soon, each infected cell is filled with thousands of new viruses, each of them looking to leave the cell to find a new home in another cell and begin reproducing there.

With this being a mutation of the influenza virus it has an envelope this makes it easier for the virus to infect the cell. It does attaches its envelope to the cell to makes the cell think that is part of it so it lets the virus in. The virus is then disassembled the RNA (ribonucleic acid) becomes available for transcription. The host cell then takes the RNA and uses it for transcription making it TRNA (Transcription ribonucleic acid). Which the nucleus then uses to manufacture the virus proteins and viral RNA and other proteins for binding the outer layer of the cell to the virus. This then lets the virus have an envelope the cell manufacters so many viruses that essentially the cell explodes shooting the virus into nearby cells to restart the process. this would cause a virulence issue as the virulence would be around 65% cell death if infected as some cells would explode, others would slowly seep the virus out of

The protective capsid helps the virus escape detection and destruction during the invasion of the host. When the virus reaches the target cell, biochemical reactions between the capsid and cell wall allow the virus to latch on and inject its genome into the cell’s interior. Once inside, the viral genetic material insinuates itself into the host’s DNA or RNA. In an efficient feat of natural bioengineering, the host cell’s genetic machinery now does the rest of the work for the virus. The cell, which had already been making copies of its own genome, now also replicates that of the virus. Coded within the viral material is the blueprint for making more copies of the viral genome. Further instructions command the production of capsids and directions for assembly of new viruses. After the host cell becomes engorged with viruses, it explodes, sending the new