GENERAL CHARCTERISTICS  Viruses come in an amazing variety of shapes and sizes.  They are very small and are measured in nanometers, which is one-billionth of a meter. Viruses can range in the size between 20 to 750nm, which is 45,000 times smaller than the width of a human hair.  The majority of viruses cannot be seen with a light microscope because the resolution of a light microscope is limited to about 200nm, so a scanning electron microscope is required to view most viruses.  The basic structure of a virus is made up of a genetic information molecule and a  protein layer that protects that information molecule.  The arrangement of the protein layer and the genetic information comes in a variety of presentations.  The core of the virus is made up of nucleic acids, which then make up the genetic information in the form of RNA or DNA.  The protein layer that surrounds and protects the nucleic acids is called the capsid.  When a single virus is in its complete form, it is known as a virion.  A virus structure can be one of the following: icosahedral, enveloped, complex or helical.  They have no cellular structure.  They have no metabolic systems of their own, but depend on the synthetic mechanism of a living host cell.

A mature virus particle is also known as a virion. It consists of either two or three basic components: — A genome of DNA or RNA, double-stranded or single-stranded, linear or circular, and in some cases segmented. A single-stranded nucleic acid can have plus or minus polarity. — The capsid, virus-coded proteins enclosing the nucleic acid of the virus and determining its antigenicity; the capsid can have a cubic (rotational), helical or complex symmetry and is made up of subunits called capsomers. — In some cases an envelope that surrounds the capsid and is always derived from cellular membranes. Other Components of Viral Particles Various enzymes. Viruses require a number of different enzymes depending on genome type and mode of infection. In several virus species enzymes are a component of the virus particle, for example the neuraminidase required for invasion and release of myxoviruses Hemagglutinin. Some viruses are capable of agglutinating various different human or animal erythrocytes.

Cubic symmetry (rotational symmetry). Viruses with rotational symmetry are icosahedrons (polyhedrons with 20 equilateral triangular faces). The number of capsomers per virion varies from 32 to 252 and depends on the number of capsomers. Helical symmetry: Helical symmetry is present when one axis of a capsid is longer than the other. Complex symmetry. Complex structural patterns are found in bacteriophages and the smallpox virus.T bacteriophages, for example, have an icosahedral head containing the DNA and a tubelike tail through which the DNA is injected into the host cell.

Envelope This virus structure is a conventional icosahedral or helical structure that is surrounded by a lipid bilayer membrane, meaning the virus is encased or enveloped. The envelope of the virus is formed when the virus is exiting the cell via budding, and the infectivity of these viruses is mostly dependent on the envelope. The most well known examples of enveloped viruses are the influenza virus, Hepatitis C and HIV.

Complex These virus structures have a combination of icosahedral and helical shape and may have a complex outer wall or head-tail morphology. The head-tail morphology structure is unique to viruses that only infect bacteria and are known as bacteriophages. Bacteriophage

Helical This virus structure has a capsid with a central cavity or hollow tube that is made by proteins arranged in a circular fashion, creating a disc like shape. The disc shapes are attached helically (like a toy slinky) creating a tube with room for the nucleic acid in the middle. All filamentous viruses are helical in shape. They are usually 15-19nm wide and range in length from 300 to 500nm depending on the genome size. An example of a virus with a helical symmetry is the tobacco mosaic virus.

 In order to survive, viruses must be able to do the following: ◦ 1. Find a host cell it can replicate in ◦ 2. Bind to that cell ◦ 3. Enter the cell ◦ 4. Release its genome in order to replicate ◦ 5. Replicate its genome ◦ 6. Transcribe and translate its viral proteins ◦ 7. Package its genome and proteins ◦ 8. Escape from the cell

The steps in viral replication are as follows:  — Adsorption of the virus to specific receptors on the cell surface.  — Penetration by the virus and intracellular release of nucleic acid.  — Proliferation of the viral components: virus-coded synthesis of capsid and non-capsid proteins, replication of nucleic acid by viral and cellular enzymes.  — Assembly of replicated nucleic acid and new capsid protein.  — Release of virus progeny from the cell.

 For each virus, there is a unique life cycle but all viruses accomplish the same steps in order to survive

 Semliki Forest Virus is an enveloped Alphavirus  It has 2 transmembrane proteins (E1 and E2) in its envelope  The virus binds to the cellular receptor, endocytosed, and fuses with the endosome membrane to release its nucleocapsid for replication

 Poliovirus is a non enveloped  It differs from SFV in that when it binds to its cellular receptor, it goes through a conformational change.  This conformational change may facilitate the release of genome into the cell for replication  Also releases from the cell by lysis instead of budding

 The first step in viral replication is to be able to bind to the correct host cell.  Virus recognize host cells by certain receptors.  Bind to these receptors through specific interactions.  Binding sites on viruses are typically conserved to ensure survival

1-Adsorption. Virus particles can only infect cells possessing surface “receptors” specific to the particular virus species. It is therefore the receptors on a cell that determine whether it can be infected by a certain virus. 1-a Receptors Some aspects of the nature of the receptors are known. These are molecules that play important roles in the life of the cell or intercellular communication: For examples: Molecules of the immunoglobulin superfamily (CD4: receptor for HIV; ICAM-1: receptor for rhinoviruses), the complement (C3) receptor that is also the receptor for the Epstein-Barr virus.

 The genome of the virus is released in order to make viral proteins and reproduce the genome.  Viruses can employ several strategies to do this: injection, release into the cytoplasm, release into the nucleus  Exception: Reoviruses

3-Replication of the nucleic acid. 1. DNA viruses: the replication of viral DNA takes place in the cell nucleus (exception: poxviruses). Some viruses (e.g., herpesviruses) possess replicases of their own. The smaller DNA viruses (e.g., polyomaviruses), code for polypeptides that modify the cellular polymerases in such a way that mainly viral DNA sequences are replicated. 2. RNA viruses: since eukaryotic cells possess no enzymes for RNA replication, the virus must supply the RNA-dependent RNA polymerase(s) (“replicase”). These enzymes are thus in any case virus-coded proteins, and in some cases are actually components of the virus particle.

4-Viral maturation (morphogenesis). In this step, the viral capsid proteins and genomes (present in multiple copies after the replication process) are assembled into new, infectious virus particles. 5-Release. The release of viral progeny in some cases correlates closely with viral maturation, whereby envelopes or components of them are acquired when the particles “bud off” of the cytoplasmic membrane and are expelled from the cell In nonenveloped viruses, release of viral progeny is realized either by means of lysis of the infected cell or more or less continuous exocytosis of the viral particles.

Possible consequences of viral infection for the host cell:  Cytocidal infection (necrosis): viral replication results directly in cell destruction (cytopathology, so-called “cytopathic effect” in cell cultures).  Apoptosis: the virus initiates a cascade of cellular events leading to cell death (“suicide”), in most cases interrupting the viral replication cycle.  Noncytocidal infection: viral replication does not destroy the host cell, although it may be destroyed by secondary immunological reactions.  Latent infection: the viral genome is inside the cell, resulting in neither viral replication nor cell destruction.  Tumor transformation: the viral infection transforms the host cell into a cancer cell, whereby viral replication may or may not take place depending on the virus and/or cell type involved.