viruses and human disease

Examples of common human diseases caused by viruses include the common cold, influenza, chickenpox and cold sores. Many serious diseases such as ebola, AIDS, avian influenza and SARS are caused by viruses. The relative ability of viruses to cause disease is described in terms of virulence. Other diseases are under investigation as to whether they too have a virus as the causative agent, such as the possible connection between human herpes virus six (HHV6) and neurological diseases such as multiple sclerosis and chronic fatigue syndrome.There is controversy over whether the borna virus, previously thought to cause neurological diseases in horses, could be responsible for psychiatric illnesses in humans.

Viruses have different mechanisms by which they produce disease in an organism, which largely depends on the viral species. Mechanisms at the cellular level primarily include cell lysis, the breaking open and subsequent death of the cell. In multicellular organisms, if enough cells die the whole organism will start to suffer the effects. Although viruses cause disruption of healthy homeostasis, resulting in disease, they may exist relatively harmlessly within an organism. An example would include the ability of the herpes simplex virus, which causes cold sores, to remain in a dormant state within the human body. This is called latencyand is a characteristic of the herpes viruses including Epstein-Barr virus, which causes glandular fever, and varicella zoster virus, which causes chickenpox and shingles. Most people have been infected with at least one of these types of herpes virus.However, these latent viruses might sometimes be beneficial, as the presence of the virus can increase immunity against bacterial pathogens, such as Yersinia pestis.

Some viruses can cause life-long or chronic infections, where the viruses continue to replicate in the body despite the host's defence mechanisms. This is common in hepatitis B virus and hepatitis C virus infections. People chronically infected are known as carriers, as they serve as reservoirs of infectious virus. In populations with a high proportion of carriers, the disease is said to be endemic.

economic importance of viruses

Virotherapy is an experimental form of cancer treatment using biotechnology to convert viruses into cancer-fighting agents by reprogramming viruses to attack cancerous cells, while healthy cells remained relatively undamaged. Usually the viruses used are herpes simplex virus or Adenoviruses.

It uses viruses as treatment against various diseases, most commonly as a vector used to specifically target cells and DNA in particular. It is not a new idea - as early as the 1950s doctors were noticing that cancer patients who suffered a non-related viral infection, or who had been vaccinated recently, showed signs of improvement[citation needed]: this has been largely attributed to the production of interferon and tumour necrosis factors in response to viral infection, but oncolytic viruses are being designed that selectively target and lyse only cancerous cells.

In the 1940s and 1950s, studies were conducted in animal models to evaluate the use of viruses in the treatment of tumors. In 1956 some of the earliest human clinical trials with oncolytic viruses for the treatment of advanced-stage cervical cancer were started[citation needed]. However, for several years research in this field was delayed due to the inadequate technology available. Research has now started to move forward more quickly in finding ways to use viruses therapeutically.

Life cycle of viruses

As stated above, the viral life cycle is dependent on a host cell. A virus is unable to replicate on its own or use "raw" materials on which to survive. Hence a virus will remain dormant until it is able to infect the next host, activate and replicate. Some viruses can live in an open environment for a short time, in some cases, only a few hours. Therefore, viruses use the most efficient method to locate a host, create progeny, and spread to other hosts.and virus are host specific

Exposure of host

Usually viral infection occurs when a virus enters the host, either:

• through a physical breach (a cut in the skin)
• direct inoculation (e.g.mosquito bite)
• direct infection of the surface itself (inhalation of the virus into trachea)

It is usually only after a virus enters a host that it can gain access to possible susceptible cells.

Viral Entry

Main article: Viral entry

In order for the virus to reproduce and thereby establish infection, it must enter cells of the host organism and use those cells' materials. In order to enter the cells, proteins found on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where viral reproduction may commence.

Viral replication

Main article: Viral replication

Next, a virus must take control of the host cell's replication mechanisms. It is at this stage a distinction between susceptibility and permissibility of a host cell is made. Permissibility determines the outcome of the infection. After control is established and the environment is set for the virus to begin making copies of itself, replication occurs quickly.

Viral shedding

Main article: Viral shedding

After a virus has made many copies of itself, it usually has exhausted the cell of its resources. The host cell is now no longer useful to the virus, therefore the cell often dies and the newly produced viruses must find a new host. The process by which virus progeny are released to find new hosts, is called shedding. This is the final stage in the viral life cycle.

Viral latency

Main article: Viral latency

Some viruses can "hide" within another cell, either to evade the host cell defenses or immune system, or simply because it is not in the best interest of the virus to continually replicate. This hiding is deemed latency. During this time, the virus will not produce any progeny, it will remain inactive until external stimuli (such as light or stress) prompts it into activation.

transmission of viruses in plant

Through sap

Viruses can be spread by direct transfer of sap by contact of a wounded plant with a healthy one. Such contact may occur during agricultural practices, as by damage caused by tools or hands, or naturally, as by an animal feeding on the plant.

Insects

Plant viruses need to be transmitted by a vector, most often insects such as leafhoppers. One class of viruses, the Rhabdoviridae, has been proposed to actually be insect viruses that have evolved to replicate in plants. The chosen insect vector of a plant virus will often be the determining factor in that virus's host range: it can only infect plants that the insect vector feeds upon.

Nematodes

Soil-borne nematodes also have been shown to transmit viruses^{[citation needed]}. They acquire and transmit them by feeding on infected roots. Viruses can be transmitted both non-persistently and persistently, but there is no evidence of viruses being able to replicate in nematodes

Plasmodiophorids

A number of virus genera are transmitted, both persistently and non-persistently, by soil borne zoosporic protozoa. These protozoa are not phytopathogenic themselves, but parasitic. Transmission of the virus takes place when they become associated with the plant roots. Examples include Polymyxa graminis, which has been shown to transmit plant viral diseases in cereal crops

Seed and pollen borne viruses

Plant virus transmission from generation to generation occurs in about 20% of plant viruses. When viruses are transmitted by seeds, the seed is infected in the generative cells and the virus is maintained in the germ cells and sometimes, but less often, in the seed coat

Direct plant-to-human transmission

Researchers from the University of the Mediterranean in Marseille, France have found evidence that suggest a virus common to peppers (the Pepper Mild Mottle Virus) may have moved on to infect humans.^[7] This is a very rare and highly unlikely event, as in order to enter a cell and replicate a virus must "bind to a receptor on its surface, and a plant virus would be highly unlikely to recognize a receptor on a human cell. One possibility is that the virus does not infect human cells directly. Instead, the naked viral RNA may alter the function of the cells through a mechanism similar to RNA interference, in which the presence of certain RNA sequences can turn genes on and off", according to Virologist Robert Garry from the Tulane University in New Orleans, Louisiana.

composition of viruses

Viruses are unique from all other life forms in that they can contain ONLY ONE FORM OF NUCLEIC ACID. Some viruses use RNA as their genetic material and other use DNA, but NEVER do they contain both. Further, this nucleic acid polymer may either exist as DOUBLE STRANDED (DS) DNA or RNA or as SINGLE STRANDED (SS) DNA or RNA. Each of these characteristics is a constant for a particular virus and is part of it description. The nucleic acid polymer may contain as few as 4 to 7 genes for very small viruses to 150 to 200 genes for very large viruses. In some viruses the nucleic acid exists in more that one molecule. Some viruses contain a few enzymes and some contain none, but no viruses contain the large numbers of enzymes found even in the smallest bacteriaAll viruses are covered with a PROTEIN COAT. This protein coat is mainly composed of a FEW TYPES of proteins of which there are many copies per virus; something like the individual threads in a shirt. These identical protein subunits are called CAPSOMERES and they are made so that they spontaneously come together (ASSEMBLE) in a PREDETERMINED way to produce the virus coat which is called the CAPSID.
If a virus has ONLY a protein capsid covering it, it is termed a NAKED CAPSID VIRUS or a NAKED VIRUS. However, some viruses pick up a lipid membrane from the host cell when it is released, that surrounds the capsid. The lipid membrane is called an ENVELOPE and such viruses are termed ENVELOPED VIRUSES. All virus contain one more important proteins type; this is ATTACHMENT PROTEIN or #docking proteins. The attachment protein is needed by the virus to ATTACH TO ITS TARGET CELL before it can enter that cell. Obviously this attachment protein must lie on the outer surface of the virus so that it is available to contact the appropriate RECEPTOR SITES on the target host cells. These attachment proteins are often called SPIKES because they can extend away from the cell so as to better be able to contact the host receptor (think of the viral AP & the host receptor site as being the pairs of a VELCRO SYSTEM). In addition, virus may contain small quantities of carbohydrate (glycoprotein).

classification of viruses

Viruses have been traditionally named by adding the word 'virus' after the disease caused in the major host, e.g. poliovirus, the causative agent of poliomyelitis.

Bacteriophages were named after laboratory code symbols e,g. φX174, P22, T7 etc.

Holmes (1948) followed the Linnaen system of binomial nomenclature. Viruses were grouped under the order Virales, which was divided into three suborders:

Phaginae - infecting bacteria.
Phytophaginae - infecting plants.
Zoophaginae - infecting animals.

Classification of Virus by Casjens and King

The Major groups of virus according to the type of nucleic acid, symmetry presence or absence of an envelope and site of assembly.

I.ssRNA VIRUSES
(A) HELICAL
a.Rigid rods :
Tobacco mosaic virus
Barely stripe mosaic virus
Tobacco rattle virus

b. Flexous rods :
Potato X and Y viruses
Clover yellow mosaic virus.

(B) ICOSAHEDRAL
a.Spherical plant viruses
(i) With 180 identical capsomers (T=3)
Cowpoa chlorotic mosaic virus
Cumumber mosaic virus
Turnip yellow moasic virus

(ii)With 60 subunits of 2 structural proteins (T=1) :
Cowpa moasic virus

b. Bacteriophages : R17, fr, f2, MS2,Q

c. Picornaviruses : (animal) -4 sub groups
(i) Human enteroviruses.Poliovirus, coxsackie and ECHO viruses
(ii) Rodent cardioviruses.Encephalomyocaritis virus, Mouse Elberfield virus, Mengovirus
(iii) Rhinoviruses. : Human respiratory infection
(iv) Foot - and mouth disease virus.

(C) ENVELOPED
(i) Spherical : Togavirus -Yellow fever
(ii) Bullet Shaped :Rhabdovirus - rabies
(iii) Spherical or filamentous : Paramyxovirus -measles Myxovirus - influenza
(iv) spherical : Coronavirus -actute upper respiratory tract infections
 

Structure of viruses

1. Size. The size range of viruses is from about 20 to 300 nm. On the whole, viruses are much smaller than bacteria. Most animal viruses and all plant viruses and phages are invisible under the light microscope.

2. Simple structure. Viruses have very simple structures. The simplest viruses are nucleoprotein particles consisting of genetic material (DNA or RNA) surrounded by a protein capsid. In this respect they differ from typical cells which arc made up) of proteins, carbohydrates, lipids and nuc1eicacids.

The more complex viruses contain lipids and carbohydrates in addition to proteins and nucleic acids, e. g. the enveloped viruses.

These viruses are surrounded by a membranous envelope which is derived from the host cell. It protects the virus and also serves for transmission from one host to another. The envelope consists of a lipid bilayer and proteins with special functions.

The membrane proteins are of two types, glycoproteins and matrix: proteins. Glycoproteins have a hydrophobic end fixed in the lipid bilayer and a hydrophilic glycosylated end which protrudes into the medium.

The spikes on the outer surface of the virions consist of glycoproteins. In the orthomyxoviruses, paramyxoviruses and rhabdoviruses, there is an unglycosylated matrix protein layer on the inner surface of the envelope. This layer appears to connect the envelope with the capsid.

The envelope and capsid proteins are specified by viral genes. The lipid and carbohydrate of the glycoprotein are derived from the host cell. Since some viruses can be grown in different cell types, they often have different lipid and carbohydrate moieties.

The surface of the virion may therefore contain polysaccharide-determined cellular antigens. The Pseudomonas phage 96 has a lipid envelope, of which the lipid bilayer appears to be assembled de novo, and is not budded from the membranes.