VIRUS: The Facts

 

                             Understanding  the  Virosphere

Millions of years of evolution has caused spectacular  changes in our life,but what remains a constant is the occurrence of diseases and viruses cause most of them. In 1857 a strange contagious disease affecting up to 80 percent of the tobacco crops. In 1879 plant pathologist Adolf Mayer named it the “ Mosaic disease of tobacco”

            In 1889 Dutch microbiologist Martinus W Beijerinck’s findings say the disease agent needed growing leaves to multiply or to infect other plants when he checked newly infected leaves,he found that with fresh infections the disease agent did not lose its disease- causing power.His conclusion was:the agent could grow on leaves but could not reproduce without them. He named this agent “Contagious vivum fluidum” or contagious living fluid. He also gave it a nickname,Viruses. Thus tobacco mosaic became the first virus to be discovered.

           The world of viruses is dense and vast. Its diversity is greater than the world that we know and interect in. Viruses are omnipresent,found in air,land,sea to every species to even in every body parts. Virus disrupts cell function in its desperation to replicate. This makes us sick. In response to infection the immune system springs into action white blood cells,antibodies and other mechanisms go on an overdrive to rid the body of the foreign invader. These cause fever,rash,headach and fatigue.

             A disease occurs when the immune system loses ground to the viruses and the later manages to establish itself in the cells for replication. The replication process typically begins when a virus infects its host by attaching to the host cell and penetrating the cell wall or membrane.

              The virus genome is then uncoated from the protein and hijacks the host cell’s machinery,forcing it to replicate the viral genome and produce viral proteins to make new capsids. The new viruses then burst out of the host cell during a process called lysis,which kills the host cell. Some viruses take a portion of the host’s membrane during the lysis process to form an envelope around the caspid. Following viral replication the new viruses then go on to infect new hosts.

              Most of the time body’s immune system is capable enough to get rid of viruses. Problem arises when the virus attacks the immune system to gain access to a cell and takes control over it . These are the ones capable of causing outbreaks and sometimes pandemics.

Viruses are microscopic parasites, generally much smaller than bacteria.They lack the capacity to thrive and reproduce outside of a host body.

            When a virus is completely assembled and capable of infection, it is known as a virion. According to the authors of “Medical Microbiology 4th Ed.” (University of Texas Medical Branch at Galveston, 1996), the structure of a simple virion comprises of an inner nucleic acid core surrounded by an outer casing of proteins known as the capsid. Capsids protect viral nucleic acids from being chewed up and destroyed by special host cell enzymes called nucleases. Some viruses have a second protective layer known as the envelope. This layer is usually derived from the cell membrane of a host; little stolen bits that are modified and repurposed for the virus to use.

              The DNA or RNA found in the core of the virus can be single stranded or double stranded. It constitutes the genome or the sum total of a virus’s genetic information. Viral genomes are generally small in size, coding only for essential proteins such as capsid proteins, enzymes, and proteins necessary for replication within a host cell.

 

                  The primary role of the virus or virion is to “deliver its DNA or RNA genome into the host cell so that the genome can be expressed (transcribed and translated) by the host cell,” according to "Medical Microbiology." 

                  First, viruses need to access the inside of a host’s body. Respiratory passages and open wounds can act as gateways for viruses. Sometimes insects provide the mode of entry. Certain viruses will hitch a ride in an insect’s saliva and enter the host’s body after the insect bites. According to the authors of “Molecular Biology of the Cell, 4th Ed” (Garland Science, 2002) such viruses can replicate inside both insect and host cells, ensuring a smooth transition from one to the other. Examples include the viruses that cause yellow fever and dengue fever. 

              Viruses will then attach themselves to host cell surfaces. They do so by recognizing and binding to cell surface receptors, like two interlocking puzzle pieces. Many different viruses can bind to the same receptor and a single virus can bind different cell surface receptors. While viruses use them to their advantage, cell surface receptors are actually designed to serve the cell. 

                            After a virus binds to the surface of the host cell, it can start to move across the outer covering or membrane of the host cell. There are many different modes of entry. HIV, a virus with an envelope, fuses with the membrane and is pushed through. Another enveloped virus, the influenza virus, is engulfed by the cell. Some non-enveloped viruses, such as the polio virus, create a porous channel of entry and burrow through the membrane.

           Once inside, viruses release their genomes and also disrupt or hijack various parts of the cellular machinery. Viral genomes direct host cells to ultimately produce viral proteins (many a time halting the synthesis of any RNA and proteins that the host cell can use). Ultimately, viruses stack the deck in their favor, both inside the host cell and within the host itself by creating conditions that allow for them to spread. For example, when suffering from the common cold, one sneeze emits 20,000 droplets containing rhinovirus or coronavirus particles, according to "Molecular Biology of the Cell." Touching or breathing those droplets in, is all it takes for a cold to spread.

                                  The recent emergence of the novel coronavirus behind the COVID-19 pandemic throws a spotlight on the risks animals can pose to humans as the source of new viruses. The virus in question, known as SARS-CoV-2, was linked to a “wet market” for wild animal trade in Wuhan, China, although it’s by no means certain this was the source of the human version of the virus. Bats were identified as the animal with the closest known equivalent virus although, again, we’re not sure that a bat provided the direct origin of SARS-CoV-2.

                   So how do new viruses actually emerge from the environment and start infecting humans? Every virus has a unique origin in terms of its timing and mechanism, but there are some general facts that are true for all species of emerging virus.

                   The first thing to know is that it is rare for viruses to jump between species. In order for a virus to successfully jump into a new species of host, it must be able to do several things.

First, it must be able to establish an infection in the new host by replicating itself there. This is not a given, as many viruses can only infect specific types of cells, such as lung cells or kidney cells. When attacking a cell, a virus binds to specific receptor molecules on the cell’s surface and so may not be able to bind to other types of cell. Or the virus may simply be unable to replicate inside the cell for whatever reason.

Once it has infected a new host, the virus must also be able to replicate itself enough to infect others and transmit itself to them. This, again, is very rare and most virus jumps will result in what we call “dead-end hosts” from which the virus cannot transmit itself and eventually dies.

For example, the influenza virus H5N1, or ‘bird flu’ can infect humans from birds, but has very limited transmission between humans. Occasionally, this barrier is overcome, and the emerging virus is able to jump to a new host, establishing a new transmission chain and a novel outbreak.

                        From research over the past few decades, we understand some of the mechanisms that contribute to virus jumps between species. Influenza virus is a classic example. The virus contains eight genome segments and if two different viruses infect the same cell, segments from both can mix to create a novel virus species. If the proteins on the surface of the new virus have significantly changed from currently circulating influenza virus strains, then no one will have immunity and the new virus can easily spread.

             This shift in the influenza virus is called antigenic shift. This is what we think happened with the 2009 H1N1 influenza epidemic, with the shift occurring in pigs and then jumping to humans to start the outbreak. There is also genetic evidence that this mechanism can occur in coronaviruses, although its role in the emergence of SARS-CoV-2 remains to be determined.

New viruses can also emerge through genetic mutations within the virus genome, which are more common among viruses that, instead of deoxyribonucleic acid (DNA), store their genetic information in the similar molecule Ribonucleic acid (RNA). This is because these viruses (with the exception of coronaviruses) lack a way to check for mistakes when they replicate. Most of the mutations produced during replication will be damaging to the virus but some will enable it to infect a new host more effectively.

                                                  New coronavirus

So what do we think happened in the case of SARS-CoV-2? Recent analysis of the genome suggest that the virus had been circulating in a very similar form to today for approximately 40 years. The closest relative of the virus that we can identify is one found in bats. However, this virus and SARS-CoV-2 probably shared a common ancestor approximately 40-70 years ago, and so this bat virus is not the cause of the outbreak.

Although these viruses share a common ancestor, 40 years of evolution since then has separated them. This means that SARS-CoV-2 may have jumped to humans from bats, or it may have come via an intermediate species. Closely related viruses have been found in pangolins, for example. But the exact path of the genetically distinct SARS-CoV-2 will remain a mystery until we are able to find closer relative species in the environment.

It is also unclear what changed in the virus to allow it to infect humans so easily. However, given that three major diseases have emerged from the coronavirus family in the last 20 years – Severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and COVID-19 – it is likely that this will not be the last time a coronavirus jumps into humans and causes a new disease outbreak.

What makes this more likely is that while they circulate in all animals in the world, viruses are only able to jump to humans when they have an opportunity from contact between us and other animals. Humans have always come into contact with new viruses as they have explored new areas and spread across the globe. But increased human activity in wild areas and the trade in wild animals creates a perfect breeding ground.

This is also compounded by our global connectedness, which enables a new disease to spread around the world in days. We must accept some responsibility for these emergence events as we continue to disturb natural environments and increase the likelihood of viruses jumping into humans.

The fact that the host range — the group of cell types that a virus can infect — is generally restricted serves as a basis for classifying viruses. A virus that infects only bacteria is called a bacteriophage, or simply a phage. Viruses that infect animal or plant cells are referred to generally as animal viruses or plant viruses. A few viruses can grow in both plants and the insects that feed on them. The highly mobile insects serve as vectors for transferring such viruses between susceptible plant hosts. An example is potato yellow dwarf virus, which can grow in leafhoppers (insects that feed on potato plant leaves) as well as in potato plants. Wide host ranges are characteristic of some strictly animal viruses, such as vesicular stomatitis virus, which grows in insects and in many different types of mammalian cells. Most animal viruses, however, do not cross phyla, and some (e.g., poliovirus) infect only closely related species such as primates. The host-cell range of some animal viruses is further restricted to a limited number of cell types because only these cells have appropriate surface receptors to which the virions can attach.