Interaction Of Animal Viruses And Their Hosts

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Interaction of Animal Viruses and Their Hosts

Introduction

Viruses tend to be species-specific as well as cell-specific. This means that they tend to

recognize their attachment sites on the cells and different species of animals. This is through the

detection of various receptors on the cell wall surfaces of these hosts. Receptors are protein

molecules, mostly consisting of carbon and hydrogen elements, to which the viruses have an

affinity for. These receptors can be grouped into two: cellular receptors and viral receptors.

Cellular receptors are found on the host whereas the viral receptors are found on the virus. These

receptors play a major role in the infection process caused by viruses. This paper focuses on the

infection process as is caused by viruses.

Infection Process

The infection process of viruses is described as the process through which viruses attach

themselves to the host, enter into the host cells, replicate, mature, and finally leave the particular

host. This eventually leads to transmission of the infection to other hosts. This process occurs in

nine distinct steps as elaborated below.

The first step in the infection process is the attachment of the virus on to the host cell.

This happens due to the diffusion and attachment of the viral receptor to the cellular receptor.

This bond is usually mediated by cell-surface molecule(s) and viral spike proteins. For example,

HIV g120 is specific for CD4, which is principally found on the T helper cells (Domingo, et

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al. 16). The attachment of the two receptors usually occurs through non-covalent interactions. In

some instances, the phages may also attach to the pili, flagella or capsules. In animal cells, the

receptors are highly specific for a given virus. Nevertheless, some viruses may use different

molecules as receptors.

Thereafter, the viruses enter into the host cell. Various viruses use different mechanisms

of entering into the cell. Some fuse with the cell’s plasma membrane. A good example of this is

the HIVgp41 which interacts with a cellular chemokine receptor to induce fusion (Domingo, et

al. 19). Other viruses enter the cell through endocytosis. In both cases, the capsid, containing the

nucleic acid and viral enzymes, joins the cytoplasm. The tail of the phage at this juncture is

usually contractile. Following the attachment, the tail core is pushed through when the

contractile rings are compressed. The DNA is then injected into the host cell. This action is

catalyzed by lysozymes as well as 144 molecules of ATP (Wagner and Hewlett 34). It is crucial

to note that enveloped viruses enter the cell by fusing their membrane with the host membrane

while others enter by receptor-mediated endocytosis.

The next step usually involves targeting the site of viral replication. Biologically, host

DNA viruses are known to replicate in the nucleus. On the other hand, RNA viruses replicate in

the cytoplasm. In some instances, some viruses integrate their double-stranded DNA into the

host cell's chromosomes. Others copy their RNA into a double-stranded DNA, which is in turn

integrated into the host cell's genome.

The fourth stage involves the uncoating of the virus. Once the virus nucleocapsid has

been injected into the host cell, the nucleic acid has to be released. This occurs in a process

known as uncoating. The capsid is composed of protein subunits. The nucleic acids usually

dissociate from the subunits. Subsequently, the capsid disintegrates hence liberating the nucleic

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acid. It is important to note that the uncoating process is pH sensitive. This process occurs at an

optimum rate when the environmental pH is at 5-6. The pH plays a role in causing a

conformational change in the capsid proteins thus prompting the release of nucleic acids. The

nucleic acids remain associated with the internal structural proteins.

Once the uncoating process ends, replication of the nucleic acids commences. This process takes

place hand-in-hand with the synthesis of proteins. RNA viruses function as two different

molecules. Some of the RNA virus genomes serve as messenger RNA. These genomes are

known as ‘plus strand' viruses. The other RNA virus genomes act as pre-packaged, virus-

encoded RNA-dependent polymerase. This group of genomes is referred to as the ‘minus strand'

viruses. The DNA viruses encode for RNA polymerase which aids in the replication process.

Other viruses have polycistronic mRNAs which are then translated into viral polypeptides by the

cell's translational machinery.

It is in this step that the virus joins the maturation phase. In this case, the polycistronic

polypeptides are cleaved into numerous sub-units. The HIV virus serves as a good illustration for

this. HIV gp160 polypeptide is cleaved into its gp120 and gp41 mature polypeptides. Based on

this, the ARV developers incorporate HIV protease inhibitors in the drug so as to inhibit this

cleavage process (Domingo, et al. 23). It is at this stage of infection that the nucleic acids and

capsid proteins spontaneously polymerize to form a nucleocapsid.

The polymerization process eventually leads to the release of the viruses from the cell.

There are two ways in which the viruses exit the cells. The first one is through cell lysis- also

known as cell death. This leads to release of the virus into the extracellular environment. The

second mechanism is budding. This is whereby the virus exits the cell, taking part of its cell

membrane. The cell membrane, in this case, serves as a viral envelope. Various viral species

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undertake budding at different locations of the cell. It can either occur at the plasma membrane,

endoplasmic reticulum, or the Golgi apparatus. It is crucial to note that if the rate of budding

exceeds the rate of membrane synthesis, the cell dies.

The last two steps involve shedding off from the host as well as transmission to other

hosts. The viruses must leave the infected host to infect other hosts. This process can be a minor

event whereby it is exhibited by symptoms such as a terminating cold. On the other hand, the

process can be a catastrophic event involving severe symptoms. Hemorrhagic fever viruses cause

such acute symptoms (Wagner and Hewlett 37). Transmission of the virus to other hosts can

occur through the various sites of infections. These sites include the skin, eyes, mouth, nose, and

body fluids.

Conclusively, animal viruses undergo a long process before finally infecting the host.

This process starts off with the attachment of the virus to the host cell- a process mediated by

specific receptors. Thereafter, the virus enters the cell and uncoats itself. This leads to the release

of its nucleic acids. Subsequently, the replication of viral DNA commences. At the same time,

protein synthesis occurs through the translation of polycistronic mRNA. Afterwards, the virus

matures and leaves the host cell. Eventually, it leaves the host body- a process which could have

both acute and minor effects on the host. The virus is then transmitted to another host and the

process starts all over again.

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Works Cited

Domingo, Esteban, et al. Origin and Evolution of Viruses. Elsevier Academic P, 2012.

Wagner, Edward K, and Martinez J. Hewlett. Basic Virology. Blackwell Science, 2015.

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