Viruses Essay Example

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Author/ Procedia Economics and Finance 00 (2012) 000–000 11

Discussion on the generic mechanism of action of viruses


virus implantation at the site of entry, spread to sites of portal exit, spread to disease sites and local replication. The circulation system plays a greater role in spreading the virus from point of entry to the target organ as well as the neural system. Viral incubation period is estimated to often take 1-3 days while in other cases it might be lengthy. Incubation period extends from the period between virus exposures to the disease onset stage. Virus pathogenesis has gotten attention to many microbiologists and health experts. The virus is always active when inside an organism (host). This is so because virus depends on the host for energy, nutrition and environment for multiplication. On entering the body, the immune system of the host will always fight back. However, since virus has various adaptive mechanisms in most cases it multiplies faster causing disease and eventually cell death. The process of virus pathogenesis entails;

Keywaords: virus, virus pathogenesis, target organ, host, virus replication

    1. Introduction

The immune system is a combination of complex interwoven network of tissues build from various cells, and organs working as a single unit to protect the body from foreign invaders. The invaders basically are tiny microbes’ fungi, parasites, virus and bacteria that causes infection. The human body is an ideal host for many microbes and thus, microorganisms will always fight to enter into it. Consequently, the immune system will react against the foreigners to deter the microbes from invading and destroy such microbes. Unfortunately, in some cases, the immune system is overwhelmed by its duty or hits the wrong target, and a disease from the microbe is presented within the body (NIAID, 2003). This research, however, will look into the viral pathogenesis mechanism in general. According to Racaniello, (2009), viral pathogenesis refers to the whole process that the viruses is involved resulting to an infection. Wong, (n.d.) adds that viral diseases can be termed as the sequential effects of reaction that are realized in the virus and the host following the microbe replication and the counter action from the immune response (Figure 1). Common interest in viral pathogenesis are triggered by the need to eliminate or treat viral diseases affecting humans. Partly this objective is attained by identifying host genes and the viral genes that trigger disease production (Racaniello, 2009).


Figure 1: A typical acute infection pathway (Medawar, n.d.)


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1.2. Virus structure

Referred to as parasitic biologic entities, virus require the host cell in order to replicate. Virus are made of double or single stranded DNA or RNA and have a protein capsid forming the virion structure. In some cases, some virus have modified lipid envelop as a result of its interaction with the host cell membrane (“Chapter 33 Virus,” 2006). Virus are termed as ubiquitous as they can infect any cell type like fungi, archae, bacteria, and eukaryotes and can exist in varied ecosystem. Although, over the history many viruses within the human population have been identified, in reference to their direct pathogenic effects there exit a broad categories of virus that causes no disease to humans. Most identified viruses are bacteriophage unlike the eukaryotic viruses.

1.3. Viral entry

Infection occurring in host follows six related components. First there should be the etiologic agent (in this case a virus), the reservoir where the agent multiplies, portal of exit (the escape route of the etiologic agent from the reservoir), transmission mode, portal of entry and presence of susceptible hosts. For a virus to successfully infect an individual host, three main factors should be in place:

  • The host anti-viral defense systems of the local host should be initially ineffective or absent

  • At the target site, the cells should be permissive, susceptible and accessible by the virus

  • The virus should be quantitatively sufficient to initiate infection.

In order to cause infection to the host, the virus must enter the cells via the surface of the body. The common entry points within the target host are: the skin, the cornea or conjunctival membranes of the eye, the urogenital tracts, alimentary canal, and the respiratory tracts mucosal lining (Racaniello, 2009).

1.4. Pathogenic mechanisms of a virus

The process by which viral infection causes disease vary. These processes are: virus implantation at the site of entry, spread to sites of portal exit, spread to disease sites and local replication. Various factors also affect pathogenic mechanisms such as susceptibility of virus to host defense, susceptibility of cell to virus multiplication and virus accessibility to tissue (Nekhai, 2012).

1.4.1. Cellular pathogenesis

The infecting virus may alter the cellular macromolecular synthesis in a cell leading to direct cell damage and or death. Virus remain active within the host environment. This is so as they cannot synthesize their structural component and genetic materials. Therefore, they exclusively depend on the cell of the host for these function. This parasitic nature of the virus robs the cell of the target host macromolecular and energy so severe that its functions are altered subsequently leading to cell disease and death. At the cellular level pathogenesis, the most rampant factor is the host cell and the virus competing for synthetic materials for survival (Figure 2) (Medawar, n.d.).

viruses 1

Figure 2: mode of virus destruction in a cell (Medawar, n.d.)

1.4.2. Tissue trophism

In most cases virus would show great viability in various tissues. Specificity of tissue trophism is determined by the host defense, PH and local temperatures, physical barriers and cells susceptibility selectiveness. Some of these viral tissue trophism include: Polioviruses. Polioviruses destroys particular nerves with high surface receptors concentration for these viruses that virus-resistant cells (Baron, Fons, & Albrecht, 1996).

1.5.0. Viral spread sequence

1.5.1. Portal of entry implantation

Often, virions enter onto living cells and implant themselves via the genital routes, skin-penetrating, gastrointestinal and the respiratory routes. The virulence, infectivity, location and dose of the virus determines the final infection outcome; whether subclinical, or lead to lethal, severe or mild disease (Baron, Fons, & Albrecht, 1996).

1.5.2. Local replication and spreading

If implantation is successful local virus replication and spread may follow. In most cases various types of viruses use extracellularly model to spread among cells, or intracellularly model or both approaches. When a local infection starts this is likely to lead to localized disease and subsequently localized virus shedding (“Chapter 3: Virus Replication Cycles,” n.d.) (Figure 3). With intracellularly spread virus find partial protection because antibody environment does not enter through the cell membranes.

viruses 2

viruses 3

Figure 3: How virus spread during localization. The numbers indicate the events as they follow on viral attack (Baron, Fons, & Albrecht, 1996).

1.5.3. Dissemination from entry point The bloodstream dissemination

From the point of entry, virus with vast multiplication find their way to the peripheral nerves and the blood the primary routes that spread the virus widely through the body. The circulation is the key player in systemic dissemination process (Table 1). The virus reaches this route through the lymphatic system. When circulated through the body, the virus enter the target site via the capillaries. This may occur through multiplication of the virus in fixed macrophages or endothelial cells, or diffuse via gaps and or be transferred via migrating leukocytes (Figure 5) (Baron, Fons, & Albrecht, 1996).

viruses 4

Figure 5: How a virus spread within a bloodstream during a generalized infection with number indicating events sequence (Baron, Fons, & Albrecht, 1996).

Table 1: Some virus pathogenesis and infections disseminated (Baron, Fons, & Albrecht, 1996).

viruses 5 Nerves dissemination

Neural dissemination is not common like bloodstream dissemination but, as seen from (Table 1) some virus use this channel to cause infection. Such virus include poliomyelitis in some cases, herpesvirus and rabies virus. These virus spread to the neurites (dendrites and axons) as well as the perineural cells where shielding of the virus from antibody takes place (Figure 6).

viruses 6

Figure 6: How virus during a generalized infection spread through nerves with numbers indicating event sequence (Baron, Fons, & Albrecht, 1996).

1.6. Incubation period

In most viral infection, through the dissemination stages symptoms do not occur. Incubation period is said to extend from the period between virus exposures to the disease onset stage. This period extends from time of implantation to the dissemination point ultimately ending when replication of the virus cause disease in the target site. Normally the period is brief from 1-3 days for short viral distance target organ from the portal of entry. Longer incubation period are likely to result from stepwise fashion viral movement in the body to the target site lysis delay or no lysis on the infected cell, late immune reaction or host cell mutation resulting into cancer development (Baron, Fons, & Albrecht, 1996).

1.7. Target organs multiplication

Like in other body sites replication of the virus in the targeted organ are similar. However, for stepwise progression, virus progression delays in systemic infections and clinical disease is evident there. Each virus stepwise progression activates the local mechanisms of recovery through the body (local immunity, local inflammation, interferon and local body defenses. Hence, by the time the target organ gets infected the sites infected earlier might be undergoing various recovery stages (Figure 7). In the target sites, virus multiplication may be sufficient to realize a dysfunction depending on the host defenses and virus balance which is manifested via disease or death.

viruses 7

Figure 7: picornavirus spread over body surface with local neutralizing activity antibody shown from eye-pharynx-intestine during natural infection (Baron, Fons, & Albrecht, 1996).

1.8. Virus shedding

Following the virus diversity, each site in the body site is viable for shedding see Table . The common sites however, includes, the alimentary tracts and the respiratory tracts (Baron, Fons, & Albrecht, 1996).

1.9. Conclusion

Virus pathogenesis is a complex process involving the interplay of the virus and the host environment.



Abeles, S.R. and Pride, D.T. (2014). Molecular bases and role of viruses in the human microbiome. J Mol Biol, 4C (7):1-15.

Baron, S., Fons, M., & Albrecht, T. (1996). Medical Microbiology: Chapter 45: Viral Pathogenesis, 4th edition. Galveston.

Chapter 3: Virus Replication Cycles, (n.d.). Retrieved 10/6/16 from,

Chapter 33: Virus, (2006). Retrieved 10/6/16 from,

Medawar, M. (n.d.). Viral Pathogenesis. Retrieved 10/6/16 from,

Nekhai, S. (2012). Viral Pathogenesis. Retrieved 10/6/16 from,

NIAID, (2003). Understanding The Immune System How It Works. Science Education, retrieved 10/6/2016 from,

Racaniello, V. (2009). Viral Pathogenesis. Retrieved 10/6/16 from,

Wong, D. (n.d.). Viral Pathogenesis. Retrieved 10/6/16 from,

* Corresponding author. Tel.: +0-000-000-0000; fax: +0-000-000-0000.1

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