Viruses Gone Viral

Viruses are tiny segments of nucleic acids with a lipoprotein coating that are usually only a few nanometers wide but have the ability to cause massive havoc within a short period, to both plants and animals. In fact, viruses are so pathogenic that they even infect other microorganisms such as bacteria as in the case of bacteriophages!

Figure 1: Morphological representation of a bacteriophage

Interestingly, viruses are likely to thrive if the host is kept alive. This means that the virus survives as a result of co-existence with its host and this relationship contributes to its spread. At times, viruses mutate to evade immune responses but this may lead to the synthesis of deadly variants that may ultimately kill the host. Furthermore, viral infections involve a relatively long latency period before illness arises in the host. During this period, the infected individual may spread the virus unknowingly leading to an increase in infected persons. For instance, the current SARS-Cov2 virus has a latency period of 14 days before the symptomatic stage. Viruses can also employ a survival mechanism that is referred to as facile transmission (from the French word ‘facile’ meaning easy). This allows the virus to spread even at acute early stages of infection as in the case of influenza and smallpox virus.

Despite them being such a great risk to our health, designing therapeutic approaches towards rendering them inactive is very complicated. In the case of treating bacterial infections, antibiotics are designed to block bacteria from replicating and increasing in number. This is somewhat less complex since the bacteria uses its own cellular machinery to replicate. Therefore, antibiotics are developed to block these cellular mechanisms. However, viral infections are hard to treat because the viruses replicate by integrating their genome into the host’s chromosomal DNA. Therefore, it is challenging to target the virus using drugs without damaging the patient’s cells. There are antiviral agents that have been developed either to reduce the rate of viral replication or antagonize the binding of the viruses to their receptors. For instance, Foscarnet is a drug that is active against HIV1 and all herpes viruses by notably inhibiting viral DNA polymerase in a non-competitive fashion and blocking the reverse transcriptase from several retroviruses. Although it is inactive against eukaryotic DNA polymerases at concentrations that inhibit viral DNA replication, it is characterized by adverse effects such as nephrotoxicity, thrombophlebitis and irritability. In line with the old adage, “Prevention is better than cure”, finding vaccines against viruses seem to be the only definitive way to conclusively counter these microbes.

Figure 2: A representation of the different antiviral drug targets in the Human Immunodeficiency Virus (HIV) life cycle. Antiviral activity may involve a range of different antagonizing effects such as prevention of viral entry, inhibition of reverse transcription as well as inhibition of viral maturation (Image from HIV I-Base – HIV Pipeline 2017, )

Novel coronavirus might change the face of antiviral preventive medicine   

The emergence of a novel coronavirus that has claimed a significant number of lives within a short period of time has necessitated the utilization of new vaccine development protocols with the aim of curbing the alarming pandemic. This has been witnessed by a race to obtain an effective vaccine against the virus which was first reported in China last year. The rapid research and formulation of potential vaccines that has involved the production of recombinant vector, mRNA and DNA vaccines may prove to be a pivotal step in the eradication of viral infections in the near future. In recent weeks, the US-based pharmaceutical company Moderna has developed an mRNA vaccine named mRNA1273 in record-breaking time. This involves administration of the messenger RNA that codes for a stabilized form of the spike protein of SARS-CoV2 virus. This stabilized antigen is then presented by the major histocompatibility complex (MHC) for recognition by the immune system. Upon recognition as a foreign entity, both the humoral and cell-mediated immune response are stimulated. Furthermore, immunological memory is induced due to long-term expression of the viral antigen. This means that the immune system will “remember” the foreign protein if they are manifested in the body again and construct an attack cascade. With the urgency that has come with finding a vaccine quickly against the Covid-19 virus, the FDA allowed phase I trials of this vaccine without any animal data.

Figure 3: Jennifer Haller receives an administration of an mRNA vaccine against the novel coronavirus developed by the biotechnology firm Moderna as human clinical trials begin (AP Photo/Ted S. Warren)

Another American pharmaceutical line known as Inovio has developed a DNA vaccine against the new coronavirus which they have termed INO-4800, set to proceed to the clinical trial stage. This type of vaccine involves the use of plasmid DNA which encodes viral antigens or proteins that are directly administered to an individual, mostly through the intramuscular route. The viral factors then stimulate the immune system and cause immune memory as in the case of the mRNA vaccine. The immune response can be further stimulated by administration of a booster shot known as a DNA prime.  A key significant advantage of DNA vaccines is that the plasmid DNA does not require refrigeration and can be used to express multiple viral proteins hence saving on time and money.

With the past success in using recombinant vector technology to produce a vaccine against Ebola, Chinese based Cansino is also in the “vaccine race”, having developed Ad5-nCoV. This vaccine uses a replication-defective adenovirus-based viral vector to carry a gene that expresses a SARS-Cov2 spike protein. When expressed in the body, the protein mimics natural infection allowing for a strong immune response.

The relatively quick manner in which vaccines have moved from conceptualization to clinical trials offer a glimpse of hope that viral infections in the near future, might be a thing of the past. However, it will take concerted scientific effort to sustain this revolutionary occurrence and stop viral pandemics, such as the one that is being witnessed currently.

About the author

My name is Simeon Hebrew. I am a final year undergraduate student taking Biochemistry and Molecular Biology at the Jomo Kenyatta University of Agriculture and Technology, Kenya. I am currently finishing my research project that entails in silico investigation of a Plasmodium falciparum protein, CX3CL1 Binding Protein 1 as a potential antimalarial drug and vaccine target supervised by Dr Daniel Kiboi. In my free time, I enjoy playing basketball and drifting into the fantasy world of video games. My twitter handle is @HebrewSimeon

Further reading

Judith A. Owen , Jenni Punt, Sharon A. Stranford. (2013). KUBY Immunology (7th ed.; C. B. Lauren Schultz, Erica Champion, Irene Pech, Allison Michael, Yassamine Ebadat, ed.). New York: W.H Freeman and Company.

Nobrega, F. L., Vlot, M., Jonge, P. A., Dreesens, L. L., Beaumont, H. J. E., Lavigne, R., … Brouns, S. J. J. (2018). Targeting mechanisms of tailed bacteriophages. Nature Reviews Microbiology.


2 thoughts on “Viruses Gone Viral

  1. Hi there,

    It’s a nice article, but I just wanted to comment on this: “However, viral infections are hard to treat because the viruses replicate by integrating their genome into the host’s chromosomal DNA.”

    The integration of viral genetic material into that of the host is not mandatory. The most well known family to do this are the retroviruses (e.g. HIV), which are RNA viruses. These viruses package an enzyme called reverse transcriptase, which converts the RNA-based genome into DNA and is then integrated into the genome of the host cell. Other non-retroviral examples include adeno-associated viruses. SARS-CoV-2, to the best of my knowledge, does not integrate into the host genetic material.

    Viruses are difficult to treat because they exist at the edge of life, and it is difficult to find compounds to selectively ‘kill’ something that doesn’t fulfil most of life’s most basic criteria. The integration of viral genomic material into the host would admittedly make this an even more complex task, however.

    Best wishes,


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