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Deondra Brown

Cell Biology
Zika paper
Zika Outbreak
Zika Biology
Zika was first discovered in 1947 and named after the Zika forest in Uganda (3).
In May 2015, an outbreak of Zika began in Brazil and is now rapidly spreading the globe.
We know that it has much more harm than the average mosquito bite. Further studies are
investigating the chance that Zika may be causing the increase of pregnancies with
microcephaly. So far, our knowledge of Zika has come a long way and we can now use
the results we have to hopefully discover how it’s linked to microcephaly and what we
can do to control it. Zika is part of the flavivirus family, which includes viruses such as
Yellow Fever, Dengue and West Nile (3). As of now there really isn’t any cure or vaccine
against the Zika virus. The best treatment is to treat its symptoms. If you are an adult the
symptoms are pretty mild, however if you are pregnant extra precaution must be taken.
Retroviruses, in general, integrate into a host’s genome by copying their own viral
genome into DNA. Once this has been done the host’s now recognizes this virus and gets
through and can integrate into a chromosome (9). However, the Zika virus does not
integrate into host’s genome. This virus is covered in a phospholipid bilayer. Its genome
contains a coding strand with two noncoding regions. The envelope is like the outer coat
of the virus. This coat is formed when the virus buds from the cell plasma membrane of
the host. After “budding” new virus particles wrap around forming the coat (8). In this
envelope, Zika expresses two glycoproteins. Glycoproteins contain oligosaccharide
chains covalently attached to polypeptide side chains (7). Zika has a simple genome
consisting of three structural proteins: envelope, membrane precursor, and capsid. As
well as, seven nonstructural proteins: NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5 and
only one noncoding RNA. These proteins are necessary for replication. The E gene is
the envelope found wrapped around the surface of the virus and it’s involved in the
replication, cell binding and membrane fusion (5). The C, capsid, outer shell allows for
the virus to penetrate the cell membrane. The prM is a precursor protein, which also
helps in the role of the assembly and fusion. It is cleaved in the Golgi and matures the
virion for fusion (1). The NS3 protease and NS5 polymerase cap and replicate the viral
RNA (6). The 3’UTR sfRNA is essential for the cause of the virus. It plays a role in
inhibiting RIG-I antiviral activity (1). The genome type of an organism tells us of its
genetic material. The structure of Zika is like all other flaviviruses. Zika is a positive
single-stranded RNA molecule with two noncoding regions (3). The specific type of
genome for Zika is +ssRNA. Its genome is directly translated because it is a positive
sense RNA strand. This single, polyprotein is cleaved by viral enzymes into three
structural proteins and seven nonstructural proteins. All are essential for assembly and
replication (12). This modification occurs at the post-transitional level. Zika replicates in
the cytoplasm of human cells. Once an infected mosquito injects the virus into the
human skin, the cells in the skin that become infected are epidermal keratinocytes,
dendritic cells or the neurons (9). When the virus enters, the virus membrane fuses with

the endosomal membrane and the ssRNA genome is released into the cytoplasm of the
host cell (5). From here it’s translated into the single polyprotein and further cleaved into
the proteins stated previously. In a mosquito, the virus is replicated in the nucleus. Once
the mosquito takes its blood meal from you, it
grows within the mosquito, replicates and then
makes its way to it’s saliva where it will pass on
the infection to the next person it bites. Skin
cells tend to be the main target of Zika. This is
easy to believe since the transmission of the
virus from mosquito to human occurs when a
mosquito injects the virus directly through the
skin. No wonder Zika is quickly and easily
spread?
Figure 1 shows the Zika virus
transmission cycle. Not only can the human be
infected from a mosquito carrying Zika, but also
a mosquito that bites an infected person will
also then become infected.
Figure 1
http://www.bbc.com/news/health35370848

Zika’s link to disease
The fact that the mosquito targets the skin cells also is very consistent in
explaining the reported symptoms of Zika virus. Only twenty percent of people infected
with the virus show symptoms but the most common symptom is a skin rash (blackboard
feedback). Maculopapular rashes have been presented by more than 90 percent of people
infected and therefore remains the main clinical symptom (12). The flavivirus family has
been show to be able to infect neurons. Neurons are one of the target spots for these
viruses. Flaviviruses such as the encephalitis viruses, West Nile, Yellow Fever and
Dengue have all show the ability to enter and infect the nervous system and neurons. The
Zika virus in particular has been shown to infect animal neurons. Scientists reported
abnormalities in the central nervous system along with congenital infections and
neurotropism of Zika in animals (11). The Zika virus RNA has been found in amniotic
fluid. In 2015, the virus was found in the amniotic fluid of two women whose babies had
microcephaly (3). Microcephaly is a neurological condition where brain fails to grow at
the normal rate. We now know it has the ability to cross into the placenta and cause
further complications to a fetus. This shows evidence that Zika has the ability to infect
neurons. We have already discovered its ability to infect animal neurons and its link to
babies with microcephaly also makes it evident. Out of thirty-eight mothers of newborns
born with microcephaly, twenty-four of them developed the common Zika skin rash
symptom (11). However, in general we have seen it infect the neurons in animals as
explained before. Scientists have already seen neurotropism of Zika demonstrated in an
animal model (11). Will all of this said I do believe Zika can cause microcephaly.
Microcephaly is when the brain fails to develop at normal pace resulting in small head
size. It can be caused by many different birth defects such as an exposure to drugs,
radiation and even from infections. Data has shown the increase of microcephaly

specifically during the Zika outbreaks. Evidence of Zika found in amniotic fluid tells us
it has the ability to infect a developing fetus. The fact that it disrupts animal neurons also
gives it the credit for causing this brain defect. According to the Center of Disease
Control, Director Dr. Thomas Frieden said, “with each day, the association of the Zika
virus and microcephaly is looking stronger and stronger” (4). Also, the CDC lab results
have shown the presence of Zika virus in the brain tissues of babies from miscarriages of
mother’s that were infected during pregnancy (4).
In conclusion, as of now all we can do is let research take over and give us all the
necessary answers about Zika. According to a paper in the journal Lancet, just between
2015 and January 2016, 4,800 infants born in Brazil had been reported to having
microcephaly whereas fewer than 200 were reported per year prior to the Zika outbreak
(4). Obviously, from these statistics we can tell that Zika is playing some role in the
escalation of microcephaly. Today, researchers at CDC are collaborating with researchers
in Brazil studying the virus and working on figuring out how Zika is damaging the brains
of fetuses (4). I enjoyed being able to find out more information about the Zika virus and
being able to understand it in its genetic form. Before this assignment I only knew the
basics along with its medical complications and how it’s transmitted. Likewise, after
reading the articles, researching and completing this paper I now feel as though I have a
much more educated understanding of Zika, its genome and the ongoing research of the
questions that still need answers.

Citations
1.

ViralZone: Zika virus (strain Mr 766). (n.d.). Retrieved April 10, 2016, from 
http://viralzone.expasy.org/all_by_species/6756.html 

2.

Zika virus animation. (2016, March 10). Retrieved April 10, 2016, from http://visual­
science.com/projects/zika/animation/ 

3.

Zika Virus. (n.d.). Modified/Retrieved April 10, 2016, from 
https://en.wikipedia.org/wiki/Zika_virus 

4.

Nierenberg, B. C. (2016, February 17). Does Zika Cause Microcephaly? CDC Seeks More 
Answers. Retrieved April 10, 2016, from http://www.livescience.com/53749­zika­microcephaly­
how­case­control­study­will­work.html 

5.

Zika Virus. (2016, February 15). Retrieved April 10, 2016, from 
https://microbewiki.kenyon.edu/index.php/Zika_virus

6.

Bollati, M., Alvarez, K., Assenberg, R., Baronti, C., Canard, B., Cook, S., . . . Bolognesi, M. 
(2010). Structure and functionality in flavivirus NS­proteins: Perspectives for drug design. 
Antiviral Research, 87(2), 125­148. doi:10.1016/j.antiviral.2009.11.009. Retrieved April 10, 2016,
from http://www.sciencedirect.com/science/article/pii/S0166354209005385

7.

Glycoprotein. (n.d.). Modified (15 March, 2016) Retrieved April 10, 2016, from 
https://en.wikipedia.org/wiki/Glycoprotein 

8.

NCI Dictionary of Cancer Terms. (n.d.). Retrieved April 10, 2016, from 
http://www.cancer.gov/publications/dictionaries/cancer­terms?cdrid=44588 

9.

Retrovirus Integration into the Human Genome. (2004). PLoS Biology PLoS Biol, 2(8). 
doi:10.1371/journal.pbio.0020281. Retrieved April 10, 2016, from 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC509317/

10. Weaver, S. C., Costa, F., Garcia-Blanco, M. A., Ko, A. I., Ribeiro, G. S.,

Saade, G., ... & Vasilakis, N. (2016). Zika Virus: History, Emergence,
Biology, and Prospects for Control. Antiviral Research.
11. Teixeira, M. G., da Conceição N. Costa, M., de Oliveira, W. K., Nunes, M.
L., & Rodrigues, L. C. (2016). The Epidemic of Zika Virus–Related
Microcephaly in Brazil: Detection, Control, Etiology, and Future
Scenarios.American journal of public health, 106(4), 601-605.
12. Hamel, R., Liégeois, F., Wichit, S., Pompon, J., Diop, F., Talignani, L., ... &

Missé, D. (2016). Zika virus: epidemiology, clinical features and hostvirus interaction. Microbes and Infection.

13. Ricketson R, Lyons-Weiler J. (2016). The Zika Virus sfRNA Secondary Structure
Reveals a miR-147a Homologue that Targets Neurofascin as a Potential Cause
of its Neurologic Syndromes. WebmedCentral VIROLOGY 7(3):WMC005076