1. 1
Filoviruses: disease and control
Abstract
This research essay is on filoviruses, focusing mainly on diseases and controls. Filoviruses
are viruses that form filamentous RNA and are spherical, elongated, curved or branched
virions. It infects primate, bats and pigs in nature. It doesn’t cause disease easily in rodents
and replicates in the cytoplasm of a host cell. It has a RNA single-stranded negative-sense
RNA genome of approximately 19 kb long.[1] Different types of filoviluses will be explored
but the ebola virus and different strains of the ebola virus will be discussed in detail due to its
current outbreak. According to World Health Organization (WHO) and respective
governments, by 18th of January 2015 the death toll from current Ebola outbreak have risen
to a total of 8,641 deaths out of 21,724 suspected cases.[2] There have been 19 outbreaks of
Ebola in last 21 years, having three alone in 2014. [3] Filovirus causes severe viral
hemorrhagic fever in humans and nonhuman primates by imparing immune responses of the
host and dysfunctioning vascular system.[4] The processes of these diseases will be examined
and the corrective measurements of controlling those diseases will be investigated.
Word count: 3488
Introduction
There are three different types of filoviruses : Marburg, Ebola and the Cueva virus.
Genus name Species name Virus name (Abbreviation)
Marburgvirus Marburg Ravn virus (RAVV)
Marburg virus (MARV)
Ebolavirus Bundibugyo Bundibugyo virus (BDBV)
Sudan Sudan virus (SUDV)
Reston Reston virus (RESTV)
Zaire Ebola virus (EBOV)
Taï Forest Taï Forest virus (TAFV)
Cuevavirus Lloviu Lloviu virus (LLOV)
Table 1 shows different types and different strains of filoviruses. There are three different
types of filoviruses : Marburg, Ebola and the Cueva virus.[5]
Marburg virus was the first filovirus discovered when a European lab worker who had
handled imported monkeys fell ill. Ebola virus was discovered in 1976 in democratic republic
of Congo. The incubation period for Ebola virus is 2-21 days. Filoviruses are so lethal
because they turn the body's own defences against it. Ebola is contagious, but spreads via
direct contact with the bodily fluids of an infected person, such as their faeces, vomit or
blood. Usually cells in the innate immune system are triggered when a virus first invades the
body, causing inflammation and other reactions to fight off the infection.[6]

2. 2
Figure 1 illustrates the structure of the Ebola virus, adapted from Ebola Virus Proteins
(October 2014 Molecule of the Month by David Goodsell doi:
10.2210/rcsb_pdb/mom_2014_10)
The Ebola virus infects and damages the innate immune cells, finishing out first line of
defence. This triggers a cytokine storm and cause the rapid death of cells that normally make
protective antibodies. Not only the immune system, Ebola virus also attacks the spleen and
kidneys, destroying cells that maintain body’s fluid and regulate chemical balance and that
make proteins to clot the blood. Lastly, Ebola virus prevents the lungs, kidneys and liver from
working, failing other organs and the blood vessels end up leaking fluid into surrounding
tissues, resulting in death.
a)

3. 3
b)
c)
Figure 2 a) shows the affect of the Ebola virus when it attacks its host, b) shows the organs
affected by the Ebola virus and c) shows structure of Ebola virus genome. All three figures
are adapted from the clinical features and pathobiology of Ebola virus infection.[7]
Main Section : Disease and control
Viral entry
Interactions of Ebola proteins with host cell proteins
Firstly, Interactions between host cellular proteins and Ebola protein results in failure of
antigen presentation, type I and type II interferon responses, T-cell-dependent B cell
responses, cell-mediated immunity, humoral antibodies and RNAi antiviral responses. This
whole system of suppression and evasion of adaptive and innate immune responses in the
target host results in a severe immune dysregulation which is a property of fatal ebolavirus
infection. [8]
Pseudotyped viruses
Ebolavirus has a high mortality comparing to its viral pathogenesis and lifecycle. Cell
adhesions increase independent of protein synthesis or mRNA. This happens due to the
infection by GP pseudovirions and the binding of the receptor binding region (RBR) of
ebolavirus glycoprotein (GP). Translocation of an RBR binding partner occurs from an
intercellular vesicle on cell adhesions to the cell surface. Suspension 293F cells are shown to
contain an RBR binding site within the organising center of microtubules and in the trans-
Golgi network. The RBR binding partner gets internalized when adherent cells are placed in
suspension and the RBR binding partner trafficking to the cell surface depends on
microtubules. Lymphocytes were thought to be lacking an RBR binding partner but it was
found to have intracellular pool of an RBR binding partner.[9]

4. 4
A system for pseudotyping of the glycoproteins is used to investigate the function of the
Ebola virus glycoprotein (Ebo-GP), by placing into murine leukemia virus (MLV). Analysis
of MLV infection dipicts that the host range conferred by Ebo-GP is very broad and extends
to cells of a variety of species. The absence of a cellular receptor for Ebo-GP on B and T cells
conveyed that all lymphoid cell lines were completely resistant to infection when it was
tested. The development of high-titer MLV pseudotypes will be beneficial for the
development of neutralizing antibodies, the analysis of glycoprotein function, isolation of the
cellular receptor(s) for the Ebola virus and analysis of immune responses to Ebola virus
infection. The replication of Ebola virus depends on the extreme pathogenicity of this virus.
[10]
No effective therapies for Ebola virus have been identified to date. To examine the entry and
fusion properties of Ebola virus, human immunodeficiency virus type 1 (HIV-1) virion-based
fusion assay was carried out by substituting Ebola virus glycoprotein (GP) for the HIV-1
envelope. Cleavage of the fluorogenic substrate CCF2 by β-lactamase-Vpr incorporated into
virions helped to detect fusion. Entry and fusion triggered by the Ebola virus GP occurred
with much slower kinetics than with vesicular stomatitis virus G protein (VSV-G), which
were blocked with bafilomycin A1 by membrane cholesterol depletion and by vesicular
acidification inhibition. Entry and fusion of Ebola virus GP pseudotypes, but not HIV-1 Env
or VSV-G pseudotypes. They were impaired in the presence of the microtubule-disrupting
agent called nocodazole but were enhanced in the presence of the microtubule-stabilizing
agent paclitaxel (Taxol). The entry and fusion of Ebola virus GP-mediated was also inhibited
by cytochalasin B, latrunculin A cytochalasin D, and jasplakinolide. This meant that both
microfilaments and microtubules may play a role in the effective trafficking of vesicles
containing Ebola virions from the cell surface to the appropriate acidified vesicular
compartment where fusion occurs. Primary macrophages were highly sensitive to entry and
fusion of Ebola virus GP-mediated, but monocytes displayed had reduced levels of entry and
fusion. Even the tumor necrosis factor alpha released by Ebola virus-infected
monocytes/macrophages, enhanced Ebola virus GP-mediated entry and fusion to human
umbilical vein endothelial cells.[11]
Requirement of Cargo Receptor ERGIC-53 for the Production of Infectious Filovirus
particles
Likewise arenaviruses and hantaviruses cause severe diseases in humans. Human proteins,
interacting with the glycoproteins (GPs) of a prototypic arenavirus and hantavirus were
identified and showed that the lectin endoplasmic reticulum (ER)-Golgi intermediate
compartment has a mass of about 53 kDa (ERGIC-53), a cargo receptor required for
glycoprotein trafficking within the early exocytic pathway, associates with arenavirus,
hantavirus, coronavirus, orthomyxovirus, and filovirus GPs. ERGIC-53 binds to arenavirus
GPs through a lectin-independent mechanism, traffics to arenavirus budding sites, and is
incorporated into virions. ERGIC-53 is required for the propagation of coronavirus,
arenavirus and filovirus. In its absence, GP-containing virus particles do form but are non-
infectious. This is because they have no ability to attach to host cells. A class of pathogen-
derived ERGIC-53 ligands are identified, a lectin-independent basis for their association with
ERGIC-53 is also identified and a role for ERGIC-53 in the propagation of several highly
pathogenic RNA virus families. ERGIC-53 is a potential antiviral target due to its ability to
associate with GPs encoded by several families of pathogenic RNA viruses and due to its role

5. 5
in the propagation of coronaviruses, arenaviruses and filoviruses. ERGIC-53 is not needed for
the formation of GP-containing arenavirus particles, but is required for their infectiousness.
[12]
There is no specific treatment for a severe haemorrhagic fever syndrome in humans caused
by Ebola virus and Marburg virus. But since filoviruses use a complex route of cell entry,
which depends on various cellular factors. It’s assumed that there may be drugs already
approved for human that might have anti-filoviral properties but used for other indications
that interfere with signal transduction or other cellular processes required for their entry.
Authentic filoviruses and lentiviral particles pseudotyped with filoviral glycoproteins are
used to identify and characterize such compounds.
Adjuvanted mAb therapy gives 100% protection for up to 72 hours post Ebola virus
infection. mAb therapy seems effective even after positive confirmation by reverse
transcription-quantitative PCR (RT-qPCR) and fever. Filovirus infections cause fatal
hemorrhagic fever after the initial onset of general symptoms, which then rapidly progresses
to severe disease, the most virulent species can cause death to their hosts within 10 days after
the appearance of symptoms. Before the use of monoclonal antibody (mAb) therapy,
infection of nonhuman primates (NHPs) was fatal with the most virulent filovirus species if
interventions were not administered within minutes. A novel nucleoside analogue, BCX4430,
has since been proven to be used as protective efficacy with a delayed treatment start. This
review summarizes and evaluates the potential of current experimental candidates for treating
filovirus disease with regard to their feasibility and use in the clinic, and assesses the most
promising strategies towards the future development of a pan-filovirus medical
countermeasure. Interventions given 1 hour after Ebola virus exposure were ineffective in
nonhuman primates (NHPs), with the exception of monoclonal antibody (mAb)-based
therapy and BCX4430. [13]
Treating with T-705 (favipiravir)
Outbreaks of Ebola hemorrhagic fever are associated with case fatality rates of up to 90% in
sub-Saharan Africa. Currently, there’s neither a vaccine nor an effective antiviral treatment
available for use in humans. The efficacy of the pyrazinecarboxamide derivative T-705
(favipiravir) against Zaire Ebola virus (EBOV) in vivo and in vitro seemed beneficial. T-705
reduced replication of Zaire EBOV in cell culture by 4 log units with an IC90 of 110 μM.
Mice lacking the type I interferon receptor (IFNAR−/−) were used as in vivo model for Zaire
EBOV-induced disease. A rapid virus clearance triggered the stimulation of T-705
administration at day 6 post infection, reduced the severity of biochemical parameters of
disease, and prevented a lethal outcome in 100% of the animals. The findings suggest that T-
705 is a candidate for treatment of Ebola hemorrhagic fever.[14]
Clathrin-mediated endocytosis
Ebola virus (EBOV) infects many cell types but viral entry is known to be pH-dependent
with the exact entry pathway(s) remain unknown. To gain insights into EBOV entry,
investigation in the role of several inhibitors of clathrin-mediated endocytosis in blocking
infection mediated by HIV pseudotyped with the EBOV envelope glycoprotein (EbGP) was
carried out. Envelope-minus HIV and Wild type HIV pseudotyped with Vesicular Stomatitis

6. 6
Virus glycoprotein (VSVg) were used as controls after inhibiting clathrin pathway to assess
cell viability. Inhibition of clathrin pathway using dominant-negative Eps15, siRNA-
mediated knockdown of clathrin heavy chain, chlorpromazine and sucrose blocked EbGP
pseudotyped HIV infection. Also, both chlorpromazine and Bafilomycin A1 inhibited entry
of infectious EBOV. Sensitivity of EbGP pseudotyped HIV as well as infectious EBOV to
inhibitors of clathrin suggests that EBOV uses clathrin-mediated endocytosis as an entry
pathway. Furthermore, since chlorpromazine inhibits EBOV infection, novel therapeutic
modalities could be designed based on this lead compound.[15]
c-Abl1 tyrosine kinase is used to replicate the Ebola virus
Ebola virus causes an infection in humans resulting in diffuse bleeding, hypotensive shock,
vascular instability and often death. Ebola virus remains a biological threat because of its
high mortality and rapid and easy transmission among humans for which therapeutic
interventions and effective preventive are required. The mechanisms of Ebola virus
pathogenesis are very important to understand in order to for develop antiviral therapeutics.
Successful replication of Ebola virus is coordinated by the c-Abl1 tyrosine kinase. Abl-
specific kinase inhibitors or c-Abl1-specific small interfering RNA (siRNA) inhibited the
release of Ebola virus-like particles (VLPs) in a cell culture co-transfection system and
required tyrosine phosphorylation of the Ebola matrix protein VP40 was needed. The release
of Ebola VLPs was declined by the expression of c-Abl1 as it stimulated an increase in
phosphorylation of tyrosine 13 (Y(13)) of VP40, resulting in a mutation of Y(13) to alanine.
The Abl-family inhibitor nilotinib or the c-Abl1-specific siRNAs inhibited the Productive
replication of the highly pathogenic Ebola virus Zaire strain by up to four orders of
magnitude. This data stated that c-Abl1 regulates release or budding of filoviruses through a
mechanism involving phosphorylation of VP40. This step of the virus life cycle therefore
may represent a target for antiviral therapy. [16]
Drugs that inhibit filovirus cell entry
Amiodarone which is a multi-ion channel inhibitor and adrenoceptor antagonist are
discovered to be a potent inhibitor of filovirus cell entry at concentrations that are routinely
reached in human serum during anti-arrhythmic therapy. The amiodarone-related agent
dronedarone and the L-type calcium channel blocker verapamil were also seen to give a
similar effect. Inhibition by amiodarone was concentration dependent and similarly affected
authentic filoviruses and also pseudoviruses. Inhibition of filovirus entry was observed with
most but not all cell types tested and a host cell-directed mechanism of action was indicated
with accentuated by the pre-treatment of cells. Amiodarone also inhibited the New World
arenavirus Guanarito but the Old World arenavirus Lassa, Bunyaviridae (Hantaan) and
members of the Rhabdoviridae (vesicular stomatitis virus) families were mostly resistant. The
ion channel blockers amiodarone, dronedarone and verapamil are proven to inhibit filoviral
cell entry. [17]

7. 7
Figure 3 illustrates the widespread of the Ebola virus since 2014, adapted from 2014 Ebola
virus epidemic timeline from wikipedia. [18]
Initial ways of controlling the Ebola disease : Isolation houses
Many of previous filovirus outbreaks have been handled using the same basic techniques
which involve isolating and treating patients then tracing and monitoring their contacts.
Public-health officials have also used this method as a measurement to reduce the spread of
Ebola virus in Nigeria and Senegal. But across West Africa as a whole, the public-health
response was completely inadequate at the start of the outbreak due to not been familiar with
the Ebola virus disease, which resulted in rapid spread of the virus. Non-profit organizations
and aid agencies found new type of controls. In Sierra Leone, officials built isolation centres
that can house patients away from their family and community, in order to prevent the virus
from spreading, but that had fewer qualified health-care workers than a standard treatment
facility.[19] Mentally, it was a controversial move, because people believed patients were
being warehoused to die. But the harsh reality was that existing clinics were full and so the
patients were left out, resulting in the widespread of disease.These smaller-level community
facilities were not ideal, but it would surely bring transmission down in communities by a
little.
ZMapp vaccine
There have been many experimental therapies and vaccines developed specifically to target
Ebola virus. However, much attention has focused on ZMapp, which is a cocktail of
antibodies that was first identified using mice vaccinated with Ebola virus proteins, and
which has been given to several people in this outbreak.[20] ZMapp proved to a highly
successful therapy, which protected 18 monkeys from dying of Ebola virus when the animals
already showed the symptoms of the disease. [21] Further tests of this and other medicines
are carried out, as well as of other experimental vaccines. [22]

8. 8
Sanitation and Hygiene
Sanitation and hygiene are very important in controlling the disease. People are taught and
trained about sanitation, about hygiene measures and about how exactly to act if a case is
suspected. Different authorities set up Ebola centres, and through leaflets, broadcasts, and
posters the governments are gave everyone a number to call if symptoms develop, so they
could be picked up by nurses and trained staff and transported to a centre. Some people
travelled to their nearest medical centre by themselves. But the major problem was that many
of them travelled by taxi, and if they were infected, then the next person to use the taxi was at
risk. Continuous spraying the inside of ambulances with chlorine spray to kill the virus,
corrodes the vehicles. Heavy-duty plastic lining material is used to line the whole of the
insides of vehicles and that seemed to be a partial solution.[23,24] But the problem is that the
plastic sheeting lining are stripped out every time after used and it’s burned. This is very
dangerous and expensive. The risk of cross infection was increased when people are waiting
for tests in public areas instead of specially built centres as some people had the ebola disease
and others didn’t. Chlorine has some ability to kill the Ebola virus but it also damaged some
surfaces, metals and electrical circuits plus it didn’t leave any traces back that could prove the
place was free of the virus. Hospitals were one of the biggest problems in Sierra Leone and
Liberia particularly. People who have other diseases didn’t wish to go to hospital because
they feared they will contract the Ebola virus disease. Therefore authorities were advised to
build new centres in suitable locations, out of tent or plastic sheeting. I think the biggest
challenge was that an infected person with Ebola used the toilet the next person to use it
could easily contract the disease. Septic tanks also had a high risk of disease. If an infected
persons wastes were treated in a safe manner then this would have a better control in
preventing the spread of the disease.
Ebola is very weak outside of the hosts’ body. It takes a chlorine solution around 10 times
more dilute to kill Ebola than it does to kill cholera. Outside of bodily fluids, the virus can
actually be killed by using soap and water. This is because its surface protection is only a
fatty fluid. [25]
People of west Africa reacted in a shock and in all sorts of different ways. Stones were
thrown at foreigner health workers by local people, tents and centres were burned and people
prevented the healthcare workers from burying the dead. [26] I think this was a big mistake
as the virus doesn’t die in a dead body, and the longer bodies are left, the fluid builds up in
the stomachs of those bodies, bursts and scatters around infected fluids. Cremation was the
best control. But many communities oppose this idea as it meant to cross a cultural boundary
for them. So bodies were left for days, which increased risk of disease spread. It was also
hard to find incinerators big enough as most hospital incinerators are used only for bags of
hospital waste, and are not big enough for bodies. [27]

9. 9
Conclusions
I think by carrying out further investigation and experiments of different filoviruses and
knowing the secret of how various strains of the same virus causes diseases to different
extents, we can find out better ways of controlling those diseases. By understanding the
structure fully we can make it possible to cure people from these deadly diseases. Further
investigation in knowing how bats can cope with ebola virus and humans can’t would give a
way to save lives of many people.
I think the major lesson to learn is to react and respond immediately. Treating a patient is
absolutely vital, but it’s also important to find the traces of first contact in order to stop the
spread of the disease. Medical services in Sierra Leone, Guinea and Liberia were totally
ruined before Ebola struck due to a condition of poverty and the poor health system.[3]
I learnt that there is no cure for Ebola, however if people are well hydrated and take
antibiotics to fight some of the symptoms of the ebola disease, they are at better position of
overcoming the disease by themselves.
In this essay, considerable knowledge on the virus and how it actually causes its fatality has
been examined and many of highly effective chemotherapeutic, preventive vaccines have also
been developed. [28]
Other ways of controlling the viral disease
•Development of a spray-on coating that is easily cleaned to protect the interior of vehicles.
•Designing new protective clothing for health workers that is reusable and is more
comfortable to wear.
•Methods of safe disposal of infected bodies in a culturally sensitive way
• Producing a suitable spray that could be used to sanitise hospital buildings. If health care is
improved, the lethality rates will decline automatically.
I think the best thing would be to produce therapies that work against all or multiple
filoviruses so that it could be used immediately when symptoms are first detected. This will
save time of trying to diagnose which virus is exactly causing the disease.
There also has been an ongoing concern that a single genetic mutation in a filovirus such as
Ebola, could result in a change in transmission system from direct body fluid transmission to
airborne transmission, as it occured in the Reston strain of EBOV among infected
macaques.[29]
Comparing to Reston strain, which had the same genotype, it would hugely increase the
disease and infection rates caused by EBOV, if a similar change occurs in the current
circulating strains of EBOV. Although, there is no record of any virus ever having made this
transition in humans because the tissue it prefers to infect is not the airway surfaces but the
vasculature. Compared to the H1N1 swine flu which had spread to an estimated 10,000 times
as many people in its first 10 months, the ebola virus disease is slow at spreading.[30]

10. 10
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