Biology Assignment: Comparative Case Study of Ebola and HIV Viruses
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Case Study
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This case study examines the Ebola and HIV viruses, comparing their mechanisms of cell invasion and their effects on the immune system. It highlights that Ebola engulfs the host cell and replicates, while HIV enters, fuses, and replicates. Both viruses harm the immune system and are fatal. The study also explores the CCR5-delta 32 mutation, a genetic mechanism that provides resistance to HIV, and discusses its use in gene therapy. Finally, the study addresses why elephants rarely get cancer, citing the role of P53 and LIF6 genes. The assignment includes citations and a reference section, providing a comprehensive analysis of the viruses and related genetic factors.

Running Head: VIRUSES
VIRUSES
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VIRUSES 2
1. QUESTION ONE
Ebola virus (filovirus) HIV - Ientivirus
It engulfs the host cell and then replicates
therefore triggering the functions of the cell.
The virus enters the host cell and then fusion
of the cell takes place and it replicates as the
cell undergoes division (Aldinucci &
Colombatti, 2014).
Ebola virus binds to the cell surface proteins
and affects the cells making even some of
them to burst (Messaoudi, Amarasinghe, &
Basler, 2015).
It targets white blood cells killing CD4 cells
thus damaging the immune system of the
body.
Ebola spreads throughout the body causing
fever and general body aches. It harms the
immune system and other organs by causing
severe and strong bleeding.
When HIV virus attacks the cells, it becomes
hard for the body to combat other
contagions. It affects the white blood cells
which are capable for fighting germs and
hence affecting the immune system
(Messaoudi, Amarasinghe, & Basler, 2015).
Similarities between Ebola and HIV virus
Both are spread by are virus and on entering the cells, they replicate.
Both are fatal since they affect the immune systems as they target cells (Messaoudi,
Amarasinghe, & Basler, 2015).
1. QUESTION ONE
Ebola virus (filovirus) HIV - Ientivirus
It engulfs the host cell and then replicates
therefore triggering the functions of the cell.
The virus enters the host cell and then fusion
of the cell takes place and it replicates as the
cell undergoes division (Aldinucci &
Colombatti, 2014).
Ebola virus binds to the cell surface proteins
and affects the cells making even some of
them to burst (Messaoudi, Amarasinghe, &
Basler, 2015).
It targets white blood cells killing CD4 cells
thus damaging the immune system of the
body.
Ebola spreads throughout the body causing
fever and general body aches. It harms the
immune system and other organs by causing
severe and strong bleeding.
When HIV virus attacks the cells, it becomes
hard for the body to combat other
contagions. It affects the white blood cells
which are capable for fighting germs and
hence affecting the immune system
(Messaoudi, Amarasinghe, & Basler, 2015).
Similarities between Ebola and HIV virus
Both are spread by are virus and on entering the cells, they replicate.
Both are fatal since they affect the immune systems as they target cells (Messaoudi,
Amarasinghe, & Basler, 2015).

VIRUSES 3
QUESTION 2
C-C chemokine receptor type 5 is a protein which lies on the surface of white blood cells
and is involved in immune system since it behaves like a receptor for chemokine. Genetic
mechanism is whereby the body undergoes mutation of the gene encrypting CCR5, which are the
co-receptor for HIV (Ren-Ping, et al., 2014). Some people have some system of resistance to
HIV. This is caused by the absence of receptors which prevent HIV from infecting CD4 which
are present on the outer region of the white blood cells. The shortening of these particular
receptors such that they are in nonterminal condition is called delta 32 mutation. The latter helps
those persons exposed to HIV so that they stay uninfected (Messaoudi, Amarasinghe, & Basler,
2015).
b) Most trials for gene therapy try to reduce the infection degree by aiming at viral
entry through CCR5 co-receptors. Therapies overpower HIV-1 and have since then improved the
survival of the infected people (Aldinucci & Colombatti, 2014). Therefore gene therapy purpose
to create population for CD4+ T cells which transports partial dysfunctional CCR5 co-receptors
since they are less vulnerable to HIV-1 infection.
QUESTION 2
C-C chemokine receptor type 5 is a protein which lies on the surface of white blood cells
and is involved in immune system since it behaves like a receptor for chemokine. Genetic
mechanism is whereby the body undergoes mutation of the gene encrypting CCR5, which are the
co-receptor for HIV (Ren-Ping, et al., 2014). Some people have some system of resistance to
HIV. This is caused by the absence of receptors which prevent HIV from infecting CD4 which
are present on the outer region of the white blood cells. The shortening of these particular
receptors such that they are in nonterminal condition is called delta 32 mutation. The latter helps
those persons exposed to HIV so that they stay uninfected (Messaoudi, Amarasinghe, & Basler,
2015).
b) Most trials for gene therapy try to reduce the infection degree by aiming at viral
entry through CCR5 co-receptors. Therapies overpower HIV-1 and have since then improved the
survival of the infected people (Aldinucci & Colombatti, 2014). Therefore gene therapy purpose
to create population for CD4+ T cells which transports partial dysfunctional CCR5 co-receptors
since they are less vulnerable to HIV-1 infection.
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VIRUSES 4
QUESTION 3
Elephants rarely get cancer due to their size and they undergo cell divisions so fast. Due
to this size and the long life span in them, they overcome getting cancer through evolving ways.
The cell kills itself and then the impaired DNA has no potential for giving rise to cancer.
Elephants have one copy of genes that reacts to dented DNA.When a cell divides the elephant
undergoes mutation therefore becomes rare for them to get cancer (Messaoudi, Amarasinghe, &
Basler, 2015). Moreover, the elephants have two more duplicates of cancer fighting genetic
factors: P53 AND LIF6. P53 is responsible for hunting those cells with miscopied DNA while
LIF6 demolishes those transformed genes before forming a cancer (Messaoudi, Amarasinghe, &
Basler, 2015).
QUESTION 3
Elephants rarely get cancer due to their size and they undergo cell divisions so fast. Due
to this size and the long life span in them, they overcome getting cancer through evolving ways.
The cell kills itself and then the impaired DNA has no potential for giving rise to cancer.
Elephants have one copy of genes that reacts to dented DNA.When a cell divides the elephant
undergoes mutation therefore becomes rare for them to get cancer (Messaoudi, Amarasinghe, &
Basler, 2015). Moreover, the elephants have two more duplicates of cancer fighting genetic
factors: P53 AND LIF6. P53 is responsible for hunting those cells with miscopied DNA while
LIF6 demolishes those transformed genes before forming a cancer (Messaoudi, Amarasinghe, &
Basler, 2015).
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VIRUSES 5
References
Aldinucci, D., & Colombatti, A. (2014). The inflammatory chemokine CCL5 and cancer
progression. Mediators of inflammation, 12(2), 104-114.
Messaoudi, I., Amarasinghe, G. K., & Basler, C. F. (2015). Filovirus pathogenesis and immune
evasion: insights from Ebola virus and Marburg virus. Nature Reviews Microbiology,
13(11), 663-665.
Ren-Ping, Z. H., Sen-Sen, L. O., Sheng-Tao, Y. A., Bo-Yang, Y. U., & Xian-Shu, B. A. (2014).
DT-13, a saponin of dwarf lilyturf tuber, exhibits anti-cancer activity by down-regulating
CC chemokine receptor type 5 and vascular endothelial growth factor in MDA-MB-435
cells. Chinese journal of natural medicines, 12(1), 24-29.
References
Aldinucci, D., & Colombatti, A. (2014). The inflammatory chemokine CCL5 and cancer
progression. Mediators of inflammation, 12(2), 104-114.
Messaoudi, I., Amarasinghe, G. K., & Basler, C. F. (2015). Filovirus pathogenesis and immune
evasion: insights from Ebola virus and Marburg virus. Nature Reviews Microbiology,
13(11), 663-665.
Ren-Ping, Z. H., Sen-Sen, L. O., Sheng-Tao, Y. A., Bo-Yang, Y. U., & Xian-Shu, B. A. (2014).
DT-13, a saponin of dwarf lilyturf tuber, exhibits anti-cancer activity by down-regulating
CC chemokine receptor type 5 and vascular endothelial growth factor in MDA-MB-435
cells. Chinese journal of natural medicines, 12(1), 24-29.
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