EGERTON UNIVERSITY.

FACULTY OF ENGINERING AND

TECHNOLOGY.
DEPARTMENT: CEEN.
CIVIL AND ENVIRONMENTAL
ENGINEERING.
NAME: EDWIN MURIMI MWANGI.
REG. NO: BP12/00234/22.

BIOLOGY OF HIV/AIDS AND

SOCIETY.
UNIT CODE: ZOOL 143.
SUBMITTED TO: DR WALTER
ESSSENDI.
1. Summarize HIV modes of transmission and the entry process.

i. Blood and blood products.

Blood transmission of HIV is virtually confined to needle and syringe sharing among injecting drug users.

ii. Mother-to-child transmission (MTCT).

Approximately 30% of infants born to untreated HIV-positive women are infected. It is not known at what
stage of the pregnancy the foetus is infected but recent evidence supports the notion that the infant often
becomes infected during the birth process.

iii. Sexual activity.

Exact levels of risk for the various forms of sexual activity are not known but some sexual practices have
higher risks associated with them than others. Transmission can occur in either direction during unprotected
vaginal intercourse. HIV can be absorbed into the woman’s bloodstream during unprotected vaginal intercourse
via tears in the vaginal wall, genital ulceration or by absorption through the membrane of the cervical canal.
Anal intercourse without a condom is the highest risk sexual activity because the rectal lining is fragile and
prone to tearing, thus allowing easy access for infected blood and semen.

2. Describe the life cycle of HIV particle.

The HIV cell bumps into a living cell that carries it on its surface for a special protein called CD4.

a. Binding.
HIV comes into contact with a T-cell and binds to specific cellular proteins that acts as a viral receptor found
on the membrane of that cell. These receptors normally function to communicate with other cells, but have
been exploited by HIV in order to initiate infection.
The initial contact and binding to the cell occurs when the viral protein gp120 binds to the cellular receptor
CD4.

b. Fusion.
Fusion between the viral and host cell membranes occurs when the gp41 binds to either CCR5 or CXCR4.

c. Infection stage.
Following the binding and fusion, infection of the t-cell by HIV occurs. During this stage, the viral and cellular
membranes ‘melt’ together and the viral core is internalized.
The nucleocaspid then breaks apart releasing the viral RNA genome and associated proteins’ such as reverse
transcriptase.

d. Reverse transcription.
In order to successfully infect a cell, the viral genome must become integrated into the hosts DNA.
For this to happen, the single stranded RNA genome must be converted into double stranded DNA. This
process is called reverse transcription and is performed by the enzyme reverse transcriptase.

e. Integration.
Once the double stranded DNA copy of the HIV genome has been produced I must integrate into the cell’s
DNA in the nucleus.
The viral enzyme integrase cuts the host DNA and pastes in the viral information. The viral genes are now a
permanent part of that cell’s DNA.
The only way to remove the viral is to destroy the infected cell.
 f. Latent infection stage.
After the integration process is complete, the cell is latently infected with HIV, which is now called provirus.

g. Transcription & translation.

If activated, the provirus begins transcription of RNA copies of its genes. Some of these copies are used to
produce viral proteins that build the new virus, while others serve as new viral genomes that will be packaged
in those viruses.

h. Assembly stage.
When viral proteins are produced they are connected to each other like beads on a string. However, in order to
function correctly and build the new viral capsid they must be cut apart. This separation or cleavage is achieved
by the protease enzyme.
After separation occurs, the structural subunits of HIV mesh with the cell’s membrane and begin to deform a
section of the membrane. Through this process, the nucleocaspid is formed and wound tightly inside.

i. Budding.
During budding, this nucleocaspid merges with the deformed cell membrane to form the viral envelope.

j. Release & maturation.

The newly created viral particle is released from the cell, taking it with a piece of the cellular membrane that
how has gp120 and gp41 inserted to it.
The virus finishes protease processing of structural proteins and is ready to infect another cell.

3. Describe the pathophysiology and stages of HIV infection.

a) Incubation/primary infection period.

This stage is asymptomatic and lasts 2-4 weeks. The initial infection with HIV generally occurs after transfer of
body fluids from an infected person to an uninfected one.

b) Acute infection.
Primary HIV infection is followed by a burst of viremia in which virus is easily detected in peripheral blood in
mononuclear cells & plasma. 28 days after exposure to the virus, up to 70% of HIV infected persons suffer flu-
like symptoms like fever, swollen lymph nodes, sore throat, vash, myalgia and mouth sores.

c) Latency period.
The burst is followed by a replication at a lower level when the patient’s immune system fights back to
dramatically reduce HIV levels with killer T cells (CD*+T), which attack and kill infected cells that are
producing virus and B-cell produced antibodies.
HIV is active within lymphoid organs where large amounts of virus become trapped in the follicular dendritic
cells (FDC) network.
Surrounding cells may also become infected cells and as free virus. Results to massive stimulation of persons B
cells impairing the ability of these cells to make antibodies against other pathogens.

d) Aids stage.
Occurs when a significant number of CD4+ lymphocytes have been destroyed and when production of new
ones cannot match destruction.
When CD4+ members decline below a critical level of 200 cells per uL.
Cell mediated immunity is lost marking the appearance of clinical AIDS.
4. Give an account of how HIV affects an individual’s health.

-Macrophages are the first cells to be infected by HIV particle, they engulf the HIV particles and
display foreign antigen on the surface of their cell membrane to alert helper Tcells to the presence of
pathogens.
Cytokines with key roles in the regulation of normal immune function may be secreted in decreased
amounts during HIV infection.
Once infected, CD4+Tcells may leave the germinal centers and infect other CD4+Tcells that
congregate in the region of the lymph node surrounding the germinal center. Because HIV
preferentially infects a subset of T lymphocytes called helper T (TH) cell, they become depleted in
the patient.
This can subvert and decimate the immune system, leading to AIDS as HIV infection progresses.
Macrophages then serve as the source of HIV production when CD4+Tcells become depleted in the
patient.

5. Explain the mechanisms used by HIV to destroy host immunity and outline how HIV ultimately
evades host community.

A) Direct cell killing.

-CD4+Tcells may be killed directly when large amounts of virus are produced and bud off from the
cell surface, disrupting the cell membrane, or when viral proteins and nucleic acid collect inside the
cell, interfering with cellular machinery.

B) Syncytia formation.
-Infected cells also may fuse with nearby uninfected cells through CD4 mediated fusion, forming
balloon like giant cells called syncytia. This mechanism of cell-to-cell spread of HIV has been
associated with the death of uninfected cells. The presence of syncytia-inducing variants of HIV has
been correlated with rapid disease progression in HIV infected individuals.

C) Apoptosis.
-Infected CD4+T cells may be killed when cellular regulation is distorted by HIV proteins, probably
leading to their suicide by a process known as programmed cell death or apoptosis.
Uninfected cells also may undergo apoptosis.
Investigators have shown in cell cultures that the HIV envelope alone or bound to antibodies sends an
inappropriate signal to CD8+Tcells causing them to undergo apoptosis even though not
Infected by HIV.

D) Innocent bystanders.
-Uninfected cells may die in an innocent bystander scenario: HIV particles may bind to the cell
surface, giving them the appearance of an infected cell and marking them for destruction by killer
Tcells.