This document discusses population genetics and ecology. It presents information from a group consisting of 8 members studying how HIV affects the body. HIV attacks CD4 cells, making the body more susceptible to other infections. When the CD4 count drops below 200, AIDS develops. The document also discusses how some individuals carry a mutation, CCR5Δ32, that protects against HIV infection by preventing the virus from entering cells. Understanding this resistance could lead to new treatments. An example calculation of allelic frequencies in a sample French population in Britain is also provided.

1. POPULATION GENETICS AND ECOLOGY
PRESENTATION
GROUP FOUR
Members Index number
• COFFIE BAIDOO RABBI UE20015317
• BUABENG ISAAC KOJO UE20015117
• DARKWAH JEPHTER UE20015717
• BALASU DELIGHT UE20014417
• BOATENG DAVID UE20014817
• BABAE THEOPHILUS UE20014217
• BRUCE BELINDAASIEDUA UE20015017
• DADEBOE VANESSA OHUI UE20014217

2. HOW DOES HIV-1 AFFECT THE BODY?
The human immunodeficiency virus is a lentivirus that causes HIV
infection and over time acquired immunodeficiency syndrome.
HIV attacks a specific type of immune system cell in the body. It is
known as the CD4 helper cell or T cell. The CD4 cell(cluster of
differentiation 4) is a glycoprotein found on the surface of immune
cells such as T helper cells, monocytes, macrophages and dendritic
cells.

3. When HIV destroy this cells, it becomes harder for the body to
fight other infections. When HIV is left untreated even a minor
infection such as cold can be much more severe because the body
has difficulty responding to new infections.
HIV does not only attack CD4 cells, it also uses the cells to make
more of the virus. HIV destroy CD4 cells by using their
replication machine to create new copies of the virus and this
causes the CD4 cells to swell and burst.
When the virus has destroyed a certain number of CD4 cells, the
CD4 count drop below 200(the normal CD4 count ranges from
approximately 500 to 1,600 cells/mm3 in healthy adults) then a
person will progress to have AIDS.

4. CERTAIN INDIVIDUALS CARRY A MUTATION
PROTECTING THEM AGAINST HIV, DISCUSS.
Some years ago, 1% descended from Northern Europeans,
particularly Swedes, were immune to HIV infection. These lucky
people are homozygous carriers of a mutated gene meaning that
they inherited a copy from both of their parents.
Just one copy of the gene does not prevent against the infection.
Hence the mutation has not been found in Africans, East Asians,
or Amerindians (NATIVE AMERICANS).

5. A genetic mutation known as CCR5Δ32 is responsible for HIV
resistance that exist. CCR5Δ32 hampers HIV ability to infilterate
immune cells.
Note; CCR5 stands for C-C Chemokine receptor type 5.
The mutations causes the CCR5 co-receptor on the outside of the
cells to develop smaller than usual and no longer sit outside of
the cell.
The CCR5 co-receptor is like the door that allows HIV entrance
into the cell. The CCR5Δ32 mutation in a sense locks the door
which prevents HIV from entering into the cell.

6. CCR5Δ32 is exciting. It present possibilities for new ways to
protect against HIV. There are some genetic test available to
see if one has the mutation. But it is not yet widespread.
The mutation is not completely full proof.

7. Cases of homozygous carrier that have become infected
with HIV have been reported.
These few exceptions have dissuaded health officials
from fully supporting genetic test over ethical concerns.
It would not be wise for those with the mutation to
assume that they can lead a dangerous lifestyle and
remain healthy.
Understanding why and how certain people are resistant
to HIV with the help of CCR5Δ32 will hopefully lead to
a new and highly successful treatments in our lifetime.

8. Consider a sample population of 100 French individuals
in Britain. Among this group 79 individuals had
genotype +/+, 20 had +/Δ32 and 1 had a genotype of
Δ32/Δ32, what are the possible allelic frequencies?
• +/+ normal allele of the gene
• Δ32/Δ32 mutant
• +/Δ32 heterozygote

9. SOLUTION
Given that;
Total population = 100
Individuals with normal allele of the gene (+/+) = 79
Individuals that carries the mutant gene (Δ32/Δ32) = 1
Heterozygous individuals of the gene (+/Δ32) = 20
To solve for the allelic frequency of +/+
= (+/+) x 2 + (+/Δ32) / (total population x 2)
= (79 x 2) + 20 / (100 x 2)
= 158 + 20 / 200
= 178 / 200
= 0.89

10. To solve for the allelic frequency of Δ32/Δ32
= (Δ32/Δ32) x 2 + (+/Δ32) / 200
= (1 x 2) + 20 / 200
= 22 / 200
= 0.11
From Hardy-Weinberg equation;
The sum of all tree genotypes is p2 + 2pq +q2 = 1
LET;
• The probability of forming an +/+ zygote = p2
• The probability of forming an Δ32/Δ32 zygote = q2
• The probability of forming an +/Δ32 zygote = (p x q) + (q x p)
• = pq + qp
• = 2pq

11. Substitute the values of p and q into the equation,
= p2 + 2pq + q2
= (0.89)2 + 2(0.89 x0.11) + (0.11)2
= 0.7921 + 0.1958 + 0.0121
= 1.
(note; the probability of 1 means certainty, and every
individual must be one of the three genotypes)
References;
Dotinga , R. “Genetic HIV Resistance Deciphered” Wired. January 7, 2005
Evolution. Double Immunity (2001).
Novembre, J., Galvani, A., and Slatkin, M. The Geographic Spread of the CCR5 Δ32
HIV Resistance Allele. PLOS Biology (2004)
Biology, BURTON S. GUTTMAN