TOPIC 1

MEANING OF HIV AND AIDS AND RELATED CONCEPTS

Section 1: Conceptualization of HIV and AIDS and related terms

It is important to understand the following terminologies/concepts that are important for the
study of this module:

a)​ HIV - Human Immune Virus

This is a virus that causes AIDS and is passed from person to person through body fluids,
particularly blood, semen and breast milk. After a person has been infected, the virus starts
breaking down their immune system. After sometime the immune system is so weak that they
become susceptive to a variety of illness.

b)​ AIDS – Acquired Immune Deficiency Syndrome

This is a cluster of medical conditions often referred to as opportunistic infections resulting from
infection by HIV virus and the eventual weakening of the body’s immune system. With time, the
immune system deteriorate as the HIV multiplies and destroys the CD4 cells and consequently
the person develops AIDS.

H-(Human) the virus can only survive in human body and can be traced in fresh human
blood outside the body.

Acquired-obtain-can only get this virus from someone else, thus acquired through
unprotected sex [semen (cum), pre-seminal fluid (pre-cum), vaginal fluid] or direct blood
contact with a person who is HIV – positive. These are blood, and breast milk.

Immune-Against infection

Deficiency- Lack of natural protection (With time – total lack of immunity)

Syndrome- A collection of many diseases/infections (syndrome means a group of

symptoms).

●​ As Virus multiples, many immune cells are destroyed, many infections and complications
occur.
●​ Complications are referred to as opportunistic infections because they take advantage of
lowered immunity.
 ●​ A collection of signs and symptoms caused by infections and other implications arising
from HIV infection is referred to as AIDS.

c)​ Epidemic
An epidemic is the occurrence in excess of normal of an illness, health event or health related
behavior that occur in a specific place or among a group e.g. AIDS.

d)​ Endemic
A disease always in the area e.g. malaria in Nyanza.

e)​ Pandemic
A disease that affects persons over a wide geographical area i.e. extensively epidemic e.g.
Nairobi, Nyanza and Coast province incidence.

The number of new cases of a disease in a population over a period of time. It measures the
frequency of additional of new cases of a disease.

f)​ Epidemiology​​
It is a study of distribution and determinants of health related states and events in specified
populations and the application of this study to the control of health problems.

It Involves:

●​ Observing, counting cases, relating cases to the population at risk, making comparisons,
making scientific references, developing hypothesis, testing hypothesis, experimenting
and intervening and evaluating World from 2004 reports.
●​ HIV the 4th commonest killer
●​ 40 million people living with HIV AIDS (note that new cases keep on being reported)
●​ 2/3 in Sub-Saharan Africa.
●​ Majority of HIV/AIDS patients are in the age group 15-49 years
●​ 50% are mothers of reproductive age
●​ 2.1m children less than 15 years are HIV infected.
●​ Mother to child transmission responsible for 90% childhood infections.

For example in Kenya

●​ 2.2 million HIV positive (note that new cases keep on being reported)
●​ Age expectancy 62-46 years
 ●​ 50%-70% medical wards in government hospitals HIV related.
●​ High death rate -500 death daily
●​ Adult infection 1.1M
●​ Women twice more likely to be infected than men [8.5-4.5]
●​ Peak age prevalence 25-29 years female 35-44 male.

Western Kenya

●​ Kakamega 9%
●​ AIDS first recognized in 1981.
●​ NB Incidence & prevalence.

g)​ Virology
Virus:

●​ Small submicroscopic biological entity which lack cellular organization (i.e. Plasma
membrane and metabolic machinery).
●​ They possess their own genetic material, genetically determined macromolecular
organization and characteristic mode of inheritance.
●​ For multiplication they require hosts cells i.e. obligate parasite.
●​ A retrovirus from a viral genus called (Retrovidae family) Lent virus.

Is a virus that is:

●​ Capable of self-reproduction.
●​ Can breath
●​ Moves independently
●​ Consumes and processes nutrients

SECTION 2: Types and sub-types of HIV

There are two types of HIV: HIV-1 and HIV-2. Both types are transmitted by sexual contact,
through blood, and from mother to child, and they appear to cause clinically indistinguishable
AIDS. However, it seems that HIV-2 is less easily transmitted, and the period between initial
infection and illness is longer in the case of HIV-2.

Worldwide, the predominant virus is HIV-1. The relatively uncommon HIV-2 type is
concentrated in West Africa and is rarely found elsewhere.

a)​ Subtypes of HIV 1

The strains of HIV-1 can be classified into three groups: the "major" group M, the "outlier"
group O and the "new" group N. These three groups may represent three separate introductions
of simian immunodeficiency virus into humans.

Group O appears to be restricted to west-central Africa and group N - discovered in 1998 in

Cameroon - is extremely rare. More than 90% of HIV-1 infections belong to HIV-1 group M.

Within group M there are known to be at least nine genetically distinct subtypes (or clades) of
HIV-1. These are subtypes A, B, C, D, F, G, H, J and K.

Occasionally, two viruses of different subtypes can meet in the cell of an infected person and mix
together their genetic material to create a new hybrid virus (a process similar to sexual
reproduction). Many of these new strains do not survive for long, but those which infect more
than one person are known as "circulating recombinant forms" or CRFs. For example, the CRF
A/B is a mixture of subtypes A and B.

The classification of HIV strains into subtypes and CRFs is a complex issue and the definitions
are subject to change as new discoveries are made. Some scientists talk about subtypes A1, A2,
A3, F1 and F2 instead of A and F, though others regard the former as sub-subtypes.

b)​ What about subtypes E and I?

One of the CRFs is called A/E because it is thought to have resulted from hybridization between
subtype A and some other "parent" subtype E. However, no-one has ever found a pure form of
subtype E. Confusingly, many people still refer to the CRF A/E as "subtype E" (in fact it is most
correctly called CRF01_AE).

A virus isolated in Cyprus was originally placed in a new subtype I, before being reclassified as a
recombinant form A/G/I. It is now thought that this virus represents an even more complex CRF
comprised of subtypes A, G, H, K and unclassified regions. The designation "I" is no longer
used.

c)​ Where are the different subtypes and CRFs found?

The HIV-1 subtypes and CRFs are very unevenly distributed throughout the world, with the most
widespread being subtypes B and C.

Subtype C is largely predominant in southern and eastern Africa, India and Nepal. It has caused
the world's worst HIV epidemics and is responsible for around half of all infections.

Historically, subtype B has been the most common subtype/CRF in Europe, the Americas, Japan
and Australia. Although this remains the case, other subtypes are becoming more frequent and
now account for at least 25% of new infections in Europe.
Subtype A and CRF A/G predominate in west and central Africa, with subtype A possibly also
causing much of the Russian epidemic. Subtype D is generally limited to east and central Africa;
A/E is prevalent in south-east Asia, but originated in central Africa; F has been found in central
Africa, South America and Eastern Europe; G and A/G have been observed in western and
eastern Africa and central Europe.

Subtype H has only been found in central Africa; J only in Central America; and K only in the
Democratic Republic of Congo and Cameroon.

d)​ Are more subtypes likely to ‘appear’?

It is almost certain that new HIV genetic subtypes and CRFs will be discovered in the future, and
indeed that new ones will develop as virus recombination and mutation continue to occur. The
current subtypes and CRFs will also continue to spread to new areas as the global epidemic
continues.

e)​ The implications of variability differences in transmission

It has been observed that certain subtypes/CRFs are predominantly associated with specific
modes of transmission. In particular, subtype B is spread mostly by homosexual contact and
intravenous drug use (essentially via blood), while subtype C and CRF A/E tend to fuel
heterosexual epidemics (via a mucosal route).

Whether there are biological causes for the observed differences in transmission routes remains
the subject of debate. Some scientists, such as Dr. Max Essex of Harvard, believe such causes do
exist. Among their claims are that subtype C and CRF A/E are transmitted much more efficiently
during heterosexual sex than subtype B. However, this theory has not been conclusively proven.

More recent studies have looked for variation between subtypes in rates of mother-to-child
transmission. It has been claimed that such transmission is more common with subtype D than
subtype A9, and that subtype C is more often transmitted than either D or A10.

f)​ Is it possible to be infected more than once?

Until about 1994, it was generally thought that individuals do not become infected with multiple
distinct HIV-1 strains. Since then, many cases of people co-infected with two or more strains
have been documented.

All cases of coinfection were once assumed to be the result of people being exposed to the
different strains more or less simultaneously, before their immune systems had had a chance to
react. However, it is now thought that "superinfection" is also occurring. In these cases, the
second infection occurred several months after the first. It would appear that the body's immune
response to the first virus is sometimes not enough to prevent infection with a second strain,
especially with a virus belonging to a different subtype. It is not yet known how commonly
superinfection occurs, or whether it can take place only in special circumstances.

g)​ Do HIV antibody tests detect all types, groups and subtypes?

Initial tests for HIV are usually conducted using the EIA (or ELISA) antibody test or a rapid
antibody test.

EIA tests which can detect either one or both types of HIV have been available for a number of
years. According to the US Centers for Disease Control and Prevention (CDC), current HIV-1
EIAs "can accurately identify infections with nearly all non-B subtypes and many infections with
group O HIV subtypes." However, because HIV-2 and group O infections are extremely rare in
most countries, routine screening programs might not be designed to test for them. Anyone who
believes they may have contracted HIV-2, HIV-1 group O or one of the rarer subtypes of group
M should seek expert advice.

Rapid tests - which can produce a result in less than an hour - are becoming increasingly popular.
Most modern rapid HIV-1 tests are capable of detecting all the major subtypes of group M. Rapid
tests which can detect HIV-2 are also now available.

h)​ What are the treatment implications?

Most current HIV-1 antiretroviral drug regimens were designed for use against subtype B, and so
hypothetically might not be equally effective in Africa or Asia where other strains are more
common. At present, there is no compelling evidence that subtypes differ in their sensitivity to
antiretroviral drugs. However, some subtypes may occasionally be more likely to develop
resistance to certain drugs. In some situations, the types of mutations associated with resistance
may vary.

The effectiveness of HIV-1 treatment is monitored using viral load tests. It has been
demonstrated that some such tests are sensitive only to subtype B and can produce a significant
underestimate of viral load if used to process other strains. The latest tests do claim to produce
accurate results for most Group M subtypes, though not necessarily for Group O. It is important
that health workers and patients are aware of the subtype/CRF they are testing for and of the
limitations of the test they are applying.

Not all of the drugs used to treat HIV-1 infection are as effective against HIV-2. In particular,
HIV-2 has a natural resistance to NNRTI antiretroviral drugs and they are therefore not
recommended. As yet there is no FDA-licensed viral load test for HIV-2 and those designed for
HIV-1 are not reliable for monitoring the other type. Instead, response to treatment may be
monitored by following CD4+ T-cell counts and indicators of immune system deterioration.
More research and clinical experience is needed to determine the most effective treatment for
HIV-2.

i)​ What are the implications for an AIDS vaccine?

The development of an AIDS vaccine is affected by the range of virus subtypes as well as by the
wide variety of human populations who need protection and who differ, for example, in their
genetic make-up and their routes of exposure to HIV. In particular, the occurrence of
superinfection indicates that an immune response triggered by a vaccine to prevent infection by
one strain of HIV may not protect against all other strains. The effectiveness of a vaccine is
likely to vary in different populations unless some innovative method is developed which guards
against many virus strains.

Inevitably, different types of candidate vaccines will have to be tested against various viral
strains in multiple vaccine trials, conducted in both high-income and developing countries.

a)​ What is the difference between HIV-1 and HIV-2?

SECTION 4: The Structure and Life Cycle of HIV

How does HIV evade the immune system so efficiently? Why are so many variants of the virus
found in a single patient? Understanding the structure and life cycle of the virus is key to
answering these questions and essential to the design of effective treatments. ​
a) The structure of HIV

●​ HIV is an enveloped RNA virus: As HIV buds out of the host cell during replication, it
acquires a phospholipid envelope. Protruding from the envelope are peg-like structures
that the viral RNA encodes. Each peg consists of three or four gp41 glycoproteins (the
stem), capped with three or four gp120 glycoproteins. Inside the envelope the
bullet-shaped nucleocapsid of the virus is composed of protein, and surrounds two single
strands of RNA. Three enzymes important to the virus's life cycle - reverse
transcriptase, integrase, and protease – are also within the nucleocapsid.​
​
Although helper T cells seem to be the main target for HIV, other cells can become
infected as well. These include monocytes and macrophages, which can hold large
numbers of viruses within themselves without being killed. Some T cells harbor similar
reservoirs of the virus. ​
​
Entry of HIV into the host cell requires the binding of one or more gp120 molecules on
the virus to CD4 molecules on the host cell's surface. Binding to a second receptor is also
required. Two different coreceptors are involved in the binding. One, CCR5, a
chemokine receptor, serves as a coreceptor early in an infection. Another chemokine
receptor (CXCR4) later serves as a coreceptor. Once introduced in Human blood stream,
the virus particle circulates through the body and only infect CD4 cells (WBC).
Mac phages and T- cells have CD4 receptor. Macrophages have another receptor CCR 5
which HIV uses to pull itself across the cell membrane.
Once inside the cells, the HIV sheds its protective coat. The virus RNA float in the
cytoplasm with a virus enzyme reverse transcriptase (it synthesizes a double strand of
DNA compliment to the virus RNA (makes mistakes often hence mutations)
The double stranded DNA directs the host cell machinery to reproduce many copies the
virus.
The new viruses are released from the cell by exocytosis
.​

The replication cycle of

HIV

HIV is a member of the group of viruses known as retroviruses, which share a unique life cycle
once HIV binds to a host cell, the viral envelope fuses with the cell membrane, and the virus's
RNA and enzymes enter the cytoplasm. HIV, like other retroviruses, contains an enzyme called
reverse transcriptase. This allows the single-stranded RNA of the virus to be copied and
double-stranded DNA (dsDNA) to be generated. The enzyme integrase then facilitates the
integration of this viral DNA into the cellular chromosome. Provirus (HIV DNA) is replicated
along with the chromosome when the cell divides. The integration of provirus into the host DNA
provides the latency that enables the virus to evade host responses so effectively. ​
​
Production of viral proteins and RNA takes place when the provirus is transcribed. Viral proteins

b) Progression of HIV Infection

Characteristically, an HIV infection can progress for eight to ten years before the clinical syndrome
(AIDS) occurs. The long latent period of the virus has contributed to many of the problems relating
to diagnosis and control. On the other hand, not all cases exhibit the long latent period, and abrupt
progression to AIDS occurs. Many factors, including genetics, determine the speed at which the
disease will progress in a given individual.
Typical progression of HIV infection and AIDS

The Centers for Disease Control and Prevention (CDC) has identified the stages of a typical HIV
infection: Categories A, B, and C. In the first stage, Category A, it can be difficult to determine
whether an individual is infected without performing a blood test. While at least half of infected
individuals will develop a mononucleosis-like illness (headache, muscle ache, sore throat, fever,
and swollen lymph nodes) within three weeks of exposure, some Category A individuals are
asymptomatic. Moreover, the symptoms themselves can be the result of many different infections.
The presence of a rash may help differentiate an HIV infection from other infections, but not all
HIV-infected individuals get a rash. Most of these signs and symptoms subside, but swollen lymph
glands and malaise can persist for years through Category A HIV. ​
​
The number of virus particles circulating in the bloodstream is usually highest soon after exposure.
At this point the CD4 cell population plunges (helper T cells are among the immune cells that
express the CD4 receptor, which can be used as a marker for counting cell types). As antibodies to
HIV appear the numbers of CD4 cells rise; however, CD4 cell levels drop again as the infection
progresses. This lowering of CD4 cell levels typically happens slowly, over the course of years.
Category C HIV (clinical AIDS) occurs once CD4 numbers have fallen substantially (to
200/mm3 from the normal level of 800-1200 cells/ mm3).

In the Category B stage indications of immune system failure begin. Persistent infections - such as
yeast infections, shingles, diarrhea, and certain cancerous conditions of the cervix - are apparent. ​
​
Category C is synonymous with AIDS. In this stage the opportunistic infections associated with
AIDS appear. According to the CDC, twenty-six known clinical conditions affect people with
AIDS; most are infections that do not usually affect healthy individuals. These include yeast
infections of the esophagus, bronchi, and lungs; Pneumocystis pneumonia (a fungal infection);
toxoplasmosis (caused by a protozoan that is spread by cats); Kaposi's sarcoma (a rare cancer of the
skin caused by a virus); cytomegalovirus (CMV) infections; and tuberculosis. In addition,
individuals who have been affected by HIV are more likely to become seriously ill or die than other
members of the population during outbreaks of infections such as cryptosporidium (a water-borne
parasite) and coccidiomycosis (a dust-borne fungus). ​
​
Cytomegalovirus (CMV) causes another opportunistic infection prevalent in AIDS patients. About
eighty percent of people in the U.S. have antibodies to this virus, but infections in normal
individuals often go undetected or seem like a mild case of mononucleosis. In the
immunocompromised, however, CMV can cause life-threatening pneumonia or encephalitis. In
AIDS patients CMV that has been latent can reactivate and sometimes cause retinitis, affecting
eyesight. ​
​
Tuberculosis (caused by Mycobacterium tuberculosis) has been on the rise in the wake of AIDS,
such that some call it a co-epidemic. M. tuberculosiscauses a respiratory infection (formerly called
consumption) that is spread by inhalation. As a result, unlike HIV, behavior modification is less
likely to reduce one's chances of exposure. The bacteria, which have an unusually waxy cell wall,
survive well in the environment. M. tuberculosis reproduces inside macrophages found in the lung,
and stimulates the production of aggregates of immune cells and connective tissue, called tubercles.
Viable organisms can be walled off within such structures for decades, only to become reactivated
when a person becomes compromised. Most tuberculosis in AIDS patients results from reactivated
infections. AIDS patients suffer not only from respiratory infection but also from disseminated
tuberculosis, which can involve the lymphatic system, peritoneum, meninges, urogenital system, or
digestive tract. Antibiotic-resistant mycobacteria are also contributing to the rise of tuberculosis, so
that second- and third-line drugs must often be used. And because treatments are prolonged, lasting
as long as a year, patients sometimes do not complete therapy appropriately. Mycobacteria other
than M. tuberculosis, particularly M. avium-intracellulare (MAC), also affect AIDS patients. ​
​
c) Why Do Some Individuals Never Get AIDS?

Despite repeated exposure, some individuals never become infected with HIV. These individuals
often have unusual helper T cells with a less-efficient variant of the coreceptor CCR5, which is
necessary for viral entry into helper T cells. ​
​
There are also individuals who become infected, but do not progress to AIDS. These long-term
survivors, or long-term non-progressors, include individuals who have been AIDS-free as long as
eighteen years after infection. A variety of factors may be responsible; for example, infection with
less-virulent viruses. Some long-term non-progressors seem to have CD8 cells, which are
particularly adept at curtailing HIV infection. (In most AIDS patients CD8 cells become less
active.) ​
​
d) Genetic variation among HIV

There are five major subtypes of HIV, designated A through E. Different subtypes predominate in
different geographical areas. For example, subtype B is more common in North America. In
contrast, subtype C predominates in sub-Saharan Africa. Considerable variation within a given
subtype also exists. In fact, any given individual infected with HIV will harbor multiple variants of
the virus. HIV makes many mistakes as is copies its viral RNA to the DNA that integrates into the
host's chromosome. Because of its sloppy copying of reverse transcriptase, HIV's mutation rate is
high, causing great variability. This large number of variants makes the virus more difficult to treat
and hinders vaccine development. In addition, because of its rapid rate of evolution, even within a
single individual, HIV can quickly evolve resistance to the drugs the individual is taking to combat
the virus.

e) Genetic Directory

RNA DNA
Has oxygen No oxygen
Single strand Double strand
Uravit base Thiamine

Genetic material

Photosphate {nucleotide sugar}

●​ Adenine
●​ Cytosine
●​ Quinine
 ●​ Uracil
●​ Thiamine

f) Disease stages

Stage 1

●​ Acute viral infection

●​ Incubation period of 1 – 3 weeks
●​ Fever, headache
●​ Sore throat
●​ Meningitis
●​ Hepatosplenopathy
●​ Hymphademophathy
●​ Encephalitis rash which appears as small pink purple or maculae or much of the body

Stage 2

●​ Asymptomatic
●​ Lasts for 6 years
●​ Large amount of HIV antibodies
●​ HIV detected in blood, semen, cervical secretaries
●​ CD4+ cells disappear from the blood
●​ HIV into blood

Stage 3

●​ Overt disease
●​ Severity directly related to the decline of CD4+ cells, macrophages and natural killer
(NK) cells that lead to opportunistic infections

g) HIV Diagnosis

●​ Common protocols used are serological or antibody based enzyme linked immune
absorbent assay (ELISA)
●​ Western blot
●​ Immunofluorescence
●​ Agglutination
●​ Virion RNA RT – PCR
●​ CDU:CD8 T cell ration
●​ Isolation and culture of virus
ELISA

HIV antibody test do not measure or detect virus but the presence of antibodies to HIV

●​ Work for antibody specific for gp120 or gp160 (4 – 8w post exposure)

●​ Very sensitive for detecting HIV antibodies

h) Phase and stages of HIV

1.​ Stages of HIV

NB Natural Progression of HIV
Viral transmission
​ Being infected (2 - 3 weeks)

Acute retroviral syndrome

(The body reacts and develops flu like illness which go away after a few weeks)

​ 2 -3 weeks

Recovery and sero conversion

(Body produces antibodies to fight the infection which then slows up in the Antibody tests)

​ 2- 4 weeks

Asymptomatic chronic HIV infection

(Body can stay well and healthy for a long period: 2 – 12 years)
​

​ Average of 8 years

Symptomatic HIV infection/AIDS

(The body immunity becomes weak and opportunistic infections start occurring with more
frequency. Having certain infection and a low CD4 count indicates a diagnosis of AIDS)

​ ​ Average 1 year – 4 months

DEATHS
2.​ Phase 1
-​ HIV present in blood but laboratory tests can’t detect it at the first 6 months
-​ Phase divided into stages:
-​ Entry stage – when the virus enters the body
-​ Window period – no sign of infection
– HIV can’t be detected by blood screening
-​ Transmission occurs

Phase 2
-​ HIV antibodies detected in blood
-​ No signs or symptoms for several years’ i.e HIV positive stage
-​ Serocouversion stage: Virus present in large quantities to produce an immune response –
antibody production
-​ Asymptomatic seropostive stage: Virus concentration high but the person infected shows
no signs unless tested

Phase 3 AIDS stage

-​ AIDS related illness stage

-​ Signs/Symptoms as diarrhea, weight loss, weakness and fatigue, loss of appetite, fever,
night sweats, patient capable of taking care of themselves

Phase 4 Full-Blown AIDS Stage

-​ Person shows pronounced and more frequent signs/symptoms

-​ Treatment (Therapy) of HIV infection
-​ It is not possible to eradicate HIV injection currently but treatment to suppress the virus
is important. Hence antiretroviral treatment (ARV)
-​ ARV – drugs that impair reproduction of the virus in the blood and limit amount damage
to the immune system.
-​ They don’t eliminate the virus thus can’t cure
-​ They suppress viral load – restore and present immunologic function
-​ Impair quality of life
-​ Reduce – HIV – related morbidity and mortality.
-​ Highly Active Antiretroviral Therapy (HAART) led to durable antiviral response. It
suppresses viral replication and halts damage to the immune system leading to partial
restoration of immune function hence fewer opportunistic infections and longer life for
the patient.
-​ Several classes of antiretroviral drugs i.e. Nucleotides-analog reverse transcriptase
inhibitor (NRTI), Non-nucleoside reverse transcriptase (NNRTIS) and protease inhibitors
(PIS)
 -​ NRTIS inhibits HIV’s reverse transcriptase by uncooperative into the DNA of the virus
hence prevent multiplication of the virus e.g. Zidovudine, Didanosine, Zalcitabine,
Starlidine etc
-​ NNRTI stops HIV production by building directly onto reverse transcriptase inhibitor
preventing conversion of RNA to DNA e.g. Nevirapine and Delavirdine.
-​ Protease inhibitors work at the last stage of virus reproduction cycle by preventing HIV
from being successfully assembled (inhibit retroviral protease from clearing the viral
protein) should not be used alone because HIV quickly becomes resistant. E.g. Saquinor,
Ritonir, Indinavir and Nelfinavir
-​ Fusion inhibitors
e.g. Enjuvirticle, Pentafuside,Fuzeona, a 36 amono acid, peptide that mimic one section
of gp 41. It inhibits virion-host cell fusion
gp 41. Is important in getting virion onto host cell should not be used alone.
-​ ARV helps those with moderate or severe symptoms of HIV infection or AIDS.
-​ Should be used in combination for patients who have the following:
i)​ Advanced HIV
ii)​ Low CD4 + cell count
iii)​ High viral load
2​ NRTIs + NNRTI or 2 NRTIs + IPIs

h)​ STDs/STIs
Caused by bacteria or viruses

Sexually transmitted diseases/infections (STDs/STIs) are a group of disease/infections whose

predominant modes of transmission is sexual intercourse

e.g . Syphilis

Caused by Bacteria Treponoma Pallidum

Stage primary syphilis

●​ Painless genital ulcers that may go away

●​ Highly infectious

Secondary

●​ 2 - 3 months later
●​ Rash on hand and feet, sore throat, sore in mouth
●​ Flat warts on genitalia
●​ Transmission through kissing
Tertiary

●​ Year later
●​ Large ulcer on the skin
●​ Brain damage
●​ Heart failure
●​ Non-infectious

Transmission – sexually or skin conduct with someone in an infectious stage

There is a high correlation between HIV and STIs.

Gonorrhea

●​ More prevalent
●​ Caused by bacteria Neisseria gonorrhea
●​ Transmitted through sexual intercourse or sexual contacts where body fluids are
exchanged (oral, anal intercourse)
●​ Infects throat, cervix, urethra, rectum
●​ Can spread to eye and internal organs causing conjunctivitis – severe eye infection)
●​ Left untreated can cause pelvic inflammatory disease (PID) a condition where fallopian
tubes become scarred and blocked – sterility.

Chlamydia

●​ Silent STD
●​ Caused by bacteria Chlamydia trachromatis
●​ Has both bacterial and viral characteristics
●​ Bacteria – susceptible to antibiotics
●​ Viral – depend on host to replicated its genetic material

Transmission – vaginal, anal or oral intercourse with infected person

Women dont experience symptoms until the infections is established

●​ Caused PID – sterility

●​ Painful urination
●​ Painful intercourse
●​ Vaginal discharge
●​ Irregular virginal bleeding
●​ Infection of cervix increases risk HIV infection in men
 ●​ Watery discharge from penis
●​ Burning or itching around urethra

i)​ Disease prevention and nutrition

Balanced diet important for health and provides nutrients. (Water Ch2O, Protein, fats, vitamins
and mineral salts)

-​ Requirements for :
-​ Energy production (CH2O, fats)
-​ Maintain water balance within the body
-​ Synthesis of complex molecules
-​ Cell building, growth and repair (protein)

A balanced diet contains all nutrients required for health in appropriate proportion.

Food

-​ Enable the immune system to work at its best

-​ Provide body with all the essential nutrients
-​ Maintain weight
-​ Improve strength and energy
-​ Prevent illness

NB:

Bread, rice, cereal and pasta – Energy giving food

Fruits and vegetables - Vitamins

Meat, fish - Proteins

Dairy products, milk cheese, minerals

Oils + fats – energy

Proteins – Growth and repair of cells and tissues

Synthesis of enzymes plasma proteins, antibodies hormones

Energy

Fats – chemical energy and heat

 -​ Transport and storage of fats soluble vitamins A,D,E,K
-​ Constituents of nerve sheath
-​ Storage of energy in a dipose tissue under skin
Vitamins – chemical compounds required in very small quantities
-​ Fat soluble – A D E & K
-​ H2O soluble – B complex
Mineral salts
-​ Health infections

NB:

-​ Eat more fresh foods and fruits

-​ Eat less cooking fat and less field foods
-​ Avoid alcohol and street drugs
-​ Flush system by drinking and clean H2O daily
Assignment

There is a widely held assertion among developing countries that there is ‘unfair distribution of
HIV infections and its impact worldwide’ discuss this assertion either agreeing or disagreeing
with examples from developing country of your choice. ​ ​ ​ (30 marks)
 TOPIC 2

THEORIES EXPLAINING ORIGIN OF HIV AND AIDS

Section 1:

a)​ Chimpanzee Theory

​ Commonly but still controversially believed that HIV evolved from primates’ (Chimps.)
SIMIAN Immunodeficiency Virus-SIV.
​ This latter changed form to HIV-1 and transferred to humans (Bailer et al,2003)
​ Actual place of transfer is also very controversial.
​ Commonly suggested is The African continent, South Cameroon forests and Congo DRC
(Annabel K. and associate, 2006).This fact is refuted by Ogot, B. 2004).

b)​ The Hunter’s Theory

​ Commonly accepted that SIV was transferred to the human hunter who killed and ate the
Chimp or got its blood into himself through cuts or wounds during a bloody hunt.
​ SIV adapted itself to the human body through a process of zoonosis (viral transfer process
between animals and human ) and hence changed to HIV-1
Transfer of SIV-HIV

​ At the 7th Conference on Retroviruses and Opportunistic Infections-OI, in Jan 2000, it is

indicated that the 1st HIV case was as early as 1930 in West Africa (Karber, B. et al.,
2006).
​ An article in the Lancet in 2004 also shows that retroviral transfer from primates to
human hunters still goes on even today as studies carried out in Cameroon (Simian
Foamy Virus-SFV) have indicated through the butchering and consumption of monkey
meat.
​ It explains the continuous evolution and appearance of the many strains of HIV

c)​ Political conspiracy Theory

​ Conspiracy theory to wipe out blacks and homosexuals in USA under the auspices of
the Federal Special Cancer, Virus (SCVP) and CIA
 ​ Ogot, B. 2004 has modified and extended it to the Kenya Government denial
conspiracy-(Homicide) between 1984 (the Kenyan 1st diagnosed case of HIV) and
2003.This refusal to accept HIV and AIDS epidemic in Kenya just to save the tourist
industry and avert international political stigma only helped enhance the spread of the
disease in Kenya without early intervention.

d)​ The Colonialism Theory (Heart of Darkness Theory)

​ Recent theory in the debate, based on the hunter’s theory and explains how the original
infection could have led to the epidemic. (1st proposed by Jim Moore-2000- website,
http://www.avert.org/origins.htm).
​ Suggest that in many colonial forced labour camps in French Equatorial Africa and in
Belgium Congo, were employed prostitutes to keep workers happy hence possibility for
onward transmission aggravated by poverty and disease ridden conditions.

e)​ The Oral Polio Vaccine-OPV (Chat)

​ Berry, N.J., Zhu T. and Blancon, P. in Kanabus, A. (2006) have been the proponents of
this theory which is still very controversial.
​ They contend that HIV was transferred iatrogenically (via medical experiments) through
some contaminated polio vaccine which caused many vaccine recipients to be infected
with HIV worldwide. (highly refuted )
​ The use of contaminated needles in the 1950s may have facilitated the monkey-to- human
transfer.

f)​ The Blood Industry (for transfusion)

​ A medical practice created a rising demand for purchase of donated blood in the USA in
the 1970s and 80s.
​ So, blood was donated for money especially by Intravenous drug users-IDU who badly
needed the money.
​ The HIV was passed to unsuspecting blood recipients worldwide.

g)​ Hemophiliacs and Factor 8

 ​ Factor 8 ,a blood coagulant is manufactured from pooled blood from hundreds of
individuals, some of whom had HIV virus. This put many hemophiliacs around the world
at risk of HIV transmission.
​ Following the Middle East and other human conflicts IDU increased especially in the
1970s. (The heroine revolution)

h)​ Ex Caelo Theory (Extraterrestrial-beyond earth)

​ The Comet Theory( one ex caelo sense,); that gas from a tail of a passing comet reached
earth and caused HIV infection
​ The 2nd ex caelo sense that HIV is a catastrophic event arising from the wrath of God to
the sinful people (promiscuous, homosexuals in rel. texts)
​ It is also an outcome of curses; chira

i)​ Patient Zero hypothesis

Could be defined in two ways;

​ 1st global/local such as 1st case in USA thought to be a gay Canadian flight attendant
known as Gaetan Dugas who willfully spread HIV to multiple sex partners and
eventually died of AIDS
​ In Kenya patient zero recorded at Kenyatta National hospital was in fact a Ugandan
national (Ogot, B., 2004)
So, patient zero may not necessarily explain the 1st HIV case.

African HIV Vulnerability (Kelly W. 2006)