2. Introduction and Definitions
• HIV belongs to the family of viruses called
retroviridae and sub family lentivirus. Lentivirus
means slow because they take along time to produce
adverse effects in the body.
• HIV stands for Human immunodeficiency virus.
• AIDS stands for Acquired immune deficiency
syndrome.
3. History of HIV
• HIV/AIDS was first noticed by physicians and
epidimiologists in 1981 in the USA when a handful of
homosexual men presented with pneumocystis
carinii(PCP) and Kaposi’s sarcoma(KS). These diseases
were resistant to any form of treatment.
• These disease were particularly rare in young adults
and indicated that some kind of immune deficiency
in was occurring in gay men.
• The first full case description already showed a
selective depletion of CD4+ T helper lymphocyte in
peripheral blood.
4. • It was shortly noticed that a larger proportion of gay
men suffered from a common syndrome i.e a
generalised, extended lymphadenopathy. The
disease was initially called gay-related immuno
deficiency(GRID). By early 1982, however,
investigators at center for disease control and
prevention at Atlanta, USA, detected similar cases of
what is now called AIDS among injecting drug users,
sex workers and recipients of blood transfusion and
blood products. These epidemiological observations
were familiar to those working with hepatitis B virus
5. In the 1970s and led to the conclusion that AIDS was
not simply a consequence of the gay lifestyle but was
caused by infectious agent spreading both by sexual
and by parenteral transmission. Similar syndrome to
AIDS in USA were recorded in Haiti, Europe and
Africa.
• The earliest known positive blood sample was
collected in 1959 in Zaire(Congo)
6. Origin of HIV
• The origin of HIV to date is not clear and a constant
debate exist among scientist and so far no body has ever
come up with a conclusive proof of its origin.
• Currently there exist several theories that have
attempted to explain the origin of HIV.
• Human immuno deficiency virus bears close resemblence
to the Simian immunodeficiency virus which inffects
monkeys.
• It has been known that certain viruses can pass between
species of animals.
• When a viral transfer between animal and human takes
place it is known as zoonosis.
7.
8. • Here are some few common theories about
how this zoonosis took place and how SIV
became HIV in humans. These theories are
advanced to the origin of HIV
9. The hunters theory
• It is the most commonly accepted theory.
• It is claimed that the Simian Immunodeficiency
virus(SIV) was transferred to human by chimpanzees.
• It is well known in Africa that chimpanzees are
hunted and eaten for food. So this theory believes
that as a result of the hunting and handling
chimpanzees carcasses, their blood got into cuts or
wounds on the hunter.
• Normally the hunters body would have fought off
SIV, but on few occasions it adapted itself within its
10. New human host and become HIV-1.
• This theory is supported by the fact that there were
several early strains of HIV, each with at least
different genetic make-up (the most common was
HIV-1 group M).
• It is believed that every time SIV passed from a
chimpanzee to man, it developed in slightly different
strain.
• On few occasions, SIV adapted itself within its new
human host and become HIV.
11. • Therefore, it is believed that HIV-1 probably
transferred to humans from chimpanzees in central
Africa.
• And HIV-2 probably transferred to humans from the
sooty Mangabey monkey in west Africa.
12. The oral polio vaccine theory
• This theory states that the virus was transmitted via
various medical experiments (iatrogenically)
especially through the polio vaccine.
• This was especially thought to be through the oral
polio vaccine called Chat that was given to millions of
people in the Belgian Congo, Rwanda and Burundi in
the late 1950s.
• In order for the vaccine to be reproduced, it needed
to be cultivated in living tissue.
13. • It was believed that the vaccine was cultivated on
kidney cells taken from chimpanzees which were
infected with SIV.
• Thus the polio vaccine became contaminated with
Siv and later infected large number of people who
developed HIV.
• However, this theory was rejected when the
scientists who developed the CHAt vaccine proved
that the only kidney cells that were used were from
Macaque monkey kidney cells which do not get
infected with SIV
14. • Another reason to reject this theory is that HIV
existed in human long before the vaccine trials were
carried out.
15. The contaminated needle theory
• According to this theory, African healthcare
professionals were using one single syringe to inject
multiple patients without any sterilization in
between.
• This could have led to the rapid transfer of infection
from individual to another resulting into mutation
from SIV to HIV.
• This theory is an extension of the hunters theory.
16. The colonialism theory
• The colonial rule Africa was particularly harsh and the
locals were forced into labor camps where sanitation was
poor and food was scarce.
• It is believed that SIV could easily have infiltrated the
labor force and taken advantage of their weakened
immune systems.
• Laborers were also being inoculated with unsterilized
against diseases such as small pox to keep them alive and
working.
• Again many of the farms actively employed prostitutes to
17. keep the workers in a good thinking mood.
• All these factors have led to the transmission
and development of AIDS as a disease.
The conspiracy theory
• Many people, especially Africans believe that HIV
was manufactured in a laboratory i.e it is a man
made.
• A survey conducted in America by African Americans
found that they believe that the virus was
manufactured as part of a biological warfare
18. Programme, designed to wipe them out in large
numbers.
• While there is no evidence, it was however not been
accepted because there were no genetic engineering
technology at that time of emergence of AIDS.
19. TRANSMISSION OF HIV
• HIV is transmitted primarily through exposure to HIV
infected blood or exchange of HIV containing bodily
fluids.
• For infection to occur, the virus needs:
High enough concentration
An entry route
Efficient transmission
• HIV can only be transferred through
Sex route 70%
20. The blood route 20%
The mother to child route(congenital) 10%
BLOOD TO BLOOD TRANSMISSION
• This is through:
Transfusion of HIV infected blood or direct contact
with the blood.
Exposure to HIV contaminated needles, syringes and
other equipment.
Donated organs.
21. Mucous membrane splash.
Sharing sharp items like razor blade, tooth brush etc.
SEXUAL CONTACT
• Unprotected vaginal, Oral, or anal intercourse.
• Direct contact with HIV infected body fluids such as
semen and cervical and vaginal secretions.
22. Biological risk factors for sex route
• High viral load
• Being the receptive partner.
• Young female.
• Sex during menstration.
• Uncircumcized male.
• Damage to genital skin/ mucous membrane
• Having a sexual transmitted infection
• Having multiple sex partners.
23. Perinatal transmission
• Mother to child
transmission of HIV
during pregnancy, labor
and delivery.
• Mother to child
transmission of HIV
during breast feeding.
HIV CAN NOT BE
TRANSMITTED BY:
• Mosquito bites
• Coughing
• Kissing
• Sharing cups or cutlery
• Hugging.
• Shaking hands.
• Using the toilet.
• Using the telephone
25. • The genetic material of the HIV virus consist of
ribonucleic acid(RNA).
• The virus consist of two short strands of RNA with
enzyme reverse transcriptase, protease, ribonucease
and integrase.
• All these are encased in a membrane lined by a
matrix protein called viral envelop.
• Projecting from this viral envelope are 72 little spikes
which are formed from the protein gp120 and gp41.
26. • Glycoprotein(gp) 120 and gp41 are the specific
envelope glycoproteins.
• Gp 120 interact with CD4 receptors on the cell
surface.
• Gp 41 mediates the fusion of the viral envelope with
the cell membrane at the time of infection.
• P 24 is the group specific antigen located in the core
are important serologic markers of infection.
27. component Description
Glycoproteins gp120/gp41 Mediate entry into the cell
Core capsid P24 is the main protein of the capsid.
Within the capsid are two identical
single strands of RNA and viral
enzymes
Core viral enzymes Reverse transcriptase, protease,
intergrase
Reverse transcriptase Converts single stranded viral RNA
into double stranded viral DNA
Integrase Facilitates integration/ incorporation
of viral DNA into host DNA
protease Breaks down macro proteins into
smaller viral particles for assembly on
a new virus
28. 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 intial infection
and illness is longer than in the case of HIV-1.
• Globally the predominant virus is HIV-1, and
generally when people refer to HIV without
specifying the type they will be referring to HIV-1.
29. SUBTYPES OF HIV-1
• The strains of HIV-1 can be classified into four groups
• The major group M
• The outlier group O
• And two new groups, N and P
• These four groups may represent four separate
introduction to immunodeficiency virus into humans.
• Group O appears to be restricted to western and
central Africa and group N-a strain discovered in
1998 in Cameroon-is extremely rare.
30. • In 2009 a new strain closely relating to gorilla SIV was
discovered in a Cameroonian woman. It was
designated HIV-1 group P
• More than 90% of HIV infections belongs to HIV-1.
• These are the subtypes A, B, C, D, F, G, H,J and K
31.
32. Life cycle of HIV
• Why is understanding the life cycle of HIV important?
• The life cycle of HIV helps to know how antiretroviral
drugs work.
• Here are the phase involved in the HIV life cycle.
• Binding
• Fusion
• Entry
• Uncoating
• Reverse transcription
33. • Integration
• Transcription or replication
• Assembly and budding
• Maturation
BINDING
• HIV infects host cell by binding to the CD4 receptor.
• CD4 is present on the surface of many lymphocytes,
which are important part of the immune body’s
system.
34. • Binding is mediated by the glycoprotein gp120 which
binds to the CD4 receptor molecule.
• Recent evidence indicates that a co-receptor is
needed for HIV to enter the cell.
• Following gp120-CD4 binding, a conformational
change occurs in the gp120.
• It then binds a co-receptor on the cell surface: a
chemokine receptor, either CCR5 or CXCR4.
35. Fusion
• Viral binding to the host cell triggers fusion of the
viral membrane to host membrane.
• Fusion is mediated by glycoprotein41, and allows
entry of the viral core into the host cell.
• This is thought to result in further conformational
changes in gp120 that expose the gp41 protein.
• This protein mediates fusion of the viral and cell
membranes.
36.
37. Uncoating
• This the process by which viral core capsid is
dissolved to release free viral RNA and viral enzymes.
• The dissolution of the capsid is achieved by the
proteoytic enzymes in the host cell cytoplasm.
• Viral enzymes released include RT, integrase,
protease and RNAse-H.
38. ENTRY
• Once the membranes of the virus and host cell are
fused, an open channels is established through which
the viral core can enter into the host cell
39.
40. REVERSE TRANSCRIPTION
• Once the viral RNA and viral enzymes are released
free into the host cytoplasm, the single stranded RNA
is converted to double stranded DNA.
• The conversion is catalysed by the enzyme reverse
transcriptase.
41.
42. INTEGRATION
• Once the genetic material of HIV has been changed
into DNA, this viral DNA enters the host cell nucleus
where it can be integrated into the genetic material
of the cell.
• The enzyme integrease catalyses this process.
• If the viral DNA is integrated into the genetic material
of the host, HIV may persist in a latent state for many
years.
• This ability of HIV to persist in certain latently
infected cells is the major barrier to eradication or
43. cure of HIV.
• For this reason, based on current knowledge,
patients must remain on anti-viral therapy for life.
44. TRANSCRIPTION OR REPLICATION
• After replication, the HIV virus turns the host cell into
a machine for producing more viruses.
• Synthesis of viral messenger RNA(mRNA) occurs.
mRNA leaves the nucleus as a complex multi-protein
molecules and enters the cytoplasm where it is
cleaved by the protease enzyme to produce less
complex viral proteins (core, envelope, and
regulatory proteins) and enzymes essential for HIV
replication
45. Assembly and budding
• The cleaved simple proteins then assemble
into functional groups at the cell membrane and
bud out of the host cell taking away with them part
of the cell membrane to form the viral membrane.
This explain why the viral membrane is said to be
similar to the host cell membrane.
46. MATURATION
• The newly produced immature viruses are non-
infectious.
• Immature virions are unable to infect other cells.
• Maturation involves the viral enzyme protease which
further structures the viral miro-proteins into
functional proteins.
• Viral particles are then infectious.
49. EFFECT OF HIV ON IMMUNE SYSTEM
• If the immune system is without the T helper cell, the
other cells of the immune system are at a loss.
• HIV attacks cells that express the CD4 receptors.
These cells are:
Microglia cells in the brain.
T-lymphocytes-CD4+cells.
Macrophages
Monocytes
Dendritic cells
50. • The halmark of HIV/AIDS is profound depletion of
CD4+ T lymphocytes.
• The CD4 T cell depletion is twofold:
1. Reduction in numbers
2. Impairment in function.
• HIV infection leads to low levels of CD4+T cells
through 3 main mechanisms:
1. Increased rate of apottosis(cell suicide) in infected
cells
2. Direct killing of infected cells
51. 3 Killing of infected CD4+ T cells by the CD8 cytotoxic
lymphocytes that recognize and eliminate infected
cells.
• When CD4+ T cell numbers decline below a critical
level, cell mediated immunity is lost, and the body
losses its ability to fight infectious diseases and
becomes progressively more susceptible to
opportunist infections.
52. HOW HIV AFFECTS ONES LIFE
• CD4 cell is kind of
white blood cell
which a friend to the
body
• Infection like cough,
diarrhoe try to attack
the body but CD4
fights them back.
• Then HIV enters and
starts to attack CD4
• CD4 can not defend
itself against HIV
53. • Later CD4 looses its
force against HIV
• CD4 losses the fight
and the body remains
without defense.
• When the body is left
lone without defense,
all kinds diseases like
cough and diarrhoea
take advantage and
starts to attack the
body
• At the end the body is
weak that all diseases
can attack without
difficulty.
54. PHASES OF HIV/AIDS
1. Infection
2. Window period
3. Seroconversion
4. Asymptomtic period
5. HIV/AIDS related illness
6. AIDS
55. Window period
• The window period is term used to describe the time
between infection and the production of
antibodies.Duration: approximately three months.
• No syndrome
• HIV test is negative( serlogical)
• Virus is multiplying rapidly-viral load is high
• Person is very infectious
56. seroconversion
• A point at which HIV test becomes positive
• Body starts making antibodies to HIV a few weeks
after infection
• HIV test become positive when Ab levels are high
enough to be measured.
• Happens about three months after infection.
• A person may have mild flu-like illness, lasting a week
or two.
• Afterwards a person is well again
57. Asymptomatic period
• Period between seroconversion and onset of
HIV/AIDS-related illness.
• Duration variable: 1 year to 15 years.
• Most people remain healthy(asymptomatic) for
about 3 years. Duration may depend on socio –
economic factors.
• The CD4 count is above 500cell/µl
58. CD4 COUNTS
• Number of CD4 cells in blood provides a measure of
immune system damage.
• CD4 count reflects phase of disease.
• CD4 count:
• 500-1200 normal
• 200-500 beginning of HIV illness
• <200; AIDS
59. HIV RELATED ILLNESS
• Period between onset of illness & diagnosis of AIDS.
• Duration is variable: Average about 5 years.
• Illness initially mild, with gradual increase in
frequency and severity
• CD4 count is between 500-200 cells/µl
AIDS
• It is the final phase of HIV/AIDS
• Duration: without antiretroviral drugs, less than 2
years
60. • CD4 count is less than 200 cells/µl
• Viral loads are high & the person is infectious.
• Serological ICT HIV test become negative.
PURPOSE FOR TESTING HIV
• To identify asymtomatic individuals.
• To diagnose HIV infection in those who practice high
risk behavior.
• To prevent secondary transmission.
• Donor screening for blood and tissue products
61. • For prophylaxis, medical mangement and treatment.
• For epidemiological survailance.
• To diagnose clinically suspected cases.
Laboratory diagnosis of HIV infection
• Direct demonstration of infective agent
Virus isolation
Antigen detection-p24 detection
Viral nucleic acid detection-PCR
62. • Indirect demonstration of infective agent
Ant-HIV antibody detection
• HIV antibody tests are the most appropriate test for
routine diagnosis of HIV among adults.
• Antibody tests are cheap and very accurate.
• Specimen to be collected for antibody detection are
whole blood, serum, plasma, saliva, urine
63. Test to detect HIV antibodies
• Screening tests(ELISA, rapid)
ELISA (2-3 hours)
Rapid tests (minutes)
• DBS(dry blood assays)
• Particle agglutination
• HIV spot tests simple(1/2 hour) based on ELISA
principle.
64. HOW DO Ab TEST WORK
• When a person is infected with HIV, the body respond by
producing Abs.
• An HIV Ab test looks for these Abs in blood, saliva or
urine.
• If Abs to HIV are detected, it means a person has the
virus.
• There are only two exception to this rule/test.
• Babies born to HIV infected mothers retain their
mother’s Abs for upto 18 months, which means they may
test positive on HIV Ab test, even if they actually HIV
negative.
65. • Some people who have taken part in HIV vaccine trials
may have HIV Abs even if they are not infected with HIV
virus.
• Therefore the presence of HIV infection during the first
month after infection and in babies born to HIV positive
mothers are not detected by Ab tests but by either viral
culture, P24 Ag test, western blot or PCR assay.
• Most people develop detectable HIV antibodies within 6-
12 weeks of infection.
• In very rare cases, it can take up to 6 months and are
66. nearly always very particular reason for Ab
developing so late as other auto-immune disorder.
• It is exceedingly unlikely that someone would take
longer than 6 months to develop antibodies.
67. PREVENTION OF HIV INFECTION
1. Prevention of sexual transmission
• A-abstain from sexual intercourse
• B-be faithful to one uninfected partner
• C-use condom correctly and consistently
2 Prevention of blood transmission
• Avoid sharing sharps like needle, razors,etc
• Testing blood for HIV before transfusion
• Prevention of mother to child transmission
