Human

Immunodeficiency Virus
(HIV)

Mohammad Al-Rawashdeh
545th course

Beginning of HIV/AIDS
The first published article related to AIDS
was in 1981. The principal authors name
was Michael Gottlieb and it appeared in
the Morbidity and Mortality Weekly Report
for June 5th. This article reported that
there was a random increase in
pneumocystis carinii pneumonia (PCP), a
rare lung infection.

Discovery of HIV infection.

In 1982, the term Acquired Immune Deficiency
Syndrome is used for the first time. The name was
designated by the CDC.
In 1983, French scientists at the Institute Pasteur found
a new virus that they called lymphadenopathyassociated virus or LAV. About a year later, Dr. Robert
Gallo, of the National Cancer institute discovered HLTVIII. The first discovery was made in France at the
Institute Pasteur, but shared credit is given to Dr. Robert
Gallo, the discoverer of AIDS and his French
counterparts for discovering HIV on April 23, 1984.

What is Human Immune

Deficiency Virus
Genus Retroviridae
Lentivirus, which literally means slow virus - it
takes such a long time to develop adverse
effects in the body.
This virus attacks the immune system
There are two strains HIV 1 & HIV 2
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What is Human Immune

Deficiency Virus
These contain RNA, the genetic material of HIV
The outer layer of the HIV virus cell is covered in
coat proteins, which can bind to certain WBCs. This
allows the virus to enter the cell, where it alters the
DNA.
The virus infects and destroys the CD4 lymphocytes
which are critical to the bodys immune response.

Family : Retroviridae
Subfamily : Lentivirus
RNA virus, 120nm in
diameter
Envelope gp160; gp120 &
gp41
Icosahedral symmetry
Nucelocapsid
Outer matrix protein (p17)
Major capsid protein (p24)
Nuclear protein (p7)

Diploid RNA with several

copies of reverse
transcriptase
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Types of HIV

Resistance
The virus are inactivated in 10 minutes at 600c and in
seconds at 1000c
At room temperature survive for seven days
HIV are inactivated in 10 minutes by treatment with 50%
ethanol
35% Isopropanol.
0.5% Lysol and paraformaldehyde
0.3% hydrogen
10% house hold bleach
Hypochlorite solution at 0.5%
2% Glutaraldehyde
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Effects of HIV on the immune system

3 areas:
1. Destruction of CD4+ T cells
population
2. Immune effects due to HIV infection
3. Progression of HIV infection to AIDS

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Blood and Body fluids contain High

concentration of Viral particles
Blood
Semen/Vaginal
fluids (as high
as blood)
Breast milk
Pus from sores

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Low concentrations of HIV

It is highly unlikely you will be infected if

you come into contact with:
Sweat
Tears
Urine
Saliva (-highly possible if blood from
mouth sores is present)

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High Risk Populations:

1. Males, homosexuals & bisexuals
2. IV drug users
3. Improperly screened transfusion
recipients
4. Sexual partners of persons infected
with HIV
5. Infants of HIV infected mothers

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How is HIV Spread?

ANY type of sexual activity (highest risk)

Sharing used drug needles
Pregnancy-from mother to child
Sharing razors- if blood is present
Kissing- if even the smallest amount of
blood is present. (-membranes of mouth
are thin enough for HIV to enter straight
into the body.)
Tattoos/body piercing if equipment is not
clean.
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HIV in Body Fluids

Blood
18,000

Semen
11,000

Vaginal
Fluid
7,000

Amniotic
Fluid
4,000

Saliva
1

Average number of HIV particles in 1 ml of these body fluids

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Transmission
Vaginal Intercourse
Anal Intercourse (10x higher infection rate than
vaginal intercourse because of tissue tear is
higher
Oral Intercourse
Blood Transfusion (risk greater than 90% if
sample is already infected)
Needles (tattoos, injections)
Infected mother to the infant through:
Pregnancy (placenta), Birth, and breastfeeding

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Pathogenesis of HIV / AIDS

Infected T-Cell

HIV
Virus

T-Cell

HIV Infected
T-Cell

New HIV
Virus

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Immune defects due to HIV infection

B cells impaired humoral response

B-cell hyper reactivity

Polyclonal hypergammaglobulinemia due to enhanced nonspecific IgG and IgA production.
Impaired Ab-isotype switching and inability to respond to specific antigen.
High incidence of B-cell lymphomas

Lymph nodes

HIV kills cells in the lymph nodes

Early HIV infection: destruction of dendritic cells
Late stage: extensive damage, tissue necrosis, a loss of follicular dendritic cells and
germinal centres.
An inability to trap Ag or support activation of T+B cells

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Progression of HIV infection

After initial infection with
HIV, there is usually an
acute flu-like illness.
This illness may include
Fever
Headache
Tiredness
Enlarged lymph nodes

But after this most

individuals are clinically
asymptomatic for years.
This is called the clinical
latency period.

Exposure to
HIV
normal
Acute HIV disease

Immune competence

Progression of HIV infection

Slightly
reduced

Clinical latency period

-declining CD4+ T cell amount

Abnormal

AIDS

Opportunistic
infections

Severely
impaired

Time

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Stage 1 - Primary
Short, flu-like illness - occurs one to six
weeks after infection
no symptoms at all
Infected person can infect other people

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Stage 2 Asymptomatic

Lasts for an average of ten years

This stage is free from symptoms
There may be swollen glands
The level of HIV in the blood drops to very
low levels
HIV antibodies are detectable in the blood

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Stage 3 - Symptomatic
The symptoms are mild
The immune system deteriorates
Emergence of opportunistic infections and
cancers

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Stage 4 - HIV AIDS

The immune
system weakens
The illnesses
become more
severe leading to
an AIDS
diagnosis

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Mother-to-Baby
Before Birth
During Birth
Postpartum
After the birth

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How is HIV not spread?

Shaking hands
Hugging
Swimming pools
Toilet seats
Insect bites
Donating blood

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Three types of tests

(i) Screening tests - ELISA and simple/rapid tests.
(ii) Confirmatory or supplemental testsWestern Blot assay.
(iii) Nucleic acid and antigen screening tests.
Polymerase chain reaction (PCR), Ligase chain
reaction (LCR), Nucleic acid based Sequence assays
(NASBA) and some ELISA tests.

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Diagnosis of HIV
Initial test for HIV is an indirect ELISA test
Economic, rapid, performed easily, high
sensitivity and specificity
Detects anti-HIV antibodies in patient serum
Antibodies are generally detectable within 3
months of infection
Antibodies are typically directed at the
envelope glycoproteins (gp120 and gp41)

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Absence of Antibodies to do not

confirm absence of HIV infection
Absence of antibody, as in window period
does not exclude the presence of the virus
which can be detected by PCR amplification
approx. ten days after infection
Window period time between infection and
detection of serological viral marker
Direct ELISA for p24 antigen can also be
used although the false negative rate is
higher

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HIV Testing
EIA/ELISA
Test
Positive

Negative
No HIV Exposure
Low Risk

HIV Exposure
High Risk
Negative

Repeat ELISA
Every 3 months
for 1 year
Repeat every
6 months for continued
High risk behavior

End Testing

Negative

Repeat
Positive

Positive

Indeterminate
Repeat at
3 weeks

Run IFA
Confirmation

Negative
Repeat at
2-4 months

Positive

HIV
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Diagnosis of HIV
Positive or indeterminate ELISA tests for antiHIV antibodies are confirmed by immunoblotting
(Western Blotting) which identifies specific HIV
virus proteins
PCR can also be used
Detects pro-viral DNA or viral RNA

It is highly sensitive and specific but is more

costly than ELISA

Can be used to test infants born to HIV-infected

mothers
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Paediatric HIV Testing

Infants born to HIV infected mothers will have
antibodies to HIV in their serum as a result of:
maternal-fetal transfer during pregnancy
delivery
breast-feeding

they may not necessarily be infected !

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Treatment of HIV

Eradication of HIV infection not possible with currently available drugs

Viral replication can not be completely suppressed
Latently infected CD4+ T cells established at early stage
Goals of antiretroviral therapy are to:
- Suppress viral replication
- Restore and/or preserve immune function
- Improve quality of life
- Reduce HIV-associated morbidity and mortality
Combinations of antiretroviral drugs are used
Referred to as HAART (highly active antiretroviral therapy)
Suppress levels of plasma viraemia for long periods
Plasma viraemia is a strong prognostic factor in HIV infection
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Antiretroviral Drugs
Significant declines in AIDS related morbidity and mortality
are seen as a result of HAART
Several strategies for development of effective antiviral
drugs
Potential therapies based on knowledge of the way in
which HIV gains access into the cells and its method of
replication
Targets for therapeutic anti-retroviral drugs:
- Inhibiting reverse transcription
- Inhibiting proteases
- Inhibiting integrate interferes with integration of viral
DNA into host genome
- Inhibiting fusion prevents virus from fusing with host cell
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Therapeutic Options
Combination of RT inhibitors protease inhibitors
results in potent anti-viral activity
In most cases, two nucleoside analogues and one
protease inhibitor are taken together
HAART lowers plasma viral loads in many cases to
levels not detectable by current methods
Has improved the health of AIDS patients to the
point that they can function at a normal level
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AIDS (Pregnancy & AIDS)

Zidovudine(AZT) recommended for px of
maternal fetal HIV transmission & adm after 14mg
AOG (PO meds); IVIT during labor; w/ neonate
post birth for 6 wks.
Postpartum monitor for s/of infxn place mother in
isolation if mother is immune suppressed.
-restrict breastfeeding infant/neonate is seen by
physician at birth, 1 wk. or 2 wks., a mos., 2 mos.,
& 4 mos. of life
* Neonate- asymptomatic for 1st several yrs. Of life &
monitored for early sign of immunodeficiency

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Antiretroviral Drugs
Nucleoside Reverse Transcriptase
inhibitors
AZT (Zidovudine)

Non-Nucleoside Transcriptase inhibitors

Viramune (Nevirapine)

Protease inhibitors
Norvir (Ritonavir)

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Prevention and control of

HIV
Education
Prevention of blood born HIV
transmission
Anti Retro Viral treatment
Combination therapy
Post exposure prophylaxis
Specific prophylaxis
Primary health care
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Sex Education Best option to Prevent

AIDS
Move from Past to Future

Dr.T.V.Rao MD

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