Human Immunodeficiency
Virus
Infection
Dr.T.V.Rao MD
Dr.T.V.Rao MD
1
Beginning of HIV/AIDS
• The first published article related to
AIDS was in 1981. The principal
author’s 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.
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2
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
lymphadenopathy-associated virus or LAV.
About a year later, Dr. Robert Gallo, of the
National Cancer institute discovered HLTV-III.
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
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23, 1984.
Dr. Luc Montagnier wins the
Nobel Prize in Medicine in 2008
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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
Dr.T.V.Rao MD
body’s immune response.
6
History of HIV
• The HIV virus first came to light during the
early 1980’s.
• A number of healthy gay men in New York
began to develop rare opportunistic
infections & cancers, that were resistant to
treatment.
• One such viral opportunistic infection is
cytomegalovirus that causes blindness &
Dr.T.V.Rao
MD
inflammation of the
colon
7
HIV Origins
• Research teams in the U.S.A & France made
independent research discoveries of the virus.
• French researchers discovered a virus linked to
AIDS in 1983, they called it LymphadenopathyAssociated Virus (LAV)
• In 1984, American researchers isolated a virus
that caused AIDS, calling it Human T-lymph
tropic Virus type III (HTLV- III )
• These two viruses were later found to be the
same virus - HIV Dr.T.V.Rao MD
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HIV Origin
• The emergence of HIV & AIDS has resulted
in countless debates as to where it originated
from
• It’s suspected that it originated from S.I.V
(Simian Immunodeficiency Virus)
• SIV affects Monkeys
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HIV Origins
• Certain strains of SIV closely resemble the two types of
HIV
• HIV 1 – was difficult to link with SIV
• In 1999 SIVcpz closely related to HIV 1
• Originated from chimpanzees but it has significant
differences from HIV-1
• HIV 2 closely related to SIVsm
• Originated from the green monkey
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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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Retroviral Genes
• gag (group-specific antigen): makes the
cone shape viral capsid.
• pol (polymerase): codes for viral enzymes
reverse transcriptase, integrase, and viral
protease.
• env (envelope): makes surface protein
gp120 and trans membrane gp41,
enabling HIV to fuse to CD4 cells.
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Genes Coding Structural
Proteins
gag
• 1 The gag gene –
core and shell
expressed as p55 – (
p18,- p17) cleaved as
p15, p18,and p24
make up as viral core
and shell
• p24 seen during early
stages reappearance in
the late stages
exacerbation of disease
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Envelop glycoprotein's
env
• The env determines the synthesizes
of envelop glycoprotein's gp160
cleaved into two envelop components
gp120 which forms the surface spike
and gp 41 which trans membrane
protein.
The gp120 antibodies are present till
the death of the patient.
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Polymerase reverse
transcriptase
pol
• The pol gene codes
for the polymerase
reverse transcriptase
and other viral
enzymes
• Expressed as
precursor protein
which is cleaved into
proteins p31, p51,and
p66
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
Genome and Proteins of
HIV
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Other genes
• Tat
The Tran activator gene influences the function of genes
some distance away. It controls transactivation of all HIV
proteins.
rev
• The differential regulator of expression of virus protein
genes.
vif
• The virus infectivity factor gene is required for infectivity
as cell-free virus.
nef
• The negative regulator factor retards HIV replication.
vpr
• The virus protein R gene has an undetermined function..
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Genes differ HIV I for HIV II
• vpu
• The virus protein U gene is required for
efficient viral replication and release. It is
found only in HIV-1.
vpx
• The virus protein X gene has an
undetermined function. It is found only in
HIV-2 and SIV.
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Types of HIV
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Subtype C is Major type in India
• Subtype C is
predominant in
Southern and East
Africa, India and
Nepal. It has caused
the world's worst HIV
epidemics and is
responsible for
around half of all
infections.
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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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HIV Replication
– Attachment
– Penetration
– Uncoating
– Reverse Transcription
– Integration
– Replication
– Assembly
– Release
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Life Cycle of HIV
1. Attachment: Virus binds to surface
molecule (CD4) of T helper cells and
macrophages.
• Coreceptors: Required for HIV infection.
• CXCR4 and CCR5 mutants are resistant to
infection.
2. Fusion: Viral envelope fuses with cell
membrane, releasing contents into the
cell.
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HIV Life Cycle: Attachment Requires CD4
Receptor plus a Coreceptor
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• The HIV receptor
• Gp160 is composed of gp41 and gp120 and forms
the receptor for binding to the host cell (CD4
positive cells).
• The gp41 portion is half embedded in the
membrane envelope and interacts with gp120
portion on the exterior side of the membrane.
• Each receptor is composed of 3 subunits of gp41
and 3 subunits of gp120.
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The HIV Receptor
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Lifecycle of HIV

HIV particles enter the body in a fluid as it can not
survive without a support medium.

The virus targets any cell expressing CD4, including T
helper cells, macrophages, dendritic cells and
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monocytes.
29
Life Cycle of HIV
3. Reverse Transcription: Viral RNA
is converted into DNA by unique
enzyme reverse transcriptase.
Reverse transcriptase
RNA ---------------------> DNA
Reverse transcriptase is the
target of several HIV drugs: AZT,
ddI, and ddC.
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Infection spread throughout the
Body
• Within the inflammatory cells of the infection (T
cells)
• Site of replication shifts to lymphoid tissues:
• Lymph nodes
• Spleen
• Liver
• Bone marrow
• Macrophages and Langerhans cells become
reservoirs and sites of replication but do not die
themselves.
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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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2.Host’s immune responses
• Both humoral and cell-mediated immune responses
partially control the viral production but in this process
they destroy the infected CD4+T cells, leading to a
gradual decline of CD4+ T cells
• HIV-specific CTLs kill infected CD4+ T cells
• Antibodies that recognize a variety of HIV antigens are
produced
Antibody
dependent
cell-mediated
cytotoxicity
• Apoptosis of infected cells
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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
Dr.T.V.Rao MD
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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Window Period
• This is the period of time after becoming
infected when an HIV test is negative
• 90 percent of cases test positive within
three months of exposure
• 10 percent of cases test positive within
three to six months of exposure
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Pathogenesis of HIV / AIDS
Infected T-Cell
HIV
Virus
T-Cell
HIV Infected
T-Cell
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New HIV
Virus
42
• Immune responses fail to eradicate all viruses.
• Viral load is maintained at low level
• Continuous decline of CD4+ T cells
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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.
MD
• An inability to trap Ag orDr.T.V.Rao
support
activation of T+B cells
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CDC Classification of HIV
• Category 1: > 500 cells/mm3 (or CD4% > 28%)
• Category 2: 200-499 cells/mm3 (or CD4% 14%-28%)
• Category 3: < 200 cells/mm3 (or CD4% < 14%)
• (CD4+ T-lymphocyte counts per microliter of blood)
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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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WHO clinical case definition for
AIDS in South-East Asia
• WHO clinical case definition for AIDS in South-East
Asia
Clinical AIDS in an adult is defined as an individual who
has been identified as meeting the two criteria A and B
below:
A. Positive test for HIV infection by two tests based on
preferably two different antigens.
B. Any one of the following criteria:
• - Weight loss of 10% body weight or cachexia, not
known to be due to a condition unrelated to HIV infection
- Chronic diarrhoea of one month's duration, intermittent
or constant
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WHO clinical case definition for
AIDS in South-East Asia
• Disseminated, miliary or extra pulmonary
tuberculosis
• Candidiasis of the oesophagus;
diagnosable as dysphasia, odynophagia
and oral Candidiasis
• Neurological impairment restricting daily
activities, not known to be due to a
condition unrelated to HIV (e.g. trauma)
• Kaposi's sarcoma.
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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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Progression to AIDS
• During the latency period, lymph nodes and the spleen are
sites of continuous HIV replication and cell destruction.
• The immune system remains competent at handling most
infections with opportunistic microbes but the number of
CD4+ T cells steadily declines.
Symptoms often experienced months to years before the onset
of AIDS.
• Lack of energy
• Weight loss
• Frequent fevers and sweats
• Persistent or frequent yeast infections
• Persistent skin rashes
• Dysfunction of CNS
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Progression to AIDS
• Final stage of HIV infection - AIDS
• Occurs when the destruction of peripheral lymphoid tissue
is complete and the blood CD4+ T cell count drops below
200 cells/mm3. (Healthy adults usually have CD4+ T-cell
counts of 1,000 or more).
• AIDS – acquired immunodeficiency syndrome – is marked
by development of various opportunistic infections and
malignancies.
• The level of virus in the blood and CD4+ T cell count can
predict the risk of developing AIDS. Voral titers often
accelerate as the patient progresses towards AIDS.
• Without treatment, at least 50% of people infected with
HIV will develop AIDS within
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MD years.
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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
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THE NATIONAL HIV TESTING POLICY
• No individual should be made to undergo a
mandatory testing for HIV
• No mandatory HIV testing should be imposed
as a precondition for
- Employment
- Providing health care services and facilities
• Any HIV testing must be accompanied by a
pretest and posttest counseling services
(through VCTC)
• Testing without consent – hindrance to the
control of the epidemic
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Counseling
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•
•
•
•
Pre-test Counseling explain to
individuals
Transmission
Prevention
Risk Factors
Voluntary &
Confidential
• Report ability of
Positive Test
Results
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Post-test Counseling
• Clarifies test
results
• Need for
additional testing
• Promotion of safe
behavior
• Release of results
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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
Repeat
Positive
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
Dr.T.V.Rao MD
Positive
Indeterminate
Repeat at
3 weeks
Run IFA
Confirmation
Negative
Repeat at
2-4 months
Positive
HIV
64
+
Diagnosis of HIV
• Positive or indeterminate ELISA tests for anti-HIV
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 mothers65
Dr.T.V.Rao MD
Indirect ELISA test
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Western blot Test
• Confirms HIV infection
• Proteins are separated by electrophoresis
and transferred to a nitrocellulose
membrane by the passage of an electric
current
• The proteins are treated with antibodies
• Similar to ELISA technique, addition of
secondary antibodies with an enzyme
attached allows the use of colour to detect
a particular protein
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Western Blotting
• A discrete protein band represents the
specific antigen that the antibody recognizes
• The bands from a positive Western blot are
from antibodies binding to specific proteins
and glycoprotein's from the HIV virus
• The CDC recommends that the blot should be
positive for two of the p24, gp41 and
gp120/160 markers (gp160 is the precursor
form of gp41 and gp120, the envelope protein)
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HIV Western blot
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Rapid Tests
• ADVANTAGES:
• quicker to perform
– do not require batching
– do not require specialised equipment or
trained personnel
– results delivered on the same day
• Only ‘WHO recommended’ Rapid HIV antibody tests
should be used to ensure quality.
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The ‘Window period’
Aware of it
Follows acute infection with HIV, before HIV
antibodies can be detected in the patient’s
blood stream.
• Patient is highly infectious, despite testing
HIV antibody negative, HIV is replicating
rapidly in all body compartments.
• Typically up to 12 weeks duration but may
be shorter in more sensitive HIV antibody
assays.
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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
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infection
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 76
Dr.T.V.Rao MD
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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HIV Occupational Exposure
• Review facility policy and report the incident
• Medical follow-up is necessary to determine
the exposure risk and course of treatment
• Baseline and follow-up HIV testing
• Four week course of medication initiated
one to two hours after exposure
• AZT (200mg)-TID
+lamivudine(3TC)(150mg)BID x 4days
• Nelfinavir (750 mg) TID ,AZT/3TC
• Exposure precautions
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MD
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HIV Non-Occupational
Exposure
PREVENTION --- FIRST
•
•
•
No data exists on the efficacy of antiretroviral
medication after non-occupational exposures
The health care provider and patient may
decide to use antiretroviral therapy after
weighing the risks and benefits
Antiretroviral should not be used for those
with low-risk transmissions or exposures
occurring more than 72 hours after exposure
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Play safe
• Use the
common sense
Be faithful to
one partner,
Use Condom.
• Antiretroviral
drugs
• Caesarean
delivery
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Abstinence
• It is the only 100 %
effective method of
not acquiring
HIV/AIDS.
• Refraining from
sexual contact:
oral, anal, or
vaginal.
• Refraining from
intravenous drug Dr.T.V.Rao MD
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Monogamous relationship
• A mutually monogamous (only one sex partner)
relationship with a person who is not infected
with HIV
• HIV testing before intercourse is necessary to
prove your partner is not infected
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Sex Education – Best option to Prevent
AIDS
Move from Past to Future
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World AIDS Day,
• World AIDS Day, observed December 1
each year, is dedicated to raising
awareness of the AIDS pandemic caused
by the spread of HIV infection. It is
common to hold memorials to honour
persons who have died from HIV/AIDS on
this day. Government and health officials
also observe the event, often with
speeches or forums on the AIDS topics.
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Do not Discriminate AIDS
Patients
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• Created by Dr.T.V.Rao MD for
Medical and Paramedical
Students in the Developing
World
• Email
• doctortvrao@gmail.com
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