THE BASIC INFORMATION ABOUT WHAT IS HIV AND HOW IT DESTRUCT THE IMMUNE SYSTEM. THEN LEADS TO AIDS. PRESENTATION ALSO EXPLAINS THE DIAGNOSIS OF HIV, ITS TREATMENT WHY WE DONT HAVE VACCINE FOR HIV AND WHAT ARE THE PRESENT SCENARIO OF VACCINE DEVELOPMENT.. I HOPE IT WILL EXPLAIN WELL ABOUT HIV INFECTION AND AIDS, MAY PROVE USEFUL FOR YOU GUYS.....

1. Human Immunodeficiency Virus
BY:
MANISH DHAWAN

2. INTRODUCTION
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Family: Retroviridae
Genus: Lentiviridae
Disease that HIV causes, AIDS was first
reported in the U.S. in 1981 in L.A. and New
York
Causative agent discovered and
characterized by Luc Montagnier of France
and Robert Gallo of the US in 1983-84.
Retrovirus having:
Reverse transcriptase

3. 
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Antigenic strains : HIV-1 and HIV-2
HIV-1(virulent strain) is most prominent in
U.S., Canada and Europe
HIV-2 (less virulent) common in certain
parts of West Africa, it is closely related to
simian immunodeficiency virus (SIV)
found in monkey
HIV-1 differs significantly from HIV-2/SIV.

4. structure
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Each virion expresses 72
glycoprotein projections composed
of gp120 and gp41
The viral envelope derives from the
host cell and contains some hostcell membrane proteins, including
class I and class II MHC molecules
Within the envelope is the viral
core, or nucleocapsid, which
includes a layer of a protein called
p17 and an inner layer of a protein
called p24.
Genome consists of two copies of
single-stranded RNA, which are
associated with two molecules of
reverse transcriptase (p64) and
nucleoid proteins p10, a protease,
and p32, an integrase.

5. 
Electron micrograph of HIV virions magnified
200,000 times. The glycoprotein projections are
faintly visible as “knobs” extending from the
periphery of each virion.

6. Genome of HIV-1
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Structural genes
gag :- Group specific antigen,
pol :- Reverse transcriptase, Protease
and Integrase,
env :- Envelope glycoprotein (gp).

7. 
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Genes essential for viral replication:
tat :- activates transcription,
rev :- export of unspliced and singly
spliced mRNAs from nucleus,
LTR sequence:- promoter and enhancer
elements
Genes not essential for viral replication:vif :- promotes maturation and infectivity
nef (negative factor) :- Down-regulates
Host-cell class I MHC and CD4
vpr , vpx and vpu

8. Stability
Inactivation By :
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Heat
a) Autoclave
b) hot air oven
Glutaraldehyde 2%
Hypochlorite 10,000 ppm : 1 in 10 dilution of domestic
bleach
Other disinfectants, including alcohols .
Survival of HIV :


Virus may survive for up to 15 days at room temperature.
At 37º C virus can survive for 10-15 days.
Over 60º C virus is inactivated 100-fold each hour.

9. Viral Infection

M-tropic, binds to CD4
and CCR5 of
macrophage

T-tropic viruses infect T
cells by binding with
CD4 and CXCR4.

10. Viral Replication

11. HIV infecting a T-lymphocyte

12. Destruction of T-cells

13. Pathogenesis :Latency Period

14. Destruction of Immune System

15. HIV-Time Course

19. Acquired Immunodeficiency Syndrome
• Disease limits the body’s ability to fight
infection due to markedly reduced helper T
cells
• CD4 count drops below 200 person is
considered to have advanced HIV disease
• If preventative medications not started the HIV
infected person is now at risk for:
– Pneumocystis carinii pneumonia (PCP)
– cryptococcal meningitis
– toxoplasmosis

20. NATURAL COURSE OF HIV/AIDS

21. Stage 1 - Primary

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Short, flu-like illness occurs one to six
weeks after infection
Mild symptoms
Infected person can
infect other people

22. 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 low levels

HIV antibodies are detectable in the blood

23. Stage 3 - Symptomatic
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The immune system deteriorates

Opportunistic infections and cancers start to
appear.

24. Stage 4 - HIV  AIDS

The immune system
weakens too much as
CD4 cells decrease in
number.

25. Opportunistic Infections associated with
AIDS
CD4<500
 Bacterial
infections
 Tuberculosis (TB)
 Herpes Simplex
 Herpes Zoster
 Vaginal candidiasis
 Hairy leukoplakia
 Kaposi’s sarcoma

26. HIV infection to -> AIDS

28. Diseases are predictive of the
progression to AIDS:
Oral Candidiasis
Kaposi’s sarcoma
Oral Hairy Leukoplakia

29. Epidemiology
Worldwide distribution

30. ESCALATING EPIDEMIC !!!
Source: WHO/UNAIDS/UN The Millennium Development Goals Report, 2009, p.32 and WHO.

31. Status in India

33. Blood Detection Tests
Screening test for HIV
HIV enzyme-linked
immunosorbent assay (ELISA) Sensitivity > 99.9%
Western blot
Confirmatory test
Speicificity > 99.9% (when combined with
ELISA)
HIV rapid antibody test
Screening test for HIV
Simple to perform
Absolute CD4 lymphocyte
count
Predictor of HIV progression
Risk of opportunistic infections and AIDS when
<200
HIV viral load tests
Best test for diagnosis of acute HIV infection
Correlates with disease progression and
response to HAART

34. Urine Testing
 Urine
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Western Blot
As sensitive as testing
blood
Safe way to screen for HIV
Can cause false positives
in certain people at high
risk for HIV

35. Oral Testing
 Orasure
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The only FDA approved
HIV antibody.
As accurate as blood
testing
Draws blood-derived
fluids from the gum
tissue.
NOT A SALIVA TEST!

36. Treatment Options

37. HAART = Highly Active AntiRetroviral Treatment

38. Antiretroviral Drugs (HAART)
 Nucleoside
 AZT
Reverse Transcriptase inhibitors
(Zidovudine), Lamivudine
 Non-Nucleoside
 Viramune
 Protease
 Norvir
Transcriptase inhibitors
(Nevirapine)
inhibitors
(Ritonavir),
 Indinavir (Crixivan)

39. HEALTH CARE FOLLOW UP OF
HIV INFECTED PATIENTS
For all HIV-infected individuals:
 CD4 counts every 3–6 months
 Viral load tests every 3–6 months and 1 month
following a change in therapy
 Toxoplasma IgG serology
 CMV IgG serology
 Pneumococcal vaccine
 Influenza vaccine in season
 Hepatitis B vaccine for those who are HBsAbnegative
 Haemophilus influenzae type b vaccination
 Papanicolaou smears every 6 months for women

40. A
Vaccine May Be the Only
Way to Stop the HIV/AIDS
Epidemic

41. Why AIDS does not fit the paradigm for classic vaccine development
• Classic vaccines mimic natural immunity against reinfection generally seen
in individuals recovered from infection; there are no recovered AIDS
patients.
• Most vaccines protect against disease, not against infection; HIV infection
may remain latent for long periods before causing AIDS.
• Most vaccines protect for years against viruses that change very little over
time; HIV-1 mutates at a rapid rate and efficiently selects mutant forms that
evade immunity.
• Most effective vaccines are whole-killed or live-attenuated organisms; killed
HIV-1 does not retain antigenicity and the use of a live retrovirus vaccine
raises safety issues.
• Most vaccines protect against infections that are infrequently encountered;
HIV may be encountered daily by individuals at high risk.
• Most vaccines protect against infections through mucosal surfaces of the
respiratory or gastrointestinal tract; the great majority of HIV infection is
through the genital tract.
• Most vaccines are tested for safety and efficacy in an animal model before
trials with human volunteers; there is no suitable animal model for HIV/AIDS
at present.

42. Vaccine strategies under study
Vaccine
constituents
Status
Advantages
Disadvantages
Viral surface
proteins,
gp120
In phase I and II
trials, which
examine safety
Safe and simple to
prepare
Vaccine –elicited
antibodies have
failed to
recognize HIV
from patients
Live vector
viruses
In phase II trials
Markers can
control amount
and kinds of viral
proteins
produced
Complicated to
prepare
Combinations of In phase II trials
elements, such
as pure gp120
protein plus
canarypox
vector
Should stimulate Complicated to
both arms of the prepare
immune
response at once