This powerpoint, deals with HIV pathophysiology, signs and symptoms, mode of transmission and diagnostic parameters. Purely based on clinical pharmacist perspective.

1. HIV PATHOPHYSIOLOGY: ALL
YOU NEED TO KNOW
Dr. Vishnu R Nair, Pharm-D, RPh,
Dip. (Nutrition),
Assistant Professor (Dept. of
Pharmacy Practice),
NIMS Institute of Pharmacy.
HIV: THE SILENT KILLER

2. DEFINITIONS:
 HIV (Human Immunodeficiency Virus): Virus, that
attacks cells which help in fighting infections 
reduces immunity of the affected person
 Refer: https://www.hiv.gov/hiv-
basics/overview/about-hiv-and-aids/what-are-hiv-
and-aids
 AIDS (Acquired Immunodeficiency Syndrome): Late
stage of HIV infection, that occurs when the body’s
immune system is badly damaged due to HIV.
EPIDEMIOLOGICAL STATISTICS:
 38 million people are living with HIV worldwide
 African region  remains worst affected (1 out of
every 25 people have HIV)
 Refer: https://www.who.int/gho/hiv/en/
 In India:
a.2.1 million people living with HIV
b.Third largest HIV epidemic in the world
c.Prevalence age of disease: 15-49 years

3. d.50% of HIV cases in India concentrated in
Maharashtra, Tamil Nadu & Andhra Pradesh
(mostly contracted heterosexually)
e.8% of HIV cases in India  concentrated in
North-East (Manipur) [among intravenous drug
abusers].
f.Refer: https://www.avert.org/professionals/hiv-
around-world/asia-pacific/india
ETIOLOGIC AGENT:
STRUCTURE OF HIV VIRUS.

4.  AIDS  caused by a HIV virus
 RNA virus in nature (retrovirus)
ROUTES OF TRANSMISSION:
1.Sexual transmission:
 Constitutes 75% of all HIV transmissions
 Other STDs (gonorrhea, chlamydial infections) 
help in HIV spreading
 Transmission from male-to-male & male-to- female
 more potent than female-to-male.
2.Transmission via blood & blood products:
 Occurs due to:
a.Intravenous drug abusers (sharing needles,
syringes)
b.Haemophiliac patients  receive large
amounts of blood from multiple donors  high
risk!
c.Blood transfusions (if blood/ blood product is
infected with HIV)

5. 3.Vertical transmission:
 Also known as perinatal transmission
 Occurs either via:
a.Mother to fetus transmission
b.Through breast milk.
4. Occupational transmission:
 Improper disposal of biological wastes 
renders health-care professionals at high risk of
HIV!
5. Transmission by other body fluids:
 Saliva, tears, sweat, urine, breast milk, CSF, etc...

6. PATHOGENESIS:
 Major principle: Depletion of CD4+ T-cells
(Helper T-cells)  results in profound
immunosuppression!!
 Explained via the following steps:
A.Selective tropism for CD4+ molecule
receptor
B.Internalisation
C.Uncoating & viral DNA formation
D.Viral integration
E.Viral replication
F.Latent period & immune attack
G.CD4+ T-cell destruction
H.Viral dissemination
I.Impact of HIV infection on other immune
cells.

7. 1. Selective tropism for CD4+ molecule receptor:
 HIV  enters into body  uses its gp120
envelope to bind to CD4+ T-cell
 Tropism means affinity
 In other words,  HIV  has affinity for
CD4+ T-cell  binds to it.
2. Internalization:
 HIV  binds to CD4+ T-cell receptor surface
 For entering into cell membrane  HIV uses
CCR (Chemokine coreceptor)
3. Uncoating & viral DNA formation:
Once virus enters into T-cell cytoplasm
Viral RNA gets converted into DNA, using
enzyme reverse transcriptase

8. ss-DNA formed
ss-DNA  forms ds-DNA using enzyme DNA
polymerase
This viral DNA  undergoes frequent mutations
Thus, HIV is incurable (less response to anti-
retroviral therapy)!!
4. Viral integration:
Viral DNA in cytoplasm
Enters into nucleus of host T-cell, using
enzyme integrase
Viral particle at this stage  provirus (stage of
virus, where it enters into T-cell DNA, and
becomes part of host cell DNA).

9. 5. Viral replication:
HIV provirus
Part of host cell DNA
Host cell DNA  transcripts for viral RNA, using tat
gene
Viral particles multiply, with the help of:
 RNA viral particles  fill cytoplasm of CD4+ T-
cell 
acquire protein coating
 Released cytokines  cause spread of infection
to other body sites (e.g., CNS infection caused
by TNF-α)
IL-4, IL-5, IL-6,
IL-10
(produced by
TH2 cells)
IL-2, Interferon-
alpha (produced
by TH1 cells)

10. 6. Latent period & immune attack:
Virus  may remain inactive in the
infected T-cell for long time periods
(known as latent period)
During latent period  immune
system gets activated
Antibodies, macrophages, CD4+ &
CD8+ T- cells  try to eliminate virus
 in vain!!!
7. CD4+ T-cell destruction:
Viral particles inside cell  form buds
on the cell-wall of host cell
Through buds  virus detaches from
host cell  causes damage to cell
membrane  death of host cell!

11. 8. Viral dissemination:
 Once host cell is killed (broken up)  viral
particles get released into blood  spread to
all body parts & infect more CD4+ T-cells!
 Causes viraemia!
 HIV  through circulation  enters lymphoid
tissues (lymph nodes, spleen)  multiplies
further
 Finally,  lymphoid tissues  become
reservoir of virus!
9. Impact of HIV infection on other immune cells:
Effects include:
Immune system
parameter
Impact of HIV infection
Macrophages Become reservoir of HIV
Infection
Dendritic
follicular cells of
lymph node
HIV  causes massive
enlargement of follicle centres 
causes lymphadenopathy

12. B-cells
 CD4+ T-cells  activate B-
cells
 Reduction in T-cells (due to
HIV infection)
 causes reduction in B-
cells
NK cells Reduced Helper T-cells 
reduced cytokine production
 reduces NK cells
CD8+ T-cells Increased.
 Net effect of HIV on immune system: Profound
immunosuppression!!!
 Severe immunosuppression  makes victim
vulnerable to opportunistic infections &
tumours  eventual death!!!

13. CLINICAL MANIFESTATIONS
OF HIV INFECTION:
Manifestation Important catchpoints
Wasting syndrome
 Involuntary loss of body weight
(>10%)
 Reasons include:
1.Malnutrition
2.Hyper-metabolism
3.Malabsorption
4.Anorexia
5.Complications of multiple
opportunistic infections.
Persistent
generalized
lymphadenopathy
 Enlarged lymph nodes
 Damage to lymph nodes 
increased risk of opportunistic
infections
GI system
 Due to opportunistic infections:
a)Chronic watery/bloody diarrhoea
b)Oral candidiasis
c)Anorexia
d)Mucosal ulcers
e)Abdominal pain
 In advanced stage/AIDS:
a) GI tumors (Kaposi’s sarcoma)

14. Pulmonary system
 Due to opportunistic infections:
a)Pneumonia
b)Lung abscess
c)ARDS
d)Secondary tumors.
Mucocutaneous
 Erythematous rashes
 Infections
 Skin cancers
Hematologic
 Anemia
 Leukopenia
 Thrombocytopenia
CNS
 Encephalopathy
 Dementia
 Meningitis
 Peripheral neuropathy
Gynaecologic
 Vaginitis
 Cervix carcinoma
Renal system
 Nephropathy
 UTI
Liver
 Steatosis (fatty liver)
 Hepatitis B/C co-infection
CVS
 Cardiomyopathy
 Pericardial effusion
 Secondary tumors
Ophthalmic
lesions
 Retinopathy
 Retinitis
 Secondary tumors

15. Musculoskeletal
System
 Osteoporosis
 Osteopenia
 Osteomyelitis
Endocrine system
 Hyperinsulinemia
 Dyslipidemia
 Lipodystrophy (buffalo hump)
 Thyroid dysfunction.
DIAGNOSIS:
Parameter Description
Antibody tests
• ELISA
• Western blot
Direct detection of HIV
• PCR
• HIV culture
Tests to detect defects
in immunity
• CD4+ T-cell count:
reduced
• CD8+ T-cell count:
• Increased
Lymphopenia
Platelet count:
Thrombocytopenia

16. IMAGE GALLERY:

18. For further reference  check on the
following links:
1.https://www.youtube.com/watch?v=5g1ijp
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2.https://www.youtube.com/watch?v=Qm2
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3.https://www.youtube.com/watch?v=8sipX8
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THANK YOU!!!