ACQUIRED
IMMUNODEFICIENCY
SYNDROME (AIDS)
Dr. J. Karthikesh MD
Epidemiology
First discovered in 1981 in the US
Now the disease involves all continents
Africa accounts for 50% of positive cases
~ 1 in 100 sexually active men are infected with HIV
worldwide
50 % of positive cases are women
5 % are children
Recent increase in the number of positive cases in India,
Thailand, Indonesia
In India, Maharashtra and Tamil Nadu account for 50% of
the positive cases through sexual route
North East state of Manipur accounts for 8% of positive
cases by IV drug abuse route
Etiology
It is a Retrovirus called Human
Immunodeficiency virus (HIV)
HIV resembles HTLV ( Human T cell leukemia-
lymphoma virus) in shape and size
Both attack CD4 molecules present on the surface
of T lymphocytes
HIV kills T lymphocytes ( cytopathic virus)
HTLV transforms T lymphocytes to leukemia
cells ( transforming virus)
HIV virus
There are 2 types of HIV
HIV 1 – Central Africa and the US
HIV 2 – West Africa & India
HIV-1 virus
Spherical in shape
100-140nm in size
It has a core which is covered by a double layer.
The core contains
Core proteins – p24 & p18
2 strands of genomic RNA
Enzyme reverse transcriptase
The double layer is composed of lipid membrane. The membrane is
studded with 2 viral glycoproteins gp120 and gp41
There are 3 genes which code for the components of the virus –
gag for core proteins, pol for reverse transcriptase and
env for envelope proteins
These act as markers for the lab diagnosis of HIV infection.
Routes of transmission
Sexual contact
Main mode of transmission – 75%
In the US, homosexual or bisexual males are more
prone
In Africa and Asia, heterosexual promiscuity is the
dominant route
Male to male or Male to female transmission is more
potent than female to male
Co-existing other forms of STD may act as cofactors in
the spread of HIV
Routes of transmission
Parenteral route
Large group – 25%
Occurs in 3 groups of high risk population
IV drug abusers sharing same needles, syringes
Hemophiliacs receiving frequent Factor VIII
concentrates
Recepients of blood or blood components such as
plasma or platelets
Routes of Transmission
Peri-natal transmission
From mother to baby
Transplacentally during pregnancy
Immediate post partum period when contact with
maternal blood, amniotic fluid or breast milk
Routes of transmission
Apart from blood HIV has been isolated in
Semen
Vaginal secretions
Cervical secretions
Breast milk
CSF
Synovial fluid
Pleural, Peritoneal and Pericardial fluids
Amniotic fluid
AIDS DOES NOT SPREAD BY
Shaking hands
Hugging
Sharing a bed
Sharing toilets
Sharing utensils
Mosquito bites
Delicate Virus - HIV
It is a relatively easy virus to kill
Hypo – Sodium hypochlorite
Formaldehyde – 5%
Ethanol – 70%
Glutaraldehyde – 2%
B-propionolactone
Heating at 56’C for 30 mts
Pathogenesis
It attacks and kills the T lymphocytes
which have CD4 markers on the surface.
This leads to profound immuno-
suppression
The body is now vulnerable to many
oppurtunistic infections and cancers
Pathogenesis
1. Selective tropism and internalisation
g.p 120 binds only to CD 4 molecule on the
surface of certain T lymphocytes
2. Uncoating and proviral DNA integration
Transcription of RNA to DNA by enzyme
reverse transcriptase to form a proviral DNA.
Later this proviral DNA gets integrated into
the T cell genome
Pathogenesis
3. Budding of viral particles and syncytia formation
Infected CD4+ T cells attract more CD4+ T cells to
form a syncytia
4. Cytopathic effects
Quantitative and Qualitative T cell destruction by the
virus leads to depletion of T lymphocytes as well as
inability to protect the body. This activation is
mediated by g.p120-CD4 interaction.
In an inactive state, the cell may remain viable for a long
time ( hence a long incubation period in some
patients)
Does HIV infect only
CD4+ T lymphocytes?
1. CD 4 molecules are present on the surface of a few
subpopulations of Mon/Mac’s such as
Dendritic cells
Microglial cells
However, there is no cytopathic effect on them.
They cause Neurological symptoms seen in AIDS.
2. The g.p 120 of HIV also causes dysfunction of the
B cells. Once again, there is no destruction of B cells but
alteration in its functions.
3. HIV also deranges the function of NK cells
Difference between HIV
infection & AIDS
A person is said to be HIV infected when
the HIV virus enters into his / her body
A person is said to have AIDS when the
virus has sufficiently replicated and has
caused damage to the immune system to
produce symptoms and signs of the disease
WHO Criteria for AIDS
At least 2 major + 1 minor signs
There should not be any other known cause
for immunosuppression.
WHO criteria for AIDS
Major signs
Weight loss > 10%
of body weight
Chronic diarrhoea >
1 month duration
Fever > 1 month
Minor signs
Recurrent Oro-pharyngeal
Candidasis
Persistent gen.
Lymphadenopathy
Persistent cough > 1 month
Generalised pruritic
dermatitis
Recurrent Herpes Zoster
Progressive Herpes Simplex
Acute HIV syndrome
1. High levels of Plasma Viremia due to replication of the
virus
Virus specific immune response leading to
seroconversion which occurs after 3-6 weeks following
exposure
Sudden marked depletion of CD4+ T cells followed by
return to normal levels
Increase in CD8+ T cells ( cytotoxic for HIV)
Mild flu like manifestations (CDC group 1) – sore throat,
fever, myalgia, skin rash, aseptic meningitis. Resolves
spontaneously within 2-3 weeks
Middle Chronic Phase
Increasing levels of Viremia as with time the host
immune system crumbles
May last for several years even upto 10 years depending
on the patients immunity
CD4+ T cells proliferate but not enough. So there is a
moderate decrease in CD4+ T cell count
CD8+ T cell count is high
Latent stage – CDC group II. If patient develops mild
constitutional symptoms or gen.lymphadenopathy \
CDC group III
Final crisis phase – lasts 18-24
months
Marked by profound immuno-suppression
Onset of full blown AIDS
Marked increase in viremia
CD4+ cell count is markedly depleted
CDC group IV – sub-classified into 5 groups
A – Constitutional symptoms
B – Neurological disease
C - Secondary oppurtunistic infections – fungal, bacterial,
parasitic
D - Secondary neoplasms – Kaposi sarcoma, NHL, Hodgkins
E – CD4+ T cell count < 200 + Pulmonary TB