AIDS
Megha J Nair
6th Batch

INTRODUCTION
 Acquired Immunodeficiency Syndrome
 First indication in 1981 with reports from
New York and Los Angeles-sudden outbreak
of two rare diseases-kaposi’s sarcoma and
Pnuemocystis carinii

HUMAN IMMUNODEFICIENCY VIRUS
 Causative agent of AIDS
 Spherical enveloped virus about 90-120 nm in
size
 Genome is diploid composed of two identical
single stranded positive RNA copies
 Along with viral RNA – reverse transcriptase
enzyme-characteristic feature of retrovirus
 When virus infects cell-reverse trancriptase
transcribe the single stranded RNA to double
stranded RNA nand then to double stranded
DNA(PROVIRUS)-integrates into human
genome!

 During viral replication , when the virus buds out of
the host cell surface membrane-acquires a lipoprotein
envelop-consists of lipid derived from the host cell
membrane and glycoproteins which are virus coded
 Major virus coded envelop protein –projecting knob
like spikes and anchoring transmembrane pedicles
 Spikes-major surface component of virus which binds
to CD4 receptors on host cells…transmembrane
proteins help in cell fusion

PATHOGENESIS
 Transmitted mainly through sexual contact or
through blood transfusion
 Transmitted when the virus enters the blood or
the tissues and come in contact with suitable
host cells
 Receptor for virus –CD4 antigen-thus infect any
cells bearing CD4 antigen on surface-primarily
the CD4+ helper T cell
 Others include B lymphocytes,monocytes and
macrophages such as specialised macrophages
of lungs langerhan cells in dermis.

 After fusion of virus with the cell-HIV genome
uncoated and internalised into the cell
 Action of reverse transcriptase enzyme-double
stranded DNA integrated into the human
genome with the help of integrase-causes
latent infection
 Long and variable incubation period is due to
latency
 Primary pathogenic mechanism-due to
damage caused to the CD4 T lymphocytes
 T4 cells decrease in number,CMI reduces
 T4:T8 ratio reverses
 Helper T cell function-essential for B cell
function-polyclonal activation of Bcells -
hypergammaglobulinemia

CLINICAL MANIFESTATIONS
 Not primarily to viral cytopathology but due to
failure of immune responses
 AIDS – only the last stage in the wide
spectrum of clinical features

STAGES OF EVOLUTION
 Acute HIV infection
 Asymptomatic or latent infection
 Persistent generalised lymphadenopathy
 AIDS related complex
 AIDS

ACUTE HIV INFECTION
 Within 3-6 weeks of infection
 Low grade fever,malaise,head
ache,lymphadenopathy,sometimes with
rashes arthropathy resembling glandular
fever.Spontaneous resolution within weeks
 Tests for HIV antibodies negative in early
stage and get positive during its course-
seroconversion illness.

ASYMPTOMATIC AND LATENT INFECTION
 Symptomless infection
 Positive HIV antibodies test
 Passes through various stages-CD4
lymphocytopaenia,minor oppurtunistic
infection,persistent generalised
lymphadenopathy,ARC and full blown AIDS
 Viral multiplication goes on-immune response
mounnted by host-only helps in limiting viral
load
 Tcell-500 from 1000/microlitre-acute infection
and when 200 or less , clinical AIDS

PGL
 Enlarged lymph nodes
 Atleast 1 cm or more
 In two or more non contiguous extrainguinal
sites-that persists for more than 3 months in the
absence of any current illness or medication

PGL

ARC
 Patients with considerable immunodeficiency
suffering from various constitutional symptoms
or minor oppurtunistic infections
 Fatigue , unexplained fever , persistent diarrhoe
, marked weight lose-symptoms-also gen.
lymphadenopathy and splenomegaly
 Oppurtunistic inf.-oral candidiasis,herpes
zoster,hairy cell luekoplakia,salmanellosis or tb

ORAL THRUSH

AIDS
• End stage disease-irreversible breakdown of
immune system-progressive oppurtunistic
infection and malignancies.
• Dry cough , dyspnea , fever , recurrent
pneumonia
• GIT-thrush , herpetic steatites , gingivitis , hairy
luekoplakia or kaposi’s sarcoma.A characteristic
intestinal pathogen is cryptosporidium

HAIRY LEUKOPLAKIA

 CNS-toxoplasmosis and
cryptococcosis,lymphomas of CNS also
seen.also can cross blood brain barrier and
cause encephalopathy leading to loss of
higher function-then dementia
 Malignancies-kaposi’s
sarcoma(nonmetastasing mucosal or
cutaneous tuour of endothelial orgin)Hodgkin
and Non Hodgkin lymphomas
 Babies born to infected mothers-also
positive-

KAPOSI’S LESIONS

DIAGNOSIS
 IMMUNOLOGICAL TESTS:
 Total luecocyte and lymphocyte count
 Tcell subset assay-ratio inversion.Absolute
CD4 cell count less than 200/cubic mm
 Platelet cout will show thrombocytopaenia
 Raised IgG and IgA levels
 Diminished CMI by skin tests
 Lymph node biopsy

 Specific tests:
 Antigen detection:major core antigen-
p24-earliest marker-p24 antigen capture
assay
 Viral isolation:cocultivation of patient’s
lymphocyte with uninfected lymphocyte in
the presence of interluekin 2.viral replicatio
detected by demo of reverse transcriptase
activity as well as antigen
 PCR:golden standard for diagnosis of all
stages of HIV infection

 Antibody detection:
 ELISA Test
 Western blot test-HIV proteins seperated
by their electrophoretic mobility by poly
acrylamide gel electrophoresis are blotted
on to the strips of nitrocellulose
paper.strips are reacted with test sera and
then with enzyme conjugated anti human
globulin

TREATMENT
Treatment and prophylaxis of infections and
tumours
General management
Immunorestortive measures(administration of
interluekin 2,thymic factors etc)
Specific anti-HIV drugs(anti retroviral drugs)