AIDS is caused by the human immunodeficiency virus (HIV) which infects and destroys CD4+ T cells. This leaves the body vulnerable to opportunistic infections and cancers. HIV is transmitted via bodily fluids and progresses from an acute infection stage to asymptomatic latency before manifesting as AIDS-related complex and finally AIDS, characterized by severe immune deficiency. Diagnosis involves immunological and virological tests to detect HIV antibodies, antigens or viral RNA. Treatment focuses on antiviral drugs and managing opportunistic infections, though there is no cure currently.
2. INTRODUCTION
ï Acquired Immunodeficiency Syndrome
ï First indication in 1981 with reports from
New York and Los Angeles-sudden outbreak
of two rare diseases-kaposiâs sarcoma and
Pnuemocystis carinii
3. HUMAN IMMUNODEFICIENCY VIRUS
ï Causative agent of AIDS
ï Spherical enveloped virus about 90-120 nm in
size
ï Genome is diploid composed of two identical
single stranded positive RNA copies
ï Along with viral RNA â reverse transcriptase
enzyme-characteristic feature of retrovirus
ï 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!
4.
5.
6. ï 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
ï Major virus coded envelop protein âprojecting knob
like spikes and anchoring transmembrane pedicles
ï Spikes-major surface component of virus which binds
to CD4 receptors on host cellsâŠtransmembrane
proteins help in cell fusion
7. PATHOGENESIS
ï Transmitted mainly through sexual contact or
through blood transfusion
ï Transmitted when the virus enters the blood or
the tissues and come in contact with suitable
host cells
ï Receptor for virus âCD4 antigen-thus infect any
cells bearing CD4 antigen on surface-primarily
the CD4+ helper T cell
ï Others include B lymphocytes,monocytes and
macrophages such as specialised macrophages
of lungs langerhan cells in dermis.
8. ï After fusion of virus with the cell-HIV genome
uncoated and internalised into the cell
ï Action of reverse transcriptase enzyme-double
stranded DNA integrated into the human
genome with the help of integrase-causes
latent infection
ï Long and variable incubation period is due to
latency
ï Primary pathogenic mechanism-due to
damage caused to the CD4 T lymphocytes
ï T4 cells decrease in number,CMI reduces
ï T4:T8 ratio reverses
ï Helper T cell function-essential for B cell
function-polyclonal activation of Bcells -
hypergammaglobulinemia
9. CLINICAL MANIFESTATIONS
ï Not primarily to viral cytopathology but due to
failure of immune responses
ï AIDS â only the last stage in the wide
spectrum of clinical features
10. STAGES OF EVOLUTION
ï¶ Acute HIV infection
ï¶ Asymptomatic or latent infection
ï¶ Persistent generalised lymphadenopathy
ï¶ AIDS related complex
ï¶ AIDS
11. ACUTE HIV INFECTION
ï Within 3-6 weeks of infection
ï Low grade fever,malaise,head
ache,lymphadenopathy,sometimes with
rashes arthropathy resembling glandular
fever.Spontaneous resolution within weeks
ï Tests for HIV antibodies negative in early
stage and get positive during its course-
seroconversion illness.
12. ASYMPTOMATIC AND LATENT INFECTION
ï Symptomless infection
ï Positive HIV antibodies test
ï Passes through various stages-CD4
lymphocytopaenia,minor oppurtunistic
infection,persistent generalised
lymphadenopathy,ARC and full blown AIDS
ï Viral multiplication goes on-immune response
mounnted by host-only helps in limiting viral
load
ï Tcell-500 from 1000/microlitre-acute infection
and when 200 or less , clinical AIDS
13. PGL
ï Enlarged lymph nodes
ï Atleast 1 cm or more
ï In two or more non contiguous extrainguinal
sites-that persists for more than 3 months in the
absence of any current illness or medication
19. ï 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
ï Malignancies-kaposiâs
sarcoma(nonmetastasing mucosal or
cutaneous tuour of endothelial orgin)Hodgkin
and Non Hodgkin lymphomas
ï Babies born to infected mothers-also
positive-
23. DIAGNOSIS
ï IMMUNOLOGICAL TESTS:
ï Total luecocyte and lymphocyte count
ï Tcell subset assay-ratio inversion.Absolute
CD4 cell count less than 200/cubic mm
ï Platelet cout will show thrombocytopaenia
ï Raised IgG and IgA levels
ï Diminished CMI by skin tests
ï Lymph node biopsy
24. ï Specific tests:
ï Antigen detection:major core antigen-
p24-earliest marker-p24 antigen capture
assay
ï Viral isolation:cocultivation of patientâs
lymphocyte with uninfected lymphocyte in
the presence of interluekin 2.viral replicatio
detected by demo of reverse transcriptase
activity as well as antigen
ï PCR:golden standard for diagnosis of all
stages of HIV infection
25. ï Antibody detection:
ï ELISA Test
ï 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
26. 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)