HIV AIDS
DR H.S.JUDGE INSTITUTE OF DENTAL SCIENCES
PUNJAB UNIVERSITY,CHANDIGARH
PRESENTED BY:-
PALLAVI CHAWLA
PALLAVI DHIMAN
(BDS – 3RD YEAR)
INDEX
• HISTORY
• MORPHOLOGY
• MODES OF TRANSMISSION
• REPLICATION OF HIV
• CELLS AFFECTED IN HIV
• CLINICAL FEATURES
• PHASES OF AIDS
• OPPORTUNISTIC INFECTIONS ASSOCIATED
WITH AIDS
• DENTAL PROBLEMS ASSOCIATED WITH AIDS
• TESTS FOR DIAGNOSIS OF AIDS
• STRATEGIES OF HIV TESTING IN INDIA
• HAART THERAPY
• POST EXPOSURE PROPHYLAXIS
HISTORY
• AIDS-acquired immunodeficiency syndrome was
first recognised in USA in 1981 amongst
homosexuals and drug addicts.The causative
agent of AIDS was reported by Luc Montagnier
and colleagues of Pasteur institute in 1983.They
called it Lymphadenopathy associated
virus{LAV}.Robert Gallo and colleagues from
national institute of health USA reported
isolation of a retrovirus and called it Human T-
cell Lymphotropic Virus -3.In 1986 international
committee on virus nomenclature gave a name-
Human Immunodeficiency Virus.
• In India it was first detected in prostitutes in
Chennai in 1986.
HIV occurs in two main types-HIV 1 isolated from
USA,Europe and Central Africa ;and;HIV 2 from
West Africa.
MORPHOLOGY
• HIV is a spherical enveloped virus,about 90-
120nm in diameter.
• It contains 2 identical copies of single
stranded,positive sense RNA genome .In
association with viral RNA is reverse
transcriptase enzyme.The virus core is
surrounded by a nucleocapsid composed of
proteins.
• The virus contains a lipoprotein envelope which
consists of lipid derived from host cell membrane
and glycoproteins which are virus coded.
• The major virus coded envelope glycoproteins are
projecting spikes on surface and anchoring
transmembrane pedicles.
• These spikes bind to CD-4 receptors on
susceptible host cells. The transmembrane
pedicles cause cell fusion.
Genes Coding For
Structural Proteins
• (i)The Gag gene-
• It codes for core and shell proteinsof virus.
• It is expressed as a precursor protein p55.it is
cleaved into 3 proteins p15,p18and p24.
• P24,major core antigen can be detected in serum
in early stages of infection till appearance of
antibodies.
• (ii)The env gene-
• It codes for envelope glycoprotein 160,gp160.
• Gp160 is cleaved into 2 envelope components,gp120
which forms surface spikes and gp41 which is
transmembrane pedicle protein.
• Gp120 is major envelope antigen.
• Antibodies to gp120 are first to appear after HIV
infection and are present in circulation til terminal
stage of infection.
• (iii)The pol gene-
• It encodes for reverse transcriptase and other
viral enzymes.
• (iv)Non structural and regulatory genes-
• The tat gene-enhance viral protein synthesis.
• The rev gene-required for expression of
structural genes.
• The vif gene-confers infectivity to virus.
• The vpr gene-stimulates promoter region of virus.
MODES OF
TRANSMISSION
• Unprotected sexual intercourse with an infected
person Sexual intercourse without a condom is
risky, because the virus, which is present in an
infected person's sexual fluids, can pass directly
into the body of their partner. This is true for
unprotected vaginal and anal sex. Oral sex
carries a lower risk, but again HIV transmission
can occur here if a condom is not used - for
example, if one partner has bleeding gums or an
open cut, however small, in their mouth.
• Contact with an infected person's blood If
sufficient blood from an infected person enters
someone else's body then it can pass on the
virus.
• From mother to child HIV can be transmitted
from an infected woman to her baby during
pregnancy, delivery and breastfeeding. There
are special drugs that can greatly reduce the
chances of this happening, but they are
unavailable in much of the developing world.
• It is not possible to become infected with
HIV through :
• sharing crockery and cutlery
• insect / animal bites
• touching, hugging or shaking hands
• eating food prepared by someone with HIV
• toilet seats
REPLICAT
ION OF
HIV
CELLS AFFECTED IN
HIV
• The virus, entering through which ever route,
acts primarily on the following cells:[66]
• Lymphoreticular system:
– CD4+ T-Helper cells
– Macrophages
– Monocytes
– B-lymphocytes
• Certain endothelial cells
• Central nervous system:
– Microglia of the nervous system
– Astrocytes
– Oligodendrocytes
– Neurones - indirectly by the action of
cytokines and the gp-120
CLINICAL FEATURES
PHASES OF
AIDS
• GROUP I-Acute HIV infection
• GROUP II-Asymptomatic infection
• GROUP III-Persistent generalised
lymphadenopathy
• GROUP IV-
i. Subgroup A-constitutional disease,AIDS
related complex
ii. Subgroup B-neurological disease
iii. Subgroup C-secondary infectious diseases
iv. Subgroup D-secondary cancers
v. Subgroup E-other conditions
• GROUP I-
• Entry of HIV into body of immunocompetent
host.
• There is high level of viraemia due to viral
replication.
• Initially marked reduction in CD4+T cells
followed by return to normal levels.
• The p24 antigen is positive in the tests but
antibodies are negative as they are
synthesised during this phase.This period is
known as WINDOW PERIOD.
• Antigens can be detected by polymerase chain
reaction.
• Manifestations include sore
throat,fever,myalgia,skin rash and sometimes
aseptic meningitis.
• GROUP II-
• This includes all infected persons who are
usually well.
• They show positive antibody tests and are
infectious.
• GROUP III-
• Phase of competition between HIV and host
immune response.
• There is increased vireamia.
o The CD4+T cells start decreasing and may fall
below 200/ul.
o CD8+T cells are markedly increased.
o Characterised by enlarged lymph nodes(more
than 1cm)at two or more extragenital sites for
atleast 3 months.
o GROUP IV-
o It is characterised by profound
immunosuppression and onset of full blown
AIDS.
1) Subgroup A-
i. Fever of more than 1month of duration.
ii. Weight loss of more than 10% of body weight.
iii. Chronic diarrhoea lasting for more than 1
month.
2) Subgroup B-
i. Aseptic meningitis
ii. Viral meningoencephalitis
iii. Periheral neuropathy
iv. AIDS sementia complex
3) Subgroup C-
i. Fungal diseases-
candidiasis,cryptococcosis,histoplasmosis.
ii. Bacterial diseases-mycobacterium avium
intercellulare , mycobacterium tuberculosis
iii. Protozoal diseases-pneumocystis carnii
pneumonia , toxoplasmosis.
4) Subgroup D-
i) Kaposi”s sarcoma
ii) Non hodgkin”s lymphoma (burkitt”s ,
immunoblastic)
iii) Hodgkin:s lymphoma
5) Subgroup E-
i) <200/ul of CD4+T cells
ii) Pulmonary tuberculosis
iii) Recurrent pneumonia
OPPORTUNISTIC
INFECTIONS
ASSOCIATED WITH AIDS
1) BACTERIAL
i) Salmonellosis
ii) Tuberculosis and other non tuberculous
infections
iii) Mycobacterium avium complex
2) VIRAL
i) Cytomegalo virus
ii) Herpes simplex
iii) Epstein barr virus
iv) Human herpes virus 6
v) Human herpes virus 8
3) FUNGAL
i) Pneumocystis carnii pneumonia
ii) Candidiasis
iii) Cryptoccocosis
iv) Aspergillosis
v) Histoplasmosis
4) PARASITIC
i) Toxoplasmosis
v) Coccidioidomycosis
vi) Cryptosporidiosis
vii) Isosporiasis
viii) Generalised strongyloidiasis
5) MALIGNANCIES
i) kaposi”s sarcoma
ii) B-cell lymphoma or non-hodgkin”s lymphoma
DENTAL PROBLEMS
ASSOCIATED WITH
HIV
• Some common dental conditions associated with
HIV / AIDS are:
• · Dry Mouth
• · Thrush
• · Swollen Glands
• · Gum Disease
• · Canker Sores
• · Herpes Simplex Lesions
• The most common side effect from HIV / AIDS
medication is dry mouth. Saliva helps wash away
bacteria and the acids that the bacteria
produces along with sugars and foods, therefore,
producing less saliva as a result of dry mouth can
contribute to tooth decay, gingivitis and gum
disease. If you have dry mouth, your dentist can
prescribe a saliva substitute or a fluoride rinse
to help decrease the risk of tooth decay. Dental
visits may become more frequent now as immune
system is more suppresed with progression of
disease.
TESTS FOR DIAGNOSIS
OF AIDS
• SPECIFIC TESTS-
i) Antigen detection
ii) Virus isolation
iii) Detection of viral nucleic acid
iv) Antibody detection-
- ELISA
- Rapid test
- Simple tests
NON SPECIFIC TESTS
• Total and differential leucocyte count
• T lymphocyte subset assay
• platelet count
• Skin tests for cell mediated immunity.
CONFIRMATORY TEST-Western blott
SPECIFIC TESTS
1)Antigen detection-p24 antigen and reverse
transcriptase enzyme are earliest markers to
appear in blood.The p24antigen capture assay using
anti p24 antibody as solid phase can be used for
detection of this antigen.
2)VIRUS ISOLATION-The virus is present in blood and
body fluids , mostly within CD4+
lymphocytes.Patient”s lymphocytes are co-
cultivated with uninfected human lymphocytes in
the presence of interleukin 2.
3)DETECTION OF VIRAL NUCLEIC ACID-Viral nucleic
acid can be detected by polymerase chain
reaction(PCR).it is also useful in diagnosis in window
period.Two types of PCR are- RNA PCR and DNA
PCR.In DNA PCR,peripheral lymphocytes are lysed
and proviral DNA is amplified.The test is highly
sensitive and specific.RNA PCR can be used for
diagnosis and for monitoring level of viraemia.
4)ANTIBODY DETECTION-It is simplest and most
commonly employed technique for diagnosis.It may
take several weeks to months for antibodies to
appear in blood.IgM antibodiesappear first
followed by
IgG antibodies.
i)ELISA-(enzyme linked immunosorbant assay)Direct
solid phase ELISA is commonly used.Antigen is
prepared from HIV grown in continuous T-
lymphocyte cell line pr by recombinant
technique.The viral antigen is coated on surface of
microtitre wells.The test serum is added and if
antibody is present it binds to viral antigen.The
unbound serum is washed away,anti-human goat
immunoglobulin linked to a suitable enzyme is
added followed by color foming substrate.If test
is posiotive,photometrically detectable color is
formed which can be read by ELISA reader.
ii)RAPID TESTS-These tests take less than 30
minutes and donot require expensive equipment.It
includes dot blot assay,particle agglutination,HIV
spot and coomb test.
iii)SIMPLE TEST-They take 1-2 hrs and donot require
expensive equipment.
CONFIRMATORY TESTS-
i)WESTERN BLOT TEST-In this test,HIV proteins are
separated by polyacrylamide gel
electrophoresis.The separated proteins are
blotted on two strips of nitrocellulose
paper.these strips are reacted with test
sera.Antibodies to HIV proteins if present in test
serum,combine with different segments of HIV.
The strips are washed and reacted with enzyme
conjugated anti-human immunoglobulin.A suitable
substrate is addedadded which produces colour
bands.The position of colour band on strip
indicates the fragment of antigen with which
antibodies have reacted.In a positive serum,bands
will be seen with multiple proteins.Antibodies to
p24(gag gene),p31(pol gene) and gp41,gp120 or
gp160(env gene) are commonly detected.A
positive reaction with proteins representing three
genes(gag,pol,env) is conclusive evidence of HIV
infection.
ii)INDIRECT IMMUNOFLUORESCENCE TEST-HIV
infected cells are fixed onto slides and then
reacted with serum followed by fluoroscein
conjugated antihuman gamma globulin.In a
positive test, apple green fluorescence appears
when examined under flourescent microscope.
STRATEGIES FOR HIV
TESTING IN INDIA
1) STRATEGY I-Serum is subjected to E/R/S test
and if positive,sample is taken as HIV
infected.If negative serum is free of HIV.This
strategy is used for donation safety.
2) STRATEGY II-Serum positive in strategyI is
again tested with a second E/R/S based on
different test principle and antigen
preparation.If test is positive,taken as HIV
positive,otherwise negative.This strategy is
used for HIV surveillance.
3) STRATEGYIII-It is similar to strategy II with
added confirmation by third E/R/S test.iIt is
again based on different test principle and
antigen preparation.Seum is always tested
positive.If this is negative,it is considered
equivocal.Such subjects should be retested
after 3 weeks.If test again negative,subject is
negative for HIV.This strategy is used in
asymptomatic individuals.
HAART
• Specific treatment wit antiretroviral drugs is
mainstay in management of HIV
infection.Highly active antiretroviral
therapy(HAART)is effective in inhibition of HIV
replication but major drawback with this is
selection of resistant mutants.
• The antiretroviral drugs used are:-
a) NUCLEOSIDE REVERSE TRANSCRIPTASE
INHIBITORS-
i) Zidovudine ii)Didanosine
iii) Zalcitabine iv)Stavudine
v) Lamivudine vi)Abacavir
b) NON-NUCLEOSIDE REVERSE
TRANSCRIPTASE INHIBITORS
i) Nevirapine ii)Delaviridine
iii) Efavirenz iv)Loviride
c) NUCLEOTIDE INHIBITOR-
i) Tenofovir
d) PROTEASE INHIBITORS
i) Saquinavir ii)Ritonavir
iii) Indinavir iv)Nelfinavir
v) Amprenavir vi)Tipranavir
e) FUSION INHIBITOR
i) enfuvirtide
POST EXPOSURE
PROPHYLAXIS-
Exposure to blood,body fluid, other potentially
infected material or an instrument
contaminated with one of these materials may
lead to risk of acquiring HIV infection.The risk
of infection varies with type of exposure and
other factors. Most exposures donot result in
infection.Health workers are normally at very
low risk of acquiring infection during
management of infected patients. Following
exposure, postexposure prophylaxis(PEP) may
be required depending upon exposure code
(EC)and HIV status code of exposure source.
• Zidovudine 300mg BD and Lamivudine 150mg BD are
used in combination for a period of four weeks.In
selected cases,Indinavir
800mg TDS is added to this combination of drugs
according to PEP guidelines.To be affective these
drugs should be started within an hour or two.Both
risk of infection and possible side effects of
antiretroviral drugs should be carefully considered
when deciding to start PEP.Besides PEP injured site
should be thoroughly washed with soap and
water.Antiseptics may also be used.
REFRENCES
• http:enwikipedia.org/wiki/AIDS
• www.colgatedentalhealth.com
• Essential pathology by HARSH MOHAN
• Textbook of microbiology by Prof.C.P.BAVEJA.
