This document discusses HIV and AIDS. It describes how HIV is caused by two types of viruses, HIV-1 and HIV-2, and how they are believed to have been transmitted from monkeys to humans. It outlines the various ways HIV can be transmitted and cannot be transmitted. It also discusses the window period, stages of HIV infection from acute to AIDS, defining diseases of AIDS, and common opportunistic infections seen in patients with AIDS. Blood tests used to detect HIV are also mentioned.

1. HIV- AIDS
BY
DR BASHIR AHMED DAR
ASSOCIATE PROFESSOR MEDICINE
CHINKI PORA SOPORE KASHMIR
EMAIL—drbashir123@gmail.com

12. • AIDS is caused by human immunodeficiency
virus
• Genetically the virus has two types
• HIV-1 (World wide)
• HIV-2 which is less aggressive slow and
restricted mainly to western Africa.

13. How it got transferred to humans
• The HIV-1 actually got
transfered from African
green monkeys or
chimpanzees

14. How it got transferred to humans
• HIV-2 got transferred
from Sooty managbey
monkeys or Chimpanzees

15. Natural transfer theory
• Commonly held theory is that HIV got
transferred through hunting and handling of
chimpanzees and through slaughtering and
eating “bush meat” of these (monkeys).The
epidemic required urbanization and increased
population mobility

16. Human error theory
• Oral polio vaccine or some other injectable
vaccines used enmass in West Africa during
the late 1950s may have been contaminated
with HIV since these vaccines were prepared
by using these monkeys or their tissues in
process of their preparation.

17. How HIV can be transmitted
• Unprotected sexual contact – be it
vaginal, oral, or anal Mucosa - with an infected
partner
• Contact of abraded skin or mucosa with body
secretions such as blood, CSF or semen;

18. Actually making sex with Bugs

19. How HIV can be transmitted
• Sharing unsterilized needles or syringes with
an HIV positive person, for example, when
using drugs or in a healthcare setting.
• During pregnancy or birth and through
breastfeeding from an HIV positive mother to
her baby.
• Blood transfusions with infected blood
• Accidental occupational exposure

21. Populations particularly at risk
• Has a sexually transmitted infections(STIs)
• Has anal sex with her/his partner(s)
• Exchanges sex for money or drugs
• Has many sex partners
• Non-circumcised

22. Populations particularly at risk
• Leads life separated from spouse due to
professional obligations (e.g., truck
drivers, laborers, migrants)
• Homosexuals/ bisexuals
• Certain sexual practices increases the disease
• Like sexual Contact with
• Male-to-male
• Female-to-female

23. How HIV can NOT be transmitted
• Through air or by coughing and sneezing
• Through food or water
• Through sweat and tears

24. How HIV can NOT be transmitted
• By sharing cups, plates, and utensils with an
infected person
• By touching, hugging and kissing an infected
person
• By sharing clothes or shaking hands with an
infected person
• By sharing toilets and bathrooms with an
infected person
• By living with an infected person
• By mosquitoes, fleas, or other insects

25. How HIV can NOT be transmitted
• While the virus has occasionally been found in
saliva, tears, urine and bronchial
secretions, transmission after contact with
these secretions has not been reported.
• No laboratory or epidemiological evidence
suggests that biting insects have transmitted
HIV infection.

26. CONCENTRATION OF VIRUS
• Blood, Menstrual Blood – Very High
• Vaginal Fluids, Semen, Pre ejaculate Fluid – High
• Bone Marrow – High
• Saliva – No
• Sweat, Tears, urine - No
26

27. HIV in Body Fluids
Blood
Semen
18,000 Vaginal
11,000
Fluid Amniotic
7,000 Fluid
4,000 Saliva
1
Average number of HIV particles in 1 ml of these body fluids

28. HIV STRUCTURE
• HIV belongs to a special class of viruses called
retroviruses. Within this class, HIV is placed in
the subgroup of lentiviruses.
• Other lentiviruses include SIV, FIV, Visna and
CAEV, which cause diseases in
monkeys, cats, sheep and goats.
• All viruses except retroviruses contain DNA

29. HIV STRUCTURE
• So Retroviruses are the exception because
their genes are composed of RNA (Ribonucleic
Acid).
• However RNA has a very similar structure to
DNA with small differences

30. HIV STRUCTURE
• HIV has just nine genes (compared to more
than 500 genes in a bacterium
• Three of the HIV genes, called gag, pol and
env, contain information needed to make
structural proteins for new virus particles.

31. HIV STRUCTURE
• The other six genes, known as
tat, rev, nef, vif, vpr and vpu, code for proteins
that control the ability of HIV to infect a
cell, produce new copies of virus, or cause
disease.

32. HIV STRUCTURE
• An HIV particle is around 100-150 billionths of
a metre in diameter. That's about the same as:
• 0.1 microns
• 4 millionths of an inch
• one twentieth of the length of an E. coli
bacterium
• one seventieth of the diameter of a human
CD4+ white blood cell.

33. HIV STRUCTURE
• HIV particles surround
themselves with a coat
of fatty material known
as the viral envelope .
• This envelope gives out
lots of little spikes
around 72 in number.

34. HIV STRUCTURE
• These spikes are made
of knobs and handles
made of proteins
gp120 and gp41
respectively.

35. HIV STRUCTURE
• Just below the viral
envelope is a layer
called the matrix, which
is made from the
protein p17(Matrix
proteins)

36. HIV STRUCTURE
• Below the matrix is
another layer of
proteins P24 forming
viral core (or capsid)
and is usually bullet-
shaped.

37. HIV STRUCTURE
• Inside the core are
three enzymes required
for HIV replication
called
• Reverse transcriptase
• Integrase
• And protease

38. HIV STRUCTURE
• Also held within the
core is HIV's genetic
material, which consists
of two identical copies
of single stranded RNA.

40. The virus, entering through which ever
route, acts primarily on the following cells:
• * Lymphoreticular system:
• o CD4+ T-Helper cells
• o CD4+ Macrophages
• o CD4+ Monocytes
• o B-lymphocytes
• *

41. The virus, entering through which ever
route, acts primarily on the following cells:
• Certain endothelial cells
• * Central nervous system:
• o Microglia of the nervous system
• o Astrocytes
• o Oligodendrocytes
• o Neurones - indirectly by the action of
cytokines and the gp-120

42. Pathogenesis
• HIV binds to CD4 molecule, CD4 molecule is
found on the T helper-cell Macrophages
etc.Binding of CD4 is not sufficient for entry
• Therefore gp120 protein also binds to co-
receptor
• CCR5 Co-receptor - is used by macrophages
• CXCR4 Co-receptor - is used by lymphocytes

43. Pathogenesis
• Binding of virus to cell surface results in fusion of viral
envelope with cell membrane of T-helper cell and thus
Viral core is released into cell cytoplasm
• After uniting with T-helper cells the T-Helper cells
through
• Th1 - activate Tc (CD8) lymphocytes, promoting cell-
mediated immunity
• Th2 - activate B lymphocytes, promoting antibody
mediated immunity

44. Pathogenesis
• CD8 Cytotoxic T lymphocyte (CTL) is Critical for
containment of HIV.Derived from T8
cells, recognize viral antigens and directly
destroy infected cells

45. Pathogenesis
• Antibodies formed bind to surface of virus to
prevent attachment to target cells
• Fc portion of antibody also binds to NK cells
and Stimulates NK cell to destroy infected cell

46. Pathogenesis
• Numerous organ systems are infected by HIV:
• Brain: macrophages and glial cells
• Lymph nodes and thymus: lymphocytes and
dendritic cells
• Blood, semen, vaginal fluids: macrophages
• Bone marrow: lymphocytes
• Skin: langerhans cells
• Colon, duodenum, rectum: chromaffin cells
• Lung: alveolar macrophages

47. Pathogenesis
• About (10 billion) virions are produced daily
• Average life-span of an HIV virion in plasma is
~6 hours
• Average life-span of an HIV-infected CD4
lymphocytes is ~1.6 days
• HIV hides in cells like CNS etc and can lie
dormant within a cell for many
years, especially in resting (memory) CD4
cells, unlike other retroviruses etc

48. Pathogenesis
• All elements of immune system are affected.
Advanced stages of HIV are associated with
destruction and disruption of lymphoid tissue(T-
helper cells etc) that result in
• Impaired ability to mount immune response
• Impaired ability to maintain memory responses
• Loss of containment of HIV replication
• ultimately results in severe immunosuppression
susceptibility to opportunistic infections

49. HIV Life Cycle
• Step 1: Attachment of
virus at the CD4
receptor and
chemokine co-receptors
CXCR4 or CCR5

50. HIV Life Cycle
• Step 2: viral fusion and
uncoating

51. HIV Life Cycle
• Steps 3-5: Reverse
transcriptase makes a
single DNA copy of the
viral RNA and then
makes another to form
a double stranded viral
DNA

52. HIV Life Cycle
• Step 6: migration to
nucleus

53. HIV Life Cycle
• Steps 7-8: Integration
of the viral DNA into
cellular DNA by the
enzyme integrase

54. HIV Life Cycle
• Steps 9-11:
Transcription and RNA
processing

55. HIV Life Cycle
• Steps 12-13:
Protein synthesis

56. HIV Life Cycle
• Step 14: protease
cleaves polypeptides
into functional HIV
proteins and the virion
assembles
• Step 15: virion budding
• Step 16: Virion
maturation

58. HIV Life Cycle

60. Window period
• The window period begins at the time of
infection and can last 4 to 8 weeks.
• During this period, a person is
infected, infectious and viremic, with a high
viral load and a negative HIV antibody test.
• The point when the HIV antibody test
becomes positive is called the point of
seroconversion.

61. Window Period
• Some times 90 percent of cases test positive
within three months of exposure
• 10 percent of cases test positive within three
to six months of exposure

62. When to suspect patient has HIV-AIDS
• Flu-like Symptoms
• When a person is first infected by the HIV
virus, he typically develops flu-like symptoms.
Since the symptoms are typically mild, most
people do not seek medical help and, if they
do, most doctors don't initially suspect HIV
because these symptoms are common for so
many diseases.

63. When to suspect patient has HIV-AIDS
• However suspicion is raised if its difficult to
treat such mild symptoms and is frustrating to
the clinician to treat such cases. Patient takes
time and relief seems delayed.

64. When to suspect patient has HIV-AIDS
• Similarly by passage of some years there may
be prolonged fever not responding to routine
drugs or a prolonged diarrhoea or weight loss
or swollen lymph glands all not responding to
routine treatment.

65. When to suspect patient has HIV-AIDS
• Clinician finds it difficult to treat such simple
cases. It is at this point one should suspect
something serious underlying disease patient
might be suffering from probably AIDS. Which
may be supported by history of sexual
promiscuity.

66. When to suspect patient has HIV-AIDS
• Or there may be no symptoms at all from the
very beginning over many years may be upto
10 years and are not typically aware that they
have HIV.

67. When to suspect patient has HIV-AIDS
• Finally over years around 10 years patient's
CD4 lymphocyte count is fewer than 200 cells
per cubic mm of blood, he begins to suffer
from so-called opportunistic infections and
thus meets the official definition for AIDS.
• Based on above facts HIV-AIDS can be divided
into four stages

68. Four Stages of HIV

69. Stage 1 - Primary
• Short, flu-like illness - occurs one to six weeks
after infection
• Or there may be no symptoms at all
• Infected person though looking normal can
infect other people

70. Stage 2 - Asymptomatic
• Lasts for an average of ten years
• This stage is free from symptoms
• There may be swollen glands
• The level of HIV in the blood drops to very low
levels
• HIV antibodies are detectable in the blood

71. Stage 3 - Symptomatic
• The symptoms are now moderate more often
and prolonged
• The immune system deteriorates

72. Stage 4 - HIV  AIDS
• The immune system weakens
• The illnesses become more severe leading to
emergence of opportunistic infections and
cancers
• A full blown AIDS has developed now

73. AIDS-DEFINING DISEASES
• Oesophageal candidiasis
• Cryptococcal meningitis
• Chronic cryptosporidial diarrhoea
• CMV retinitis or colitis
• Chronic mucocutaneous herpes simplex
• Disseminated Mycobacterium avium
intracellulare
• Pulmonary or extrapulmonary tuberculosis
• Pneumocystis carinii (jirovecii) pneumonia

74. AIDS-DEFINING DISEASES
• Progressive multifocal leucoencephalopathy
• Recurrent non-typhi Salmonella septicaemia
• Cerebral toxoplasmosis
• Extrapulmonary coccidioidomycosis
• Invasive cervical cancer
• Extrapulmonary histoplasmosis
• Kaposi's sarcoma
• Non-Hodgkin lymphoma
• Primary cerebral lymphoma
• HIV-associated wasting
• HIV-associated dementia

78. Oral Candidiasis (thrush)

79. Opportunistic Oral Yeast Infection by Candida
albicans in an AIDS Patient

80. Chronic Herpes Simplex infection with lesions on tongue and lips.
.

83. Oral Hairy Leukoplakia
• Being that HIV reduces immunologic activity, the intraoral
environment is a prime target for chronic secondary infections
and inflammatory processes, including OHL, which is due to
the Epstein-Barr virus under immunosuppressed conditions

90. Kaposi’s sarcoma (KS)
• Kaposi’s sarcoma (shown) is
a rare cancer of the blood
vessels that is associated
with HIV. It manifests as
bluish-red oval-shaped
patches that may eventually
become thickened. Lesions
may appear singly or in
clusters.

91. Extensive tumor lesions of Kaposi's sarcoma in AIDS patient.

98. Pneumocystis pneumonia
• X-ray of Pneumocystis
jirovecii caused
pneumonia. There is
increased white
(opacity) in the lower
lungs on both
sides, characteristic of
Pneumocystis
pneumonia

99. Pneumocystis pneumonia
• Pneumocystis pneumonia
(originally known as
Pneumocystis carinii
pneumonia, and still
abbreviated as PCP, which
now stands for
Pneumocystis pneumonia)
is relatively rare in
healthy, immunocompetent
people, but common among
HIV-infected individuals. It is
caused by Pneumocystis
jirovecii.

101. Non-Hodgkin’s Lymphoma & ascites in AIDS patient

102. African AIDS patient with slim disease

103. Blood Detection Tests
• Enzyme-Linked Immunosorbent Assay/Enzyme
Immunoassay (ELISA/EIA)
• Radio Immunoprecipitation Assay/Indirect
Fluorescent Antibody Assay (RIP/IFA)
• Polymerase Chain Reaction (PCR)
• Western Blot Confirmatory test

104. Immunologic Manifestations
• Antibodies are produced to all major antigens.
– First antibodies detected produced against gag
proteins p24 and p55.
– Followed by antibody to p51, p120 and gp41
– As disease progresses antibody levels decrease.

105. ELISA Testing
• First serological test developed to detect HIV
infection.
– Easy to perform.
– Easily adapted to batch testing.
– Highly sensitive and specific.
• Antibodies detected in ELISA include those
directed against: p24, gp120, gp160 and
gp41, detected first in infection and appear in
most individuals

106. Western Blot
• Most popular confirmatory test.
– Utilizes a lysate prepared from HIV virus.
– The lysate is electrophoresed to separate out the HIV
proteins (antigens).
– The paper is cut into strips and reacted with test sera.
– After incubation and washing anti-antibody tagged with
radioisotope or enzyme is added.
– Specific bands form where antibody has reacted with
different antigens.
– Most critical reagent of test is purest quality HIV antigen.
– The following antigens must be present:
p17, p24, p31, gp41, p51, p55, p66, gp120 and gp160.

107. Western Blot
• Antibodies to p24 and p55 appear earliest but
decrease or become undetectable.
• Antibodies to gp31, gp41, gp 120, and gp160
appear later but are present throughout all
stages of the disease.

108. Western Blot
• Interpretation of results.
– No bands, negative.
– In order to be interpreted as positive a minimum
of 3 bands directed against the following antigens
must be present: p24, p31, gp41 or gp120/160.
• CDC criteria require 2 bands of the following:
p24, gp41 or gp120/160.

109. Western Blot
• Expensive – $ 80 - 100
• technically more difficult
• visual interpretation
• lack standardisation
– - performance
– - interpretation
– - indeterminate reactions –
resolution of ??
• ‘Gold Standard’ for
confirmation

110. Virus isolation
• Virus isolation can be used to definitively diagnose
HIV.
• Best sample is peripheral blood, but can use
CSF, saliva, cervical secretions, semen, tears or
material from organ biopsy.
• Cell growth in culture is stimulated, amplifies
number of cells releasing virus.
• Cultures incubated one month, infection confirmed
by detecting reverse transcriptase or p24 antigen in
supernatant.

111. Urine Testing
• Urine Western Blot
– As sensitive as testing blood
– Safe way to screen for HIV
– Can cause false positives in
certain people at high risk for
HIV

112. Oral Testing
Orasure
– The only FDA approved
HIV antibody.
– As accurate as blood
testing
– Draws blood-derived
fluids from the gum
tissue.
– NOT A SALIVA TEST!

113. Indirect immunofluorescence
• Can be used to detect both virus and antibody
to it.
• Antibody detected by testing patient serum
against antigen applied to a
slide, incubated, washed and a fluorescent
antibody added.
• Virus is detected by fixing patient cells to
slide, incubating with antibody.

115. Polymerase Chain Reaction (PCR)
• Looks for HIV DNA in the WBCs of a person.
• PCR amplifies tiny quantities of the HIV DNA present, each
cycle of PCR results in doubling of the DNA sequences
present.
• The DNA is detected by using radioactive or biotinylated
probes.
• Once DNA is amplified it is placed on nitrocellulose paper and
allowed to react with a radiolabeled probe, a single stranded
DNA fragment unique to HIV, which will hybridize with the
patient’s HIV DNA if present.
• Radioactivity is determined.

116. Virus isolation
• Virus isolation can be used to definitively diagnose
HIV.
• Best sample is peripheral blood, but can use
CSF, saliva, cervical secretions, semen, tears or
material from organ biopsy.
• Cell growth in culture is stimulated, amplifies
number of cells releasing virus.
• Cultures incubated one month, infection confirmed
by detecting reverse transcriptase or p24 antigen in
supernatant.

117. Viral Load Tests
• Viral load or viral burden is the quantity of
HIV-RNA that is in the blood.
• RNA is the genetic material of HIV that
contains information to make more virus.

118. Viral Load Tests
• Viral load tests measure the amount of HIV-RNA in
one milliliter of blood.
• Take 2 measurements 2-3 weeks apart to determine
baseline.
• Repeat every 3-6 months in conjunction with CD4
counts to monitor viral load ant T-cell count.
• Repeat 4-6 weeks after starting or changing
antiretroviral therapy to determine effect on viral
load.

119. Testing of Neonates
• Difficult due to presence of maternal IgG
antibodies.
• Use tests to detect IgM or IgA antibodies, IgM
lacks sensitivity, IgA more promising.
• Measurement of p24 antigen.
• PCR testing may be helpful but still not
detecting antigen soon enough: 38 days to 6
months to be positive.

120. INVESTIGATIONS UNDER DIFFERENT
CONDITIONS
To all:
CD4 count and Viral load
Hepatitis B and C Ab
HIVResistant Test
Cervical Smear in women
Hep A IgG Antibody
Toxoplasma Ab
Cytomegalovirus Ig G Ab
Treponema Serology
Genitourinary Medicine Screen

121. INVESTIGATIONS UNDER DIFFERENT
CONDITIONS
For CD4 < 200/mm3
• CXR
• HCV-RNA
• Cryptococcal Ag
• Stool for Ova ,cyst and parasites.
For CD4 < 100/mm3
• CMV –PCR
• Dilated Fundoscopy
• Electroencephalogram(EEG)
• Mycobacterial Blood Culture

122. Who Should be Treated
• HIV ELISA positive, confirmed with Western
blot
• HIV RNA >55,000 copies/ml
• CD4 <350 cells/mm3
• Special considerations:
– Pregnant women
– Acute HIV infection
– Exposed healthcare workers

123. Who Should be Treated
• Viral load is an indication of the amount of
virus in the bloodstream in HIV infection
• The viral load can also serve as a means to
identify when HAART should be started.
HAART is commenced when the CD4 cell
count is less than 350 cells/mm3, sometimes
as low as 200 cells/mm3.

124. Who Should be Treated
• Considering starting HAART based on the viral
load, however, is not as simple and many
doctors may advise patients on HAART with a
viral anywhere between 10,000 to 30,000
copies/mL

125. Who Should be Treated
• A viral load exceeding 10,000 copies is
considered to be high. A viral load below 500
copies/mL is considered as low. However, a
level below 500 copies/mL is a good indication
that viral replication has drastically slow or
ceased.

126. Who Should be Treated
• An undetectable viral load is reported when
the level drops to below 50 copies/ milliliter.
This does not mean that the virus has been
eradicated from the bloodstream or that the
patient is “cured”.

127. Who Should be Treated
• The viral RNA may just be below the threshold
and cannot be detected. Eventually the viral
load will rise again and regular monitoring
even with an undetectable viral load is
therefore essential. The aim of treatment is to
maintain the viral load at undetectable levels
as long as possible.

128. Who Should be Treated
• When the CD4 count drops below 200 due to
advanced HIV disease, a person is diagnosed
with AIDS. A normal range for CD4 cells is
between 500 and 1,500.
• Usually, when a person with low CD4 cells
starts HIV medicines, the CD4 cell count
increases as the HIV virus is controlled.

129. Who Should be Treated
• The same test that measures your CD4 count
usually includes a CD8 cell count, too. CD8
cells (also known as CD8+ T cells) are another
type of white blood cell that seek out and
destroy cells infected with viruses, including
HIV-infected cells.

130. Who Should be Treated
• CD8 counts in normal person are between 375
and 1100
• The ratio of CD4 cells to CD8 cells is often
reported. This is calculated by dividing the CD4
value by the CD8 value. In healthy people, this
ratio is between 0.9 and 1.9, meaning that there
are about 1 to 2 CD4 cells for every CD8 cell. In
people with HIV infection, this ratio drops
dramatically, meaning that there are many times
more CD8 cells than CD4 cells.

131. When to start drugs to prevent
opportunistic infections
• when CD4 levels are:
• •Less than 200: Pneumocystis pneumonia
(PCP)
• •Less than 100: toxoplasmosis and
cryptococcosis
• •Less than 75: mycobacterium avium complex
(MAC).

132. Combination Therapy
• Combination therapy often called HAART is standard
care for people with HIV.
• Monotherapy created virus resistance to the
individual drug. Some combination therapies
increase the time it takes for the virus to become
resistant.
• Combinations of a PI or NNRTI with one or two
NRTI’s is often recommended.
• Combination therapy may reduce individual drug
toxicity by lowering the dosage of each drug

133. Treatment
 HAART: Highly Affective Anti-Retro Viral
Therapy:
 Anti-retro viral therapy is recommended if:
► Patient is asymptomatic/ symptomatic + CD4 count
of <350/µl / any AIDS defining condition / plasma HIV
RNA greater than 100,000 copies/ml
 HAART combines two types of antiretroviral drugs:
Triple cocktail
◦ 2NRTI’S + 1PI or
◦ 2NRTI’S + 1NNRTI

134. Treatment
► Entry inhibitors/Fusion inhibitors: Maraviroc, Enfuvirtide
• Integrase inhibitors: Raltegravir
• Maturation Inhibitors under trails: Bevirimat & vivicon

135. Treatment
 For needle stick: Post exposure Prophylaxis
 ZDV+3TC 28 days, but in high risk (high viral RNA copies) a combination of
ZDV+3TC+Indinavir
 Pregnancy:
 ZDV full dose, trimester 2 and 3+ 6 weeks to neonate reduces vertical transmission
by 80%
 ZDV restricted to intrapartum period + NEVIRAPINE- 1 dose at onset of delivery+
AZT+3TC for 1 week after delivery
 Neonate: 1 dose of Nevirapine within 24-72 hrs after birth + ZDV for 1 week
 Symptomatic tx and antibiotics/antivirals/glucocorticoids/thalidomide
/antifungals/metronidazole for bacterial, viral, autoimmune, fungal and parasitic
infections.

136. HAART (highly active antiretroviral therapy)
• Four approved classes of drugs in the HAART
regimens
– Nucleoside and nucleotide reverse transcriptase
inhibitors
– Non-nucleoside reverse transcriptase inhibitors
– Protease inhibitors
– Fusion inhibitors

137. Currently Available Drugs
• Nucleoside analogue reverse transcriptase inhibitors
– Zidovudine
– Lamivudine
– Stavudine
– Didanosine
– Zalcitabine
– Abacavir
• Nucleotide …
– Tenofovir

138. Currently Available Drugs
• Non-nucleoside reverse transcriptase inhibitors
– Nevirapine
– Delavridine
– Efavirenz
• Fusion Inhibitors
– Enfuvirtide

139. Currently Available Drugs
• Protease Inhibitors
• Indinavir
• Nelfinavir
• Ritonavir
• Saquinavir soft gel
• Amprenavir
• Lopinavir/ritonavir
• Amprenavir/ritonavir

140. What is the Best Initial Treatment
• What we know
– Two is better than one
– Three is better than two
• What we are trying to find out
– Is four better than three????

141. Choice of Initial Regimen
2 NRTI 1 PI
2 NRTI 1 NNRTI
3 NRTI 3rd NRTI is abacavir
2 NRTI 1 nucleotide RTI
(Tenofovir)
2 NRTI 2 PI (ritonavir as
booster)

142. Choice of Regimen
• NNRTIs • PIs
• Nevirapine (2 tab) • Indinavir (6 or 12 cap)
• Efavirenz (3 cap) • Nelfinavir (10 tab)
• Ritonavir (don’t even go
• Delavridine (6 or
there)
12)
• Saquinavir soft gel (18
cap)
• Amprenavir (16 cap)
• Lopinavir/ritonavir (6
cap)

143. Averting Failure — Promote Adherence
• HAART has increased long-term survival of patients with HIV
– Before HAART, median survival: 8 to 10 years
– After HAART, median survival: may be 36 years
• Drug “holidays” or treatment interruptions result in
rapid viral rebound within 2 to 3 weeks of
treatment discontinuation
• Simplification of dosing regimens to twice or once
daily may improve long-term adherence

144. Summary
• When to start treatment
• CD4<350
• VL> 55,000
• Choice of initial regimen
• 3 drugs
• Appropriate prophylaxis
• Primary: PCP, MAC
• Secondary: PCP, MAC, Toxo, candidiasis, CMV, etc.

145. Nucleoside Analogues (NA’s) or
NRTI’s
Abbreviated Generic Name Trade Name Dose
Name
AZT Zidovudine Retrovir 200 mg TID
300 mg BID
ddI Didanosine Videx 200 mg BID
400 mg QD
ddC Zalcitibine Hivid 0.75 mg TID
d4T Stavudine Zerit 20 mg BID
40 mg BID
3TC Lamivudine Epivir 150 mg BID
AZT/3TC Combivir One BID
ABC Abacavir Ziagen 300 mg BID
AZT/3TC/ABC Trizivir One BID

146. Nucleotide Analogues
• Tenofovir
• Dose: 300 mg once daily
• Take with food for optimal absorption

147. Non-Nucleoside Reverse Transcriptase Inhibitors
(NNRTI’s)
Generic Name Trade Name Usual Dose
Nevirapine Viramune 200 mg QD x14
days, then
200 mg BID
Delavirdine Rescriptor 400 mg TID
Efavirenz SustivaTM 600 mg QD

148. Protease Inhibitors (PI’s)
Generic Name Trade Name Usual Dose
Saquinavir Invirase 400 mg BID with RTV
Fortovase 1200 mg TID
Indinavir Crixivan 800 mg q8h
Ritonavir Norvir 600 mg BID
400 mg BID with SQV
Nelfinavir Viracept 750 mg TID or
1250 mg BID
TM
Amprenavir Agenerase 1200 mg BID
TM
Lopinavir/ Kaletra 400 mg lopinavir/100 mg ritonavir
Ritonavir BID= 3 caps BID

149. Some Alternative Therapies
• Virus adsorption inhibitors – interfere with
virus binding to cell surface by shielding the
positively charged sites on the gp-120
glycoprotein
– Polyanionic compounds
• Viral co receptor antagonists – compete for
binding at the CXCR4 (X4) and CCR5 (R5)
coreceptors
– bicyclams and ligands

150. HIV Occupational Exposure
• Review facility policy and report the incident
• Medical follow-up is necessary to determine
the exposure risk and course of treatment
• Baseline and follow-up HIV testing
• Four week course of medication initiated one to
two hours after exposure
• AZT (200mg)-TID +lamivudine(3TC)(150mg)BID
x 4days
• Nelfinavir (750 mg) TID ,AZT/3TC
• Exposure precautions practiced

151. Why Does Treatment Fail?
• Intolerance
• Infection with a resistant virus
• Malabsorption
• NON-ADHERENCE TOPS THE LIST
– Rates of adherence have a direct correlation
with success of HAART1
– Near perfect viral suppression in DOT trials2

152. Averting Failure — Promote Adherence
• HAART has increased long-term survival of patients with HIV
– Before HAART, median survival: 8 to 10 years
– After HAART, median survival: may be 36 years
• Drug “holidays” or treatment interruptions result in
rapid viral rebound within 2 to 3 weeks of
treatment discontinuation
• Simplification of dosing regimens to twice or once
daily may improve long-term adherence

153. Prevention and control of HIV
• Education
• Prevention of blood born HIV transmission
• Anti Retro Viral treatment
• Combination therapy
• Post exposure prophylaxis
• Specific prophylaxis
• Primary health care

154. Four ways to protect yourself?
• Abstinence
• Monogamous Relationship
• Protected Sex
• Sterile needles

155. Protected Sex
• Use condoms (female or male) every time you
have sex (vaginal or anal)
• Always use latex or polyurethane condom (not a
natural skin condom)
• Always use a latex barrier during oral sex

156. When Using A Condom
Remember To:
• Make sure the package is not expired
• Make sure to check the package for damages
• Do not open the package with your teeth for
risk of tearing
• Never use the condom more than once
• Use water-based rather than oil-based
condoms

157. THANK YOU
• There is no end to education. It is not that
you read a book, pass an examination, and
finish with education. The whole of life, from
the moment you are born to the moment you
die, is a process of learning.

158. Thank You again
• Any question ?
• or
• Doubt !
• EMAIL AT- (drbashir123@gmail.com)